var title_f0_45_720="Cholangioscopy-directed biopsy";

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" Cholangioscopy-directed biopsy of a stricture",
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" <div class=\"lgnd\">",
" Fiberoptic cholangioscopy showing biopsy forceps obtaining a tissue sample
from an ulcerated stricture due to cholangiocarcinoma.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" </div>",
" </div>",
" </div>",
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" </div>",
" <div class=\"lgnd\">",
" Barium radiograph in a patient with small bowel scleroderma and pseudo-
obstruction syndrome reveals a dilated post-bulbar duodenum (megaduodenum) and
jejunum, with infiltrated valvulae conniventes (white arrow) in the lower jejunal
loop.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Courtesy of Michael Camilleri, MD.",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
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var outline_f0_45_721=null;
var title_f0_45_722="Port wine stain - V2 child";
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" ^{",
" &reg;",
"}",
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title=\"Email graphic(s)\"/>",
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" <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
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" </div>",
" <div class=\"graphic\">",
" <div class=\"figure\" style=\"width: 470px\">",
" <div class=\"ttl\">",
" Port wine stain",
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" </div>",
" <div class=\"lgnd\">",
" A port wine stain, represented by an erythematous patch, is present in the V2
distribution on the face of this child.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Reproduced with permission from: www.visualdx.com. Copyright Logical Images,
Inc.",
" </div>",
" </div>",
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var outline_f0_45_722=null;
var title_f0_45_723="EBUS tissue core";
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" <div class=\"lgnd\">",
" Tissue core obtained by endobronchial ultrasound-guided sampling.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" </div>",
" </div>",
" </div>",
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" <div class=\"lgnd\">",
" <div class=\"footnotes\">",
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var script_f0_45_724=[""].join("\n");
var outline_f0_45_724=null;
var title_f0_45_725="Acute subacute paracocci";
var content_f0_45_725=[" <div id=\"graphicsToolbar\">",
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" &copy;2013 UpToDate",
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" </div>",
" <div class=\"graphic\">",
" <div class=\"figure\" style=\"width: 470px\">",
" <div class=\"ttl\">",
" Clinical presentations of acute/subacute paracoccidioidomycosis",
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" </div>",
" <div class=\"lgnd\">",
" Young adults with acute/subacute paracoccidioidomycosis. A. Lymphadenopathy in
the supraclavicular, cervical, and submandibular regions. B. The lymphadenopathy of
paracoccidioidomycosis must be differentiated from hematologic diseases, such as
lymphoma. C. Ulcerating lesions on the cheek and near the ear with a verrucous
appearance resulting from hematologic dissemination. D. Papulonodular and
ulcerating lesions resulting from hematologic dissemination.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Reproduced with permission from: Shikanai-Yasuda, MA, Queiroz Telles Filho,
F, Mendes, RP, et al. Consenso em paracoccidioidomicose [Guidelines in
paracoccidioidomycosis]. Revista da Sociedade Brasileira de Medicina Tropical 2006;
39:297-310. Copyright &copy;2006 Sociedade Brasileira de Medicina Tropical.",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
var script_f0_45_725=[""].join("\n");
var outline_f0_45_725=null;
var title_f0_45_726="NHLBI pediatric risk stratification associated with CVD";
var content_f0_45_726=[" <div id=\"graphicsToolbar\">",
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" &copy;2013 UpToDate",
" ^{",
" &reg;",
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" </div>",
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" <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
title=\"Print this page\"/>",
" </a>",
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%2F54963&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\"
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" Print",
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" <a class=\"etacLink\" href=\"#\">",
" <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
title=\"Email graphic(s)\"/>",
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" <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
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" </div>",
" <div class=\"graphic\">",
" <div class=\"figure\" style=\"width: 626px\">",
" <div class=\"ttl\">",
" Risk stratification and management for children with conditions predisposing
to accelerated atherosclerosis and early cardiovascular disease from the 2011 NHLBI
Expert Panel",
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" </div>",
" <div class=\"lgnd\">",
" <strong>",
" Step 1:",
" </strong>",
" Risk stratification by disease state or condition.",
" <br/>",
" <strong>",
" Step 2:",
" </strong>",
" Assess all cardiovascular risk factors. If there are &ge;2 comorbidities, move
tier II patient to tier I for subsequent management.",
" <br/>",
" <strong>",
" Step 3:",
" </strong>",
" Tier-specific treatment goals/cut points defined.",
" <br/>",
" <strong>",
" Step 4:",
" </strong>",
" Initial therapy: For tier I, initial management is therapeutic lifestyle
change PLUS disease-specific management. For tier II, initial management is
therapeutic lifestyle change.",
" <br/>",
" <strong>",
" Step 5:",
" </strong>",
" For tier I conditions, if goals are not met, consider pharmacological
therapy.",
" <div class=\"footnotes\">",
" CVD: cardiovascular disease; NHLBI: National Heart, Lung, and Blood
Institute; CV: cardiovascular; LDL-C: low-density lipoprotein cholesterol; HDL-C:
high-density lipoprotein cholesterol; TG: triglycerides; BP: blood pressure; BMI:
body mass index; HgbA1c: hemoglobin A1c.",
" </div>",
" <div class=\"reference\">",
" Reproduced from: Daniels SR, Benuck I, Christakis DA, et al. Expert panel on
integrated guidelines for cardiovascular health and risk reduction in children and
adolescents: Full report, 2011. National Heart Lung and Blood Institute. Available
at: file://www.nhlbi.nih.gov/guidelines/cvd_ped/peds_guidelines_full.pdf.",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
var script_f0_45_726=[""].join("\n");
var outline_f0_45_726=null;
var title_f0_45_727="Items for nasal foreign body removal";
var content_f0_45_727=[" <div id=\"graphicsToolbar\">",
" <div id=\"graphicsCopy\">",
" &copy;2013 UpToDate",
" ^{",
" &reg;",
"}",
" </div>",
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" <a href=\"?imageKey=EM
%2F86450&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=2\" onclick=\"\">",
" <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
title=\"Print this page\"/>",
" </a>",
" <a class=\"icontxt textLink\" href=\"?imageKey=EM
%2F86450&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=2\" onclick=\"\"
title=\"Print this page\">",
" Print",
" </a>",
" <a class=\"etacLink\" href=\"#\">",
" <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
title=\"Email graphic(s)\"/>",
" </a>",
" <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
" Email",
" </a>",
" </div>",
" </div>",
" <div class=\"graphic\">",
" <div class=\"figure\" style=\"width: 610px\">",
" <div class=\"ttl\">",
" Instruments and topical anesthetic for nasal foreign body removal",
" </div>",
" <div class=\"cntnt\" style=\"width: 590px; height: 440px; background-image:
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" </div>",
" <div class=\"lgnd\">",
" The headlamp frees both hands for instrumentation. When dosing the lidocaine
and oxymetazoline mixture ensure no more than&nbsp;1 mg/kg (0.1 mL per kg of the 2
percent lidocaine mixture) is administered. Instruments pictured from top to
bottom: right angle Day hook,&nbsp;Lucae bayonet forceps, alligator forceps.",
" <div class=\"footnotes\">",
" %: percent.",
" </div>",
" <div class=\"reference\">",
" Courtesty of Glenn C Isaacson, MD.",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
var script_f0_45_727=[""].join("\n");
var outline_f0_45_727=null;
var title_f0_45_728="Famotidine: Drug information";
var content_f0_45_728=[" <noscript>",
" <div id=\"javascriptDisabled\">",
" It seems to us that you have your JavaScript turned off on your browser.
JavaScript is required in order for our site to behave correctly. Please enable
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" </noscript>",
" <div id=\"printHeader\">",
" <div id=\"printHeaderLogo\">",
" <img alt=\"UpToDate\" src=\"./../images/wk_utd-rgb.myextg\" width=\"220px\">",
" </img>",
" </div>",
" <div id=\"printHeaderText\">",
" Official reprint from UpToDate",
" ^{",
" &reg;",
"}",
" <a href=\"file://www.uptodate.com\">",
" www.uptodate.com",
" </a>",
" <br>",
" &copy;2013 UpToDate",
" ^{",
" &reg;",
"}",
" </br>",
" </div>",
" <div id=\"printHeaderLinks\">",
" <a class=\"TOPIC\" href=\"#\" id=\"printHeaderPrint\" rel=\"2\" title=\"Click
here to print\">",
" Print",
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" |",
" </span>",
" <a href=\"#\" id=\"printHeaderBack\" title=\"Back to normal view\">",
" Back",
" </a>",
" </div>",
" </div>",
" <!-- TC:TOPIC_PAGE -->",
" <div id=\"topicContent\">",
" <div id=\"drugTitle\">",
" Famotidine: Drug information",
" </div>",
" <div id=\"lexiTitleImg\">",
" <img height=\"17\" src=\"./../images/lexiComp/Lexicomp_2012_71x17.myextg\"
width=\"71\"/>",
" </div>",
" <div class=\"clear\">",
" </div>",
" <div id=\"drugCopy\">",
" Copyright 1978-2013 Lexicomp, Inc. All rights reserved.",
" </div>",
" <div id=\"topicText\">",
" (For additional information",
" <a class=\"drug drug_patient\" href=\"UTD.htm?16/10/16549?source=see_link\">",
" see \"Famotidine: Patient drug information\"",
" </a>",
" and",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/61/29655?
source=see_link\">",
" see \"Famotidine: Pediatric drug information\"",
" </a>",
" )",
" <br/>",
" For abbreviations and symbols that may be used in Lexicomp (",
" <a class=\"graphic graphic_table\" href=\"UTD.htm?23/39/24183\">",
" show table",
" </a>",
" )",
" <div class=\"list ubnlist drugH1Div drugBrandNames\" id=\"F169927\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Brand Names: U.S.",
" </span>",
" <ul>",
" <li>",
" Heartburn Relief Maximum Strength [OTC];",
" </li>",
" <li>",
" Heartburn Relief [OTC];",
" </li>",
" <li>",
" Pepcid&reg;;",
" </li>",
" <li>",
" Pepcid&reg; AC Maximum Strength [OTC];",
" </li>",
" <li>",
" Pepcid&reg; AC [OTC]",
" </li>",
" </ul>",
" </div>",
" <div class=\"list cbnlist drugH1Div drugBrandNames\" id=\"F169928\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Brand Names: Canada",
" </span>",
" <ul>",
" <li>",
" Acid Control;",
" </li>",
" <li>",
" Apo-Famotidine&reg;;",
" </li>",
" <li>",
" Apo-Famotidine&reg; Injectable;",
" </li>",
" <li>",
" Famotidine Omega;",
" </li>",
" <li>",
" Mylan-Famotidine;",
" </li>",
" <li>",
" Novo-Famotidine;",
" </li>",
" <li>",
" Nu-Famotidine;",
" </li>",
" <li>",
" Pepcid&reg;;",
" </li>",
" <li>",
" Pepcid&reg; AC;",
" </li>",
" <li>",
" Pepcid&reg; I.V.;",
" </li>",
" <li>",
" Ulcidine",
" </li>",
" </ul>",
" </div>",
" <div class=\"ex_sect_xr thclist drugH1Div drugBrandNames\" id=\"F169978\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Pharmacologic Category",
" </span>",
" <ul>",
" <li>",
" Histamine H",
" _{",
" 2",
"}",
" Antagonist",
" </li>",
" </ul>",
" </div>",
" <div class=\"block doa drugH1Div\" id=\"F169931\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Dosing: Adult",
" </span>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Duodenal ulcer:",
" </b>",
" Oral: Acute therapy: 40 mg/day at bedtime (or 20 mg twice daily) for 4-8
weeks; maintenance therapy: 20 mg/day at bedtime",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Gastric ulcer:",
" </b>",
" Oral: Acute therapy: 40 mg/day at bedtime",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" GERD:",
" </b>",
" Oral: 20 mg twice daily for 6 weeks",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Hypersecretory conditions:",
" </b>",
" Oral: Initial: 20 mg every 6 hours, may increase in increments up to 160 mg
every 6 hours",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Esophagitis and accompanying symptoms due to GERD:",
" </b>",
" Oral: 20 mg or 40 mg twice daily for up to 12 weeks",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Peptic ulcer disease: Eradication of",
" </b>",
" <b>",
" <i>",
" Helicobacter pylori",
" </i>",
" </b>",
" <b>",
" (unlabeled use):",
" </b>",
" Oral: 40 mg once daily; requires combination therapy with antibiotics",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Stress ulcer prophylaxis (unlabeled use; ASHP, 1999):",
" </b>",
" Oral, I.V., or nasogastric (NG) tube: 20 mg twice daily;",
" <b>",
" Note:",
" </b>",
" Intended for patients with associated risk factors (eg, coagulopathy,
mechanical ventilation for &gt;48 hours, severe sepsis); discontinue use once risk
factors have resolved.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Patients unable to take oral medication:",
" </b>",
" I.V.: 20 mg every 12 hours",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Heartburn, indigestion, sour stomach:",
" </b>",
" OTC labeling: Oral: 10-20 mg every 12 hours; dose may be taken 15-60 minutes
before eating foods known to cause heartburn",
" </p>",
" </div>",
" <div class=\"block dop drugH1Div\" id=\"F169952\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Dosing: Pediatric",
" </span>",
" <p>",
" (For additional information",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/61/29655?
source=see_link\">",
" see \"Famotidine: Pediatric drug information\"",
" </a>",
" )",
" </p>",
" <p style=\"text-indent:0em;display:inline\">",
" Treatment duration and dose should be individualized",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Peptic ulcer:",
" </b>",
" 1-16 years:",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Oral: 0.5 mg/kg/day at bedtime or divided twice daily (maximum dose: 40
mg/day); doses of up to 1 mg/kg/day have been used in clinical studies",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" I.V.: 0.25 mg/kg every 12 hours (maximum dose: 40 mg/day); doses of up to 0.5
mg/kg have been used in clinical studies",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" GERD:",
" </b>",
" Oral:",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" &lt;3 months: 0.5 mg/kg once daily",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 3-12 months: 0.5 mg/kg twice daily",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 1-16 years: 1 mg/kg/day divided twice daily (maximum dose: 40 mg twice
daily); doses of up to 2 mg/kg/day have been used in clinical studies",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Heartburn, indigestion, sour stomach:",
" </b>",
" OTC labeling: Oral: Children &ge;12 years: Refer to adult dosing.",
" </p>",
" </div>",
" <div class=\"block doe drugH1Div\" id=\"F169932\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Dosing: Geriatric",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Refer to adult dosing.",
" </p>",
" </div>",
" <div class=\"block dor drugH1Div\" id=\"F169933\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Dosing: Renal Impairment",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Cl",
" _{",
" cr",
"}",
" &lt;50 mL/minute: Manufacturer recommendation: Administer 50% of dose",
" <b>",
" or",
" </b>",
" increase the dosing interval to every 36-48 hours (to limit potential CNS
adverse effects).",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;margin-top:0em;text-
align:justify;\">",
" Stress ulcer prophylaxis (ASHP, 1999): Adults: Cl",
" _{",
" cr",
"}",
" &lt;30 mL/minute: Oral, I.V., or nasogastric (NG) tube: 20 mg once daily",
" </p>",
" </div>",
" <div class=\"block foc drugH1Div\" id=\"F169901\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Dosage Forms: U.S.",
" </span>",
" <p style=\"text-indent:0em;text-align:justify;display:inline\">",
" Excipient information presented when available (limited, particularly for
generics); consult specific product labeling.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Infusion, premixed in NS [preservative free]: 20 mg (50 mL)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Injection, solution: 10 mg/mL (4 mL, 20 mL, 50 mL)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Injection, solution [preservative free]: 10 mg/mL (2 mL)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Powder for suspension, oral: 40 mg/5 mL (50 mL)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Pepcid&reg;: 40 mg/5 mL (50 mL) [contains sodium benzoate; cherry-banana-mint
flavor]",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Tablet, oral: 10 mg, 20 mg, 40 mg",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Heartburn Relief: 10 mg",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Heartburn Relief Maximum Strength: 20 mg",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Pepcid&reg;: 20 mg, 40 mg",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Pepcid&reg; AC: 10 mg",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Pepcid&reg; AC Maximum Strength: 20 mg",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Tablet, chewable, oral:",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Pepcid&reg; AC Maximum Strength: 20 mg [berries 'n' cream flavor]",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Pepcid&reg; AC Maximum Strength: 20 mg [cool mint flavor]",
" </p>",
" </div>",
" <div class=\"block geq drugH1Div\" id=\"F169887\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Generic Equivalent Available: U.S.",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Yes: Infusion, Injection, oral suspension, tablet",
" </p>",
" </div>",
" <div class=\"block adm drugH1Div\" id=\"F169904\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Administration",
" </span>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Oral: May administer with antacids.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Suspension: Shake vigorously before use. May be taken without regard to
meals.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Tablet: May be taken without regard to meals.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" I.V.:",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" I.V. push: Inject over at least 2 minutes.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Solution for infusion: Administer over 15-30 minutes.",
" </p>",
" </div>",
" <div class=\"block scp drugH1Div\" id=\"F169985\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Compatibility",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Stable in D",
" _{",
" 5",
"}",
" W, D",
" _{",
" 10",
"}",
" W, LR, fat emulsion 10%, NS, sodium bicarbonate 5%;",
" <b>",
" variable stability (consult detailed reference)",
" </b>",
" in TPN.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Y-site administration: Compatible:",
" </b>",
" Acyclovir, allopurinol, amifostine, aminophylline, amiodarone, ampicillin,
ampicillin/sulbactam, amsacrine, anakinra, anidulafungin, atropine, aztreonam,
bivalirudin, calcium gluconate, caspofungin, cefazolin, cefotaxime, cefotetan,
cefoxitin, ceftazidime, cefuroxime, chlorpromazine, cisatracurium, cisplatin,
cladribine, clindamycin, cyanocobalamin, cyclosporine, cyclophosphamide,
cytarabine, dexamethasone sodium phosphate, dexmedetomidine, dextran 40, digoxin,
diphenhydramine, dobutamine, docetaxel, dopamine, doripenem, doxorubicin,
doxorubicin liposome, doxycycline, droperidol, enalaprilat, ephedrine, epinephrine,
erythromycin lactobionate, esmolol, etoposide phosphate, fenoldopam, filgrastim,
fluconazole, fludarabine, folic acid, gemcitabine, gentamicin, granisetron,
haloperidol, heparin, hetastarch in lactate electrolyte injection (Hextend&reg;),
hydrocortisone sodium succinate, hydromorphone, hydroxyzine, imipenem/cilastatin,
inamrinone, insulin (regular), isoproterenol, labetalol, lidocaine, linezolid,
lorazepam, magnesium sulfate, melphalan, meperidine, methotrexate,
methylprednisolone sodium succinate, metoclopramide, midazolam, morphine,
nafcillin, nicardipine, nitroglycerin, nitroprusside, norepinephrine, ondansetron,
oxacillin, oxaliplatin, oxytocin, paclitaxel, palonosetron, pemetrexed,
phenylephrine, phytonadione, phenytoin, piperacillin, potassium chloride, potassium
phosphate, procainamide, propofol, remifentanil, sargramostim, sodium bicarbonate,
telavancin, teniposide, theophylline, thiamine, thiotepa, ticarcillin/clavulanate
potassium, tirofiban, verapamil, vinorelbine.",
" <b>",
" Incompatible:",
" </b>",
" Amphotericin B cholesteryl sulfate complex, azithromycin, cefepime,
piperacillin/tazobactam, sulfamethoxazole/trimethoprim.",
" <b>",
" Variable (consult detailed reference):",
" </b>",
" Furosemide.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Compatibility in syringe: Incompatible:",
" </b>",
" Ceftriaxone, dexamethasone sodium phosphate.",
" </p>",
" </div>",
" <div class=\"block use drugH1Div\" id=\"F169903\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Use",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Maintenance therapy and treatment of duodenal ulcer; treatment of
gastroesophageal reflux disease (GERD), active benign gastric ulcer; pathological
hypersecretory conditions",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" OTC labeling: Relief of heartburn, acid indigestion, and sour stomach",
" </p>",
" </div>",
" <div class=\"block usu drugH1Div\" id=\"F169974\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Use - Unlabeled",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Part of a multidrug regimen for",
" <i>",
" H. pylori",
" </i>",
" eradication to reduce the risk of duodenal ulcer recurrence; stress ulcer
prophylaxis in critically-ill patients; symptomatic relief in gastritis",
" </p>",
" </div>",
" <div class=\"block mst drugH1Div\" id=\"F7305905\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Medication Safety Issues",
" </span>",
" <div class=\"collapsible\">",
" <span class=\"collapsible-title\">",
" Sound-alike/look-alike issues:",
" </span>",
" <div class=\"collapsible-wrap\">",
" <p style=\"text-indent:-2em;margin-left:4em;\">",
" Famotidine may be confused with FLUoxetine, furosemide",
" </p>",
" </div>",
" </div>",
" </div>",
" <div class=\"block ars drugH1Div\" id=\"F169976\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Adverse Reactions Significant",
" </span>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Note:",
" </b>",
" Agitation and vomiting have been reported in up to 14% of pediatric patients
&lt;1 year of age.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" 1% to 10%:",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Central nervous system: Headache (5%), dizziness (1%)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Gastrointestinal: Diarrhea (2%), constipation (1%), necrotizing enterocolitis
(VLBW neonates; Guillet, 2006)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" &lt;1% (Limited to important or life-threatening): Abdominal discomfort,
acne, agitation, agranulocytosis, allergic reaction, alopecia, anaphylaxis,
angioedema, anorexia, anxiety, arrhythmia, arthralgia, AV block, bronchospasm,
cholestatic jaundice, confusion, conjunctival injection, depression, dry skin,
facial edema, fatigue, fever, flushing, hallucinations, hepatitis, injection site
reactions, insomnia, interstitial pneumonia, leukopenia, libido decreased, liver
function tests increased, muscle cramps, nausea, palpitation, pancytopenia,
paresthesia, pruritus, QT-interval prolongation, rash, seizure, somnolence,
Stevens-Johnson syndrome, taste disorder, tinnitus, thrombocytopenia, torsade de
pointes, toxic epidermal necrolysis, urticaria, vomiting, weakness, xerostomia",
" </p>",
" </div>",
" <div class=\"block coi drugH1Div\" id=\"F169907\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Contraindications",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Hypersensitivity to famotidine, other H",
" _{",
" 2",
"}",
" antagonists, or any component of the formulation",
" </p>",
" </div>",
" <div class=\"block war drugH1Div\" id=\"F169891\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Warnings/Precautions",
" </span>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" <i>",
" Concerns related to adverse effects.",
" </i>",
" </b>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" &bull; Confusion: Reversible confusional states, usually clearing within 3-4
days after discontinuation, have been linked to use. Increased age (&gt;50 years)
and renal or hepatic impairment are thought to be associated.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" &bull; ECG changes: Prolonged QT interval has been reported in patients with
renal dysfunction. The FDA has received reports of torsade de pointes occurring
with famotidine (Poluzzi, 2009).",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" <i>",
" Disease-related concerns:",
" </i>",
" </b>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" &bull; Gastric malignancy: Relief of symptoms does not preclude the presence
of a gastric malignancy.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" &bull; Renal impairment: Use with caution in patients with moderate-to-severe
renal impairment (Cl",
" _{",
" cr",
"}",
" &lt;50 mL/minute); dosage adjustment recommended.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" <i>",
" Dosage form specific issues:",
" </i>",
" </b>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" &bull; Benzyl alcohol: Multidose vials for injection contain benzyl alcohol
which has been associated with \"gasping syndrome\" in neonates.",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" <i>",
" Other warnings/precautions:",
" </i>",
" </b>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" &bull; OTC labeling: When used for self-medication, patients should be
instructed not to use if they have difficulty swallowing, are vomiting blood, or
have bloody or black stools. Not for use with other acid reducers.",
" </p>",
" </div>",
" <div class=\"block cyt drugH1Div\" id=\"F13299312\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Metabolism/Transport Effects",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" None known.",
" </p>",
" </div>",
" <div class=\"block dri drugH1Div\" id=\"F169896\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Drug Interactions",
" </span>",
" <br/>",
" <br/>",
" <div class=\"lexi\" id=\"lexiInteractAddInfo\">",
" (For additional information:",
" <a class=\"dip\" href=\"./drug-interaction\" target=\"_blank\">",
" Launch Lexi-Interact&trade; Drug Interactions Program",
" </a>",
" )",
" </div>",
" <div class=\"lexi\" id=\"lexiInteractImgB\">",
" <img border=\"0\" height=\"17\"
src=\"./../images/lexiComp/Lexicomp_2012_71x17.myextg\" width=\"71\"/>",
" </div>",
" <div class=\"clear\">",
" </div>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Atazanavir: H2-Antagonists may decrease the serum concentration of
Atazanavir. Management: Specific dose limitations and administration guidelines
exist; consult full interaction monograph or atazanavir prescribing information.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Bosutinib: H2-Antagonists may decrease the serum concentration of Bosutinib.
Management: Administer histamine H2 receptor antagonists more than 2 hours before
or after bosutinib.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Cefditoren: H2-Antagonists may decrease the serum concentration of
Cefditoren. Management: Concomitant use of cefditoren with H2-antagonists and
antacids is not recommended. Consider alternative methods to control acid reflux
(eg, diet modification) or alternative antimicrobial therapy if use of H2-
antagonists can not be avoided.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Cefpodoxime: H2-Antagonists may decrease the absorption of Cefpodoxime.
Separate oral doses by at least 2 hours.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Cefuroxime: H2-Antagonists may decrease the absorption of Cefuroxime.
Separate oral doses by at least 2 hours.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Dasatinib: H2-Antagonists may decrease the absorption of Dasatinib.
Management: Antacids (taken 2 hours before or after dasatinib administration) can
be used in place of H2-antagonists if some acid-reducing therapy is needed.",
" <i>",
" Risk X: Avoid combination",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Delavirdine: H2-Antagonists may decrease the serum concentration of
Delavirdine. Management: Chronic therapy with H2-antagonists should be avoided in
patients who are being treated with delavirdine. The clinical significance of
short-term H2-antagonist therapy with delavirdine is uncertain, but such therapy
should be undertaken with caution.",
" <i>",
" Risk X: Avoid combination",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Dexmethylphenidate: H2-Antagonists may increase the absorption of
Dexmethylphenidate. Specifically, H2-antagonists may interfere with the normal
release of drug from the extended-release capsules (Focalin XR brand), which could
result in both increased absorption (early) and decreased delayed absorption.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Erlotinib: H2-Antagonists may decrease the serum concentration of Erlotinib.
Management: Avoid H2-antagonists in patients receiving erlotinib when possible. If
concomitant treatment cannot be avoided, erlotinib should be dosed once daily, 10
hours after and at least 2 hours before H2-antagonist dosing.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Fosamprenavir: H2-Antagonists may decrease the serum concentration of
Fosamprenavir. Cimetidine may also inhibit the metabolism of the active metabolite
amprenavir, making its effects on fosamprenavir/amprenavir concentrations difficult
to predict.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Gefitinib: H2-Antagonists may decrease the serum concentration of
Gefitinib.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Highest Risk QTc-Prolonging Agents: QTc-Prolonging Agents (Indeterminate Risk
and Risk Modifying) may enhance the QTc-prolonging effect of Highest Risk QTc-
Prolonging Agents. Management: Avoid such combinations when possible. Use should
be accompanied by close monitoring for evidence of QT prolongation or other
alterations of cardiac rhythm.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Indinavir: H2-Antagonists may decrease the serum concentration of
Indinavir.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Iron Salts: H2-Antagonists may decrease the absorption of Iron Salts.",
" <b>",
" Exceptions:",
" </b>",
" Ferric Gluconate; Ferumoxytol; Iron Dextran Complex; Iron Sucrose.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Itraconazole: H2-Antagonists may decrease the serum concentration of
Itraconazole. Management: When this combination is used, the itraconazole should
be administered with a cola beverage (8 ounces). Itraconazole oral suspension may
be less sensitive to this interaction. Monitor patient response to itraconazole
closely.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Ketoconazole (Systemic): H2-Antagonists may decrease the serum concentration
of Ketoconazole (Systemic). Management: Administer oral ketoconazole at least 2
hours prior to use of any H2-receptor antagonist. Monitor patients closely for
signs of inadequate clinical response to ketoconazole.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Mesalamine: H2-Antagonists may diminish the therapeutic effect of Mesalamine.
Histamine H2-Antagonist-mediated increases in gastrointestinal pH may cause the
premature release of mesalamine from specific sustained-release mesalamine
products. Management: Consider avoiding concurrent administration of high-dose
histamine H2-receptor antagonists with sustained-release mesalamine products.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Methylphenidate: H2-Antagonists may increase the absorption of
Methylphenidate. Specifically, H2-antagonists may interfere with the normal release
of drug from the extended-release capsules (Ritalin LA brand), which could result
in both increased absorption (early) and decreased delayed absorption.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Mifepristone: May enhance the QTc-prolonging effect of QTc-Prolonging Agents
(Indeterminate Risk and Risk Modifying). Management: Though the drugs listed here
have uncertain QT-prolonging effects, they all have some possible association with
QT prolongation and should generally be avoided when possible.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Moderate Risk QTc-Prolonging Agents: QTc-Prolonging Agents (Indeterminate
Risk and Risk Modifying) may enhance the QTc-prolonging effect of Moderate Risk
QTc-Prolonging Agents.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Multivitamins/Minerals (with ADEK, Folate, Iron): H2-Antagonists may decrease
the serum concentration of Multivitamins/Minerals (with ADEK, Folate, Iron).
Specifically, the absorption of iron may be impaired by H2-antagonists.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Nelfinavir: H2-Antagonists may decrease the serum concentration of
Nelfinavir. Concentrations of the active M8 metabolite may also be reduced.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Nilotinib: H2-Antagonists may decrease the serum concentration of Nilotinib.
Management: Separate the administration of nilotinib and the H2 receptor antagonist
by several hours whenever possible in order to minimize the risk of a significant
interaction.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Ponatinib: H2-Antagonists may decrease the serum concentration of
Ponatinib.",
" <i>",
" Risk X: Avoid combination",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Posaconazole: H2-Antagonists may decrease the serum concentration of
Posaconazole. Management: Avoid concurrent use whenever possible. Monitor
patients closely for decreased antifungal effects if this combination is used.
Consider using a noninteracting antifungal as appropriate.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Rilpivirine: H2-Antagonists may decrease the serum concentration of
Rilpivirine. Management: Administer histamine H2 receptor antagonists at least 12
hours before or 4 hours after rilpivirine.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Risedronate: H2-Antagonists may increase the serum concentration of
Risedronate. This applies specifically to delayed-release risedronate.",
" <i>",
" Risk X: Avoid combination",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Saquinavir: H2-Antagonists may increase the serum concentration of
Saquinavir.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Varenicline: H2-Antagonists may increase the serum concentration of
Varenicline. Management: Monitor for increased varenicline adverse effects with
concomitant use of cimetidine or other H2-antagonists, particularly in patients
with severe renal impairment. International product labeling recommendations vary.
Consult appropriate labeling.",
" <i>",
" Risk C: Monitor therapy",
" </i>",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;\">",
" Vismodegib: H2-Antagonists may decrease the serum concentration of
Vismodegib. Management: Carefully consider the need for any medication that
increases the pH of the upper GI tract (PPIs, H2RAs, antacids), as these could
significantly reduce vismodegib systemic exposure. Vismodegib dose increases are
unlikely to compensate for this effect.",
" <i>",
" Risk D: Consider therapy modification",
" </i>",
" </p>",
" </div>",
" <div class=\"block foi drugH1Div\" id=\"F169924\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Ethanol/Nutrition/Herb Interactions",
" </span>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Ethanol: Avoid ethanol (may cause gastric mucosal irritation).",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Food: Famotidine bioavailability may be increased if taken with food.",
" </p>",
" </div>",
" <div class=\"block prf drugH1Div\" id=\"F169898\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Pregnancy Risk Factor",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" B (",
" <a class=\"graphic graphic_table\" href=\"UTD.htm?16/42/17068\">",
" show table",
" </a>",
" )",
" </p>",
" </div>",
" <div class=\"block pri drugH1Div\" id=\"F169910\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Pregnancy Implications",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Adverse events have not been observed in animal reproduction studies;
therefore, famotidine is classified as pregnancy category B. Famotidine crosses the
placenta. An increased risk of congenital malformations or adverse events in the
newborn has generally not been observed following maternal use of famotidine during
pregnancy. Histamine H",
" _{",
" 2",
"}",
" antagonists have been evaluated for the treatment of gastroesophageal reflux
disease (GERD), as well as gastric and duodenal ulcers, during pregnancy. Although
if needed, famotidine is not the agent of choice. Histamine H",
" _{",
" 2",
"}",
" antagonists may be used for aspiration prophylaxis prior to cesarean
delivery.",
" </p>",
" </div>",
" <div class=\"block lac drugH1Div\" id=\"F169937\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Lactation",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Enters breast milk/not recommended",
" </p>",
" </div>",
" <div class=\"block brc drugH1Div\" id=\"F169911\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Breast-Feeding Considerations",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Famotidine is excreted into breast milk with peak concentrations occurring ~6
hours after the maternal dose. According to the manufacturer, the decision to
continue or discontinue breast-feeding during therapy should take into account the
risk of exposure to the infant and the benefits of treatment to the mother.",
" </p>",
" </div>",
" <div class=\"block dic drugH1Div\" id=\"F9537094\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Dietary Considerations",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" May be taken without regard to meals.",
" </p>",
" </div>",
" <div class=\"block fee drugH1Div\" id=\"F169909\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Pricing: U.S. (Medi-Span&reg;)",
" </span>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Chewable",
" </b>",
" (Pepcid AC Maximum Strength Oral)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 20 mg (25): $9.92",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Chewable",
" </b>",
" (Pepcid AC Oral)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 10 mg (60): $16.98",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Solution",
" </b>",
" (Famotidine Intravenous)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 10 mg/mL (2 mL): $1.07",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Suspension (reconstituted)",
" </b>",
" (Famotidine Oral)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 40 mg/5 mL (50 mL): $176.95",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Suspension (reconstituted)",
" </b>",
" (Pepcid Oral)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 40 mg/5 mL (50 mL): $196.61",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Tablets",
" </b>",
" (Famotidine Oral)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 10 mg (30): $1.62",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 20 mg (100): $173.50",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 40 mg (100): $335.00",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Tablets",
" </b>",
" (Pepcid AC Maximum Strength Oral)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 20 mg (25): $9.92",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Tablets",
" </b>",
" (Pepcid AC Oral)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 10 mg (30): $8.99",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" <b>",
" Tablets",
" </b>",
" (Pepcid Oral)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 20 mg (30): $80.00",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" 40 mg (30): $154.62",
" </p>",
" </div>",
" <div class=\"list fbnlist drugH1Div drugBrandNames\" id=\"F169913\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" International Brand Names",
" </span>",
" <ul>",
" <li>",
" Androtin (MX);",
" </li>",
" <li>",
" Antiflam (UY);",
" </li>",
" <li>",
" Antodine (AE, BH, CY, EG, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SY, YE);",
" </li>",
" <li>",
" Asid (BR);",
" </li>",
" <li>",
" Aulzadin (HK);",
" </li>",
" <li>",
" Ausfam (AU);",
" </li>",
" <li>",
" Denufam (ID);",
" </li>",
" <li>",
" Durater (CR, DO, GT, HN, MX, NI, PA, SV);",
" </li>",
" <li>",
" Facid (ID, IN);",
" </li>",
" <li>",
" Facidex (MX);",
" </li>",
" <li>",
" Fadin (TW);",
" </li>",
" <li>",
" Fadine (AE, BH, CY, EG, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SY, YE);",
" </li>",
" <li>",
" Fadul (DE);",
" </li>",
" <li>",
" Famagen (KP);",
" </li>",
" <li>",
" Famo (IL);",
" </li>",
" <li>",
" Famoc (SG);",
" </li>",
" <li>",
" Famocid (BF, BJ, CI, ET, GH, GM, GN, IN, KE, LR, MA, ML, MR, MU, MW, NE, NG,
SC, SD, SL, SN, TN, TZ, UG, ZM, ZW);",
" </li>",
" <li>",
" Famodar (AE, BH, CY, EG, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SY, YE);",
" </li>",
" <li>",
" Famodil (IT);",
" </li>",
" <li>",
" Famodine (AE, BH, CY, EG, IL, IQ, IR, JO, KW, LB, LY, MY, OM, PK, QA, SA,
SY, YE);",
" </li>",
" <li>",
" Famogal (CO);",
" </li>",
" <li>",
" Famogard (RU);",
" </li>",
" <li>",
" Famohexal (AU);",
" </li>",
" <li>",
" Famonerton (DE);",
" </li>",
" <li>",
" Famosan (CZ, EE, HR);",
" </li>",
" <li>",
" Famosia (TH);",
" </li>",
" <li>",
" Famotin (SG);",
" </li>",
" <li>",
" Famowal (IN);",
" </li>",
" <li>",
" Famox (HK, NZ, TW);",
" </li>",
" <li>",
" Farotin (KP);",
" </li>",
" <li>",
" Ferotine (KP);",
" </li>",
" <li>",
" Fibonel (CN);",
" </li>",
" <li>",
" Fudone (BF, BJ, CI, ET, GH, GM, GN, KE, LR, MA, ML, MR, MU, MW, NE, NG, SC,
SD, SL, SN, TN, TZ, UG, ZM, ZW);",
" </li>",
" <li>",
" Fuweidin (TW);",
" </li>",
" <li>",
" Gasafe (TW);",
" </li>",
" <li>",
" Gaster (CL, JP, TW);",
" </li>",
" <li>",
" Gastren (PY);",
" </li>",
" <li>",
" Gastridin (IT);",
" </li>",
" <li>",
" Gastro (IL);",
" </li>",
" <li>",
" Gastrodomina (BF, BJ, CI, ET, GH, GM, GN, HU, KE, LR, MA, ML, MR, MU, MW,
NE, NG, SC, SD, SL, SN, TN, TZ, UG, ZM, ZW);",
" </li>",
" <li>",
" Gastrum (CO);",
" </li>",
" <li>",
" H2 Bloc (PH);",
" </li>",
" <li>",
" Hista-Bloc (PH);",
" </li>",
" <li>",
" Interfam (HK);",
" </li>",
" <li>",
" Kimodin (TW);",
" </li>",
" <li>",
" Logos (ZA);",
" </li>",
" <li>",
" Ludex (MX);",
" </li>",
" <li>",
" Modin (PH);",
" </li>",
" <li>",
" Motiax (IT);",
" </li>",
" <li>",
" Motidine (HK);",
" </li>",
" <li>",
" Pamacid (AU);",
" </li>",
" <li>",
" Pepcid (BB, BM, BS, BZ, GB, GY, JM, SE, SR, TT);",
" </li>",
" <li>",
" Pepcid AC (CH, IE);",
" </li>",
" <li>",
" Pepcidac (FR);",
" </li>",
" <li>",
" Pepcidin (DK, FI, NL, NO, SE);",
" </li>",
" <li>",
" Pepcidin Rapitab (NO);",
" </li>",
" <li>",
" Pepcidina (PT);",
" </li>",
" <li>",
" Pepcidine (AT, AU, BE, CH, HK, LU, MX, NZ, PE);",
" </li>",
" <li>",
" Pepdif (TR);",
" </li>",
" <li>",
" Pepdine (BF, BJ, CI, ET, FR, GH, GM, GN, KE, LR, MA, ML, MR, MU, MW, NE, NG,
SC, SD, SL, SN, TN, TZ, UG, ZM, ZW);",
" </li>",
" <li>",
" Pepfamin (TH);",
" </li>",
" <li>",
" Peptifam (AE, BH, CY, EG, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SY, YE);",
" </li>",
" <li>",
" Peptoci (TH);",
" </li>",
" <li>",
" Peptodin (PH);",
" </li>",
" <li>",
" Pepzan (MY, NZ);",
" </li>",
" <li>",
" Pharmotidine (PH);",
" </li>",
" <li>",
" Quamatel (HU);",
" </li>",
" <li>",
" Quamtel (BB, BM, BS, BZ, GY, JM, SR, TT);",
" </li>",
" <li>",
" Rogasti (IL);",
" </li>",
" <li>",
" Sedanium-R (GR);",
" </li>",
" <li>",
" Stadin (KP);",
" </li>",
" <li>",
" Stomax (AE, BH, CY, EG, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SY, YE);",
" </li>",
" <li>",
" Supertidine (TW);",
" </li>",
" <li>",
" Tamin (ES);",
" </li>",
" <li>",
" Topcid (IN);",
" </li>",
" <li>",
" Ulcatif (AE, BH, CY, EG, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SY, YE);",
" </li>",
" <li>",
" Ulcelac (AR);",
" </li>",
" <li>",
" Ulcenol (VE);",
" </li>",
" <li>",
" Ulceran (AE, BG, BH, CY, EG, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SG, SY,
YE);",
" </li>",
" <li>",
" Ulfadin (CO);",
" </li>",
" <li>",
" Ulfagel (EC);",
" </li>",
" <li>",
" Ulfamid (HR, HU, PL);",
" </li>",
" <li>",
" Ulmo (ID);",
" </li>",
" <li>",
" Voker (MY);",
" </li>",
" <li>",
" Weimok (TW);",
" </li>",
" <li>",
" Winiful (TW)",
" </li>",
" </ul>",
" </div>",
" <div class=\"block pha drugH1Div\" id=\"F169890\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Mechanism of Action",
" </span>",
" <p style=\"text-indent:0em;display:inline\">",
" Competitive inhibition of histamine at H",
" _{",
" 2",
"}",
" receptors of the gastric parietal cells, which inhibits gastric acid
secretion",
" </p>",
" </div>",
" <div class=\"block phk drugH1Div\" id=\"F169906\"
xmlns=\"file://www.w3.org/1999/xhtml\">",
" <span class=\"drugH1\">",
" Pharmacodynamics/Kinetics",
" </span>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Onset of action: Antisecretory effect: Oral: Within 1 hour; I.V.: Within 30
minutes",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Peak effect: Antisecretory effect: Oral: Within 1-3 hours (dose-dependent)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Duration: Antisecretory effect: I.V., Oral: 10-12 hours",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Absorption: Oral: Incompletely absorbed",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Distribution: V",
" _{",
" d",
"}",
" :",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Infants: 0-3 months: ~1.4-1.8 L/kg; &gt;3-12 months: ~2.3 L/kg",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Children: ~2 L/kg",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Adults: ~1 L/kg",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Protein binding: 15% to 20%",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Metabolism: Minimal first-pass metabolism; forms one metabolite (S-oxide)",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Bioavailability: Oral: 40% to 45%",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Half-life elimination:",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Infants: 0-3 months: ~8-10.5 hours; &gt;3-12 months: ~4.5 hours",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Children: 3.4 hours",
" </p>",
" <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
" Adults: 2.5-3.5 hours; prolonged with renal impairment; Oliguria: &gt;20
hours",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Time to peak, serum: Oral: ~1-3 hours",
" </p>",
" <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
" Excretion: Urine (25% to 30% [oral], 65% to 70% [I.V.] as unchanged drug)",
" </p>",
" </div>",
" </div>",
" <div id=\"topicAgreement\">",
" Use of UpToDate is subject to the",
" <a class=\"licenseLink\" href=\"./license\" id=\"sla_in_page\"
target=\"_blank\">",
" Subscription and License Agreement",
" </a>",
" .",
" </div>",
" <div class=\"headingAnchor\" id=\"references\">",
" <h1>",
" REFERENCES",
" </h1>",
" <ol id=\"reference\">",
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" <div class=\"reference\">",
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" Dellinger RP, Levy MM, Rhodes A, et al, &ldquo;Surviving Sepsis Campaign:
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" Fennerty MD and Higbee M, &ldquo;Drug Therapy of Gastrointestinal
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" , Bressler R and Katz MD, eds, New York, NY: McGraw-Hill, 1993, 585-608.",
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" 2019939",
" </a>",
" ]",
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var title_f0_45_729="Pathophysiology of psoriasis";
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" Pathophysiology of psoriasis",
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0/45/729/contributors\">",
" Andrew Blauvelt, MD",
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0/45/729/contributors\">",
" Benjamin D Ehst, MD, PhD",
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href=\"UTD.htm?0/45/729/contributors\">",
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0/45/729/contributors\">",
" Kristina Callis Duffin, MD",
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href=\"UTD.htm?0/45/729/contributors\">",
" Deputy Editor",
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0/45/729/contributors\">",
" Abena O Ofori, MD",
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" Literature review current through:",
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" </div>",
" <div id=\"topicText\">",
" <p class=\"headingAnchor\" id=\"H12219610\">",
" <span class=\"h1\">",
" INTRODUCTION",
" </span>",
" &nbsp;&mdash;&nbsp;Psoriasis is a complex autoimmune inflammatory disease that
occurs in genetically susceptible individuals and presents with the development of
inflammatory plaques on the skin (",
" <a class=\"graphic graphic_picture graphicRef54581 graphicRef78531 \"
href=\"UTD.htm?2/26/2473\">",
" picture 1A-B",
" </a>",
" ). Although early concepts of the pathogenesis of psoriasis focused primarily
on keratinocyte hyperproliferation, dysregulation of the immune system is now
recognized as a critical event in this disease. The evolving knowledge of the role
of the immune system in psoriasis has had a significant impact on treatment
development. Many new and emerging therapeutic agents target specific immunologic
aspects of psoriatic disease. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/6/40042?
source=see_link\">",
" \"Treatment of psoriasis\"",
" </a>",
" .)",
" </p>",
" <p>",
" The pathophysiology of psoriasis will be discussed here. The epidemiology,
genetics, clinical features, diagnosis, and management of psoriasis are reviewed
separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?26/62/27625?
source=see_link\">",
" \"Epidemiology, clinical manifestations, and diagnosis of psoriasis\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?14/31/14842?
source=see_link\">",
" \"Treatment selection for moderate to severe plaque psoriasis in special
populations\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219617\">",
" <span class=\"h1\">",
" OVERVIEW",
" </span>",
" &nbsp;&mdash;&nbsp;Involvement of the immune system in psoriasis was first
indicated in early studies that identified complex infiltrates of leukocytes
involved in both innate and adaptive immunity in psoriatic skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/1,2\">",
" 1,2",
" </a>",
" ]. Subsequent studies have supported the concept that interactions between
dendritic cells, T cells, keratinocytes, neutrophils, and the cytokines released
from immune cells likely contribute to the initiation and perpetuation of the
cutaneous inflammation that is characteristic of psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/3\">",
" 3",
" </a>",
" ]. A basic sequence of the immunologic events that are theorized to occur in
psoriasis is described below [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/3\">",
" 3",
" </a>",
" ]:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Antigenic stimuli contribute to the activation of plasmacytoid dendritic
cells and other innate immune cells in the skin.",
" </li>",
" <li>",
" Proinflammatory cytokines produced by innate immune cells, including
interferon (IFN)-alpha, stimulate the activation of myeloid dendritic cells in the
skin.",
" </li>",
" <li>",
" Myeloid dendritic cells produce cytokines, such as interleukin (IL)-23 and
IL-12 that stimulate the attraction, activation, and differentiation of T cells.",
" </li>",
" <li>",
" Recruited T cells produce cytokines that stimulate keratinocytes to
proliferate and produce proinflammatory antimicrobial peptides and cytokines.",
" </li>",
" <li>",
" Cytokines produced by immune cells and keratinocytes perpetuate the
inflammatory process via participation in positive feedback loops.",
" </li>",
" </ul>",
" </p>",
" <p>",
" The specific components of this pathway are reviewed below.",
" </p>",
" <p class=\"headingAnchor\" id=\"H481234\">",
" <span class=\"h1\">",
" THE INNATE IMMUNE RESPONSE",
" </span>",
" &nbsp;&mdash;&nbsp;The cellular components of the innate immune system that
have been linked to the pathophysiology of psoriasis include dendritic cells,
macrophages, and neutrophils. The cytokines produced by these cells that appear to
play major roles in the development of psoriasis include interferon (IFN)-alpha,
tumor necrosis factor (TNF)-alpha, interleukin (IL)-23, and IL-12.",
" </p>",
" <p class=\"headingAnchor\" id=\"H481641\">",
" <span class=\"h2\">",
" Cellular components",
" </span>",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219638\">",
" <span class=\"h3\">",
" Dendritic cells",
" </span>",
" &nbsp;&mdash;&nbsp;Two types of dendritic cells (plasmacytoid dendritic cells
and myeloid dendritic cells) have been implicated as contributors to psoriasis.",
" </p>",
" <p>",
" <ul class=\"bulletCompact-block\">",
" <li>",
" <strong>",
" Plasmacytoid dendritic cells",
" </strong>",
" &ndash; Plasmacytoid dendritic cells are largely absent from normal human
skin, but are increased in number in early lesions of psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/4\">",
" 4",
" </a>",
" ]. These cells are the primary producers of IFN-alpha, a key cytokine
involved in the initiation of autoimmune responses and antiviral immunity. (See",
" <a class=\"local\" href=\"#H481370\">",
" 'Interferon-alpha'",
" </a>",
" below.)",
" <br/>",
" <br/>",
" Upregulation of IFN-alpha has been detected in early psoriatic lesions [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/5\">",
" 5",
" </a>",
" ]. In addition, in a mouse xenograft model of psoriasis, the development of
psoriatic lesions was dependent on IFN-alpha production by plasmacytoid dendritic
cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/6\">",
" 6",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" <strong>",
" Myeloid dendritic cells",
" </strong>",
" &ndash; The numbers of myeloid dendritic cells are markedly elevated in
psoriatic skin. In particular, an inflammatory subset of myeloid dendritic cells
that is likely recruited in response to the release of IFN-alpha and other
proinflammatory cytokines and chemokines has been detected in psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/7-10\">",
" 7-10",
" </a>",
" ].",
" <br/>",
" <br/>",
" Myeloid dendritic cells are potent antigen presenting cells that produce an
array of inflammatory cytokines that influence T cell activity, such as TNF-alpha.
(See",
" <a class=\"local\" href=\"#H481514\">",
" 'Tumor necrosis factor-alpha'",
" </a>",
" below.) Myeloid dendritic cells also produce IL-23, a cytokine that causes
the differentiation of precursor CD4+ cells into Th17 cells, and IL-12, a cytokine
that stimulates the development of Th1 cells and effector CD8+ T cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/11\">",
" 11",
" </a>",
" ]. (See",
" <a class=\"local\" href=\"#H12219645\">",
" 'Interleukin-23'",
" </a>",
" below and",
" <a class=\"local\" href=\"#H12219659\">",
" 'Interleukin-12'",
" </a>",
" below.) Myeloid dendritic cells also affect keratinocytes and the skin
vasculature through the production of IL-20 (a modulator of keratinocyte function)
and nitric oxide (a vasodilating agent) [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/12\">",
" 12",
" </a>",
" ]. (See",
" <a class=\"local\" href=\"#H12219729\">",
" 'Keratinocytes'",
" </a>",
" below and",
" <a class=\"local\" href=\"#H12219736\">",
" 'Vascular changes'",
" </a>",
" below.)",
" </li>",
" </ul>",
" </p>",
" <p class=\"headingAnchor\" id=\"H481271\">",
" <span class=\"h3\">",
" Macrophages and neutrophils",
" </span>",
" &nbsp;&mdash;&nbsp;The importance of macrophages in psoriasis in humans is not
well-understood. Macrophages accumulate in psoriatic skin near the basement
membrane [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/13\">",
" 13",
" </a>",
" ] and may contribute to psoriasis through antigen presentation to T cells as
well as cytokine production. The depletion of macrophages can reverse psoriasis-
like skin changes in mouse models [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/14\">",
" 14",
" </a>",
" ].",
" </p>",
" <p>",
" Neutrophils are prominent in lesions of psoriasis, and are found in
collections throughout the epidermis that are referred to as Munro microabscesses.
The neutrophil chemoattractant IL-8 is highly elevated in psoriatic skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/15,16\">",
" 15,16",
" </a>",
" ]. Like macrophages, neutrophils are believed to participate in psoriatic
inflammation. However, it is conceivable that neutrophils do not play a central
pathogenic role.",
" </p>",
" <p class=\"headingAnchor\" id=\"H481603\">",
" <span class=\"h2\">",
" Cytokines",
" </span>",
" </p>",
" <p class=\"headingAnchor\" id=\"H481370\">",
" <span class=\"h3\">",
" Interferon-alpha",
" </span>",
" &nbsp;&mdash;&nbsp;Type I interferon pathways are upregulated in early lesions
of psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/5\">",
" 5",
" </a>",
" ]. IFN-alpha present in psoriatic skin is largely derived from plasmacytoid
dendritic cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/5\">",
" 5",
" </a>",
" ]. (See",
" <a class=\"local\" href=\"#H12219638\">",
" 'Dendritic cells'",
" </a>",
" above.)",
" </p>",
" <p>",
" Evidence in support of a key role for IFN-alpha in psoriasis includes the
observation that systemic treatment with IFN-alpha can exacerbate psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/17,18\">",
" 17,18",
" </a>",
" ]. In addition, topical treatment with",
" <a class=\"drug drug_general\" href=\"UTD.htm?19/59/20406?source=see_link\">",
" imiquimod",
" </a>",
" , which induces local production of IFN-alpha in the skin, has stimulated the
development of psoriasis in humans and psoriasis-like disease in mice [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/19,20\">",
" 19,20",
" </a>",
" ]. Furthermore, mice that lack a transcription factor that represses type I
interferon signaling develop psoriasis-like disease [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/21\">",
" 21",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H481514\">",
" <span class=\"h3\">",
" Tumor necrosis factor-alpha",
" </span>",
" &nbsp;&mdash;&nbsp;TNF-alpha is a critical proinflammatory cytokine common to
many inflammatory disease states, including psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/22\">",
" 22",
" </a>",
" ]. Activated dendritic cells, Th17 and Th1 cells, and keratinocytes in
psoriatic skin produce TNF-alpha and respond to its effects. TNF-alpha also
functions synergistically with other cytokines to promote disease pathogenesis.",
" </p>",
" <p>",
" The following observations support an important role for TNF-alpha in
psoriasis:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Elevated levels of TNF-alpha are found in lesional skin of psoriatic
patients [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/23\">",
" 23",
" </a>",
" ].",
" </li>",
" <li>",
" Dramatic clinical improvement of psoriasis is seen with pharmacologic
inhibitors of TNF-alpha (",
" <a class=\"drug drug_general\" href=\"UTD.htm?28/6/28776?
source=see_link\">",
" infliximab",
" </a>",
" ,",
" <a class=\"drug drug_general\" href=\"UTD.htm?38/24/39303?
source=see_link\">",
" adalimumab",
" </a>",
" , and",
" <a class=\"drug drug_general\" href=\"UTD.htm?27/31/28151?
source=see_link\">",
" etanercept",
" </a>",
" ) [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/24-26\">",
" 24-26",
" </a>",
" ].",
" </li>",
" <li>",
" Removal of circulating TNF-alpha via the administration of",
" <a class=\"drug drug_general\" href=\"UTD.htm?27/31/28151?
source=see_link\">",
" etanercept",
" </a>",
" (a TNF-alpha inhibitor) results in decreased numbers of dendritic cells and
T cells along with a reduction of epidermal hyperplasia in psoriatic skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/9\">",
" 9",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p>",
" The central role of TNF-alpha in both innate and adaptive immune responses
makes this cytokine an ideal target for therapeutic blockade. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/6/40042?
source=see_link&amp;anchor=H36#H36\">",
" \"Treatment of psoriasis\", section on 'Biologic agents'",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219645\">",
" <span class=\"h3\">",
" Interleukin-23",
" </span>",
" &nbsp;&mdash;&nbsp;IL-23 is the cytokine responsible for proliferation and
survival of Th17 cells, which is an increasingly important T cell subset in many
autoimmune diseases, including psoriasis and Crohn&rsquo;s disease [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/27-29\">",
" 27-29",
" </a>",
" ]. IL-23 is produced by myeloid dendritic cells and at low levels by
keratinocytes [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/30,31\">",
" 30,31",
" </a>",
" ]. Production of this cytokine by dendritic cells can occur through toll-like
receptor signaling pathways [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/32,33\">",
" 32,33",
" </a>",
" ]. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?22/54/23401?
source=see_link\">",
" \"Toll-like receptors: Roles in disease and therapy\"",
" </a>",
" .)",
" </p>",
" <p>",
" The importance of IL-23 to the pathogenesis of psoriasis has been demonstrated
by the following:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" In psoriatics, IL-23 is elevated in lesions of psoriasis compared with
unaffected skin and localizes to dermal dendritic cells and keratinocytes; levels
of IL-23 fall with effective treatment of psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/34-38\">",
" 34-38",
" </a>",
" ].",
" </li>",
" <li>",
" Injection of IL-23 into normal mouse skin produces changes that are
clinically and histologically similar to psoriasis; this process depends on
downstream production of IL-22 and IL-17A [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/34,39,40\">",
" 34,39,40",
" </a>",
" ].",
" </li>",
" <li>",
" Polymorphisms in the genes encoding a component of the IL-23 receptor,",
" <em>",
" IL23R",
" </em>",
" , and the p40 and p19 subunits of IL-23 have been linked to psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/41\">",
" 41",
" </a>",
" ].",
" </li>",
" <li>",
" <a class=\"drug drug_general\" href=\"UTD.htm?0/46/742?source=see_link\">",
" Ustekinumab",
" </a>",
" , a monoclonal antibody that blocks IL-23 effects on Th17 cells by
inhibiting binding of IL-23 to the IL-23 receptor, has shown great efficacy in
treating psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/42\">",
" 42",
" </a>",
" ]. Additional biologic agents that selectively block IL-23 actions hold
promise for future treatment [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/43\">",
" 43",
" </a>",
" ]. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/6/40042?
source=see_link&amp;anchor=H42#H42\">",
" \"Treatment of psoriasis\", section on 'Ustekinumab'",
" </a>",
" .)",
" </li>",
" </ul>",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219659\">",
" <span class=\"h3\">",
" Interleukin-12",
" </span>",
" &nbsp;&mdash;&nbsp;IL-12 is produced by activated myeloid dendritic cells.
This cytokine promotes the differentiation of Th1 cells, which are considered
important in the pathogenesis of psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/42\">",
" 42",
" </a>",
" ]. Indirect evidence for a contributory role for IL-12 in psoriasis comes from
findings of increased Th1 cells and IFN-gamma (a product of Th1 cells) in psoriatic
skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/43,44\">",
" 43,44",
" </a>",
" ]. However, the degree to which IL-12 contributes to psoriasis is brought into
question by the failure of a study to detect upregulation of the p35 subunit of IL-
12 in psoriatic skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/36\">",
" 36",
" </a>",
" ]. It is possible that",
" <a class=\"drug drug_general\" href=\"UTD.htm?0/46/742?source=see_link\">",
" ustekinumab",
" </a>",
" , an effective biologic agent for psoriasis that targets both IL-12 and IL-23
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/45,46\">",
" 45,46",
" </a>",
" ], may function primarily through the drug&rsquo;s effects on the IL-23
pathway. (See",
" <a class=\"local\" href=\"#H12219694\">",
" 'T helper type 1 cells'",
" </a>",
" below and",
" <a class=\"local\" href=\"#H12219645\">",
" 'Interleukin-23'",
" </a>",
" above and",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/6/40042?
source=see_link&amp;anchor=H42#H42\">",
" \"Treatment of psoriasis\", section on 'Ustekinumab'",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219673\">",
" <span class=\"h1\">",
" THE ADAPTIVE IMMUNE RESPONSE",
" </span>",
" &nbsp;&mdash;&nbsp;The importance of T cells and their effector cytokines in
psoriasis was established early on with the success of medications that inhibit
global T cell responses, such as",
" <a class=\"drug drug_general\" href=\"UTD.htm?31/39/32368?source=see_link\">",
" cyclosporine",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/47\">",
" 47",
" </a>",
" ]. Therapies that block T cell activation or induce T cell death, such as
alefacept (an inhibitor of the T cell-activating interaction between LFA3 on
antigen presenting cells and CD2 on T cells that is no longer commercially
available) have been effective for psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/48\">",
" 48",
" </a>",
" ]. In addition, injection of lymphocytes from psoriatics can induce psoriatic
features in nonlesional human skin transplanted onto severe combined
immunodeficient (SCID) mice [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/49\">",
" 49",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H1279163\">",
" <span class=\"h2\">",
" Cellular components",
" </span>",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219680\">",
" <span class=\"h3\">",
" CD4+ T cells",
" </span>",
" &nbsp;&mdash;&nbsp;CD4+ helper T cells are found throughout dermal
inflammatory infiltrates in psoriatic skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/50\">",
" 50",
" </a>",
" ]. Data in support of a role for these cells include the finding that the
injection of CD4+ (but not CD8+) T cells from patients with psoriasis into graft
sites on SCID mice transplanted with human skin induces psoriatic changes in the
engrafted skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/51\">",
" 51",
" </a>",
" ]. In addition, clinical improvement has occurred in patients with psoriasis
treated with monoclonal antibodies against the CD4+ molecule on T cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/52\">",
" 52",
" </a>",
" ].",
" </p>",
" <p>",
" Both Th17 and Th1 subsets of CD4+ T cells have been implicated in psoriasis.
Early investigational studies presumed a dominating role for Th1 cells; however,
Th17 cells are now believed to play a greater role. The effects of these cells and
other components of the adaptive immune system in psoriasis are reviewed below.",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219687\">",
" <span class=\"h4\">",
" T helper type 17 cells",
" </span>",
" &nbsp;&mdash;&nbsp;The discovery of Th17 cells has led to important insights
on the pathophysiology of psoriasis and new target-specific approaches to
treatment. Th17 cells develop in psoriatic skin under the polarizing effects of IL-
1, IL-6, transforming growth factor (TGF)-beta, and IL-23 produced by inflammatory
dendritic cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/53\">",
" 53",
" </a>",
" ]. (See",
" <a class=\"local\" href=\"#H12219638\">",
" 'Dendritic cells'",
" </a>",
" above.) The activation of Th17 cells by IL-23 stimulates these cells to
produce IL-17A and IL-22, cytokines that promote keratinocyte activation and growth
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/39,54,55\">",
" 39,54,55",
" </a>",
" ]. (See",
" <a class=\"local\" href=\"#H12219701\">",
" 'Interleukin-17A'",
" </a>",
" below and",
" <a class=\"local\" href=\"#H12219708\">",
" 'Interleukin-22'",
" </a>",
" below.)",
" </p>",
" <p>",
" The following study results highlight the role of these cells in psoriasis:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Th17 cells produce an array of proinflammatory cytokines, including IL-17A,
IL-17F, IL-21, IL-22, IL-6, and TNF-alpha [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/29\">",
" 29",
" </a>",
" ], all of which have been linked to psoriasis.",
" </li>",
" <li>",
" Th17 cells are found in lesional skin and at elevated levels in the
circulation in patients with psoriasis, and IL-17A is abundantly expressed by these
cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/43,56,57\">",
" 43,56,57",
" </a>",
" ].",
" </li>",
" <li>",
" Transgenic mice overexpressing the p19 subunit of IL-23, a key factor for
Th17 cell functioning, have severe widespread inflammatory disease that includes
inflammation of the skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/58\">",
" 58",
" </a>",
" ].",
" </li>",
" <li>",
" Effective therapies for psoriasis, such as phototherapy,",
" <a class=\"drug drug_general\" href=\"UTD.htm?31/39/32368?
source=see_link\">",
" cyclosporine",
" </a>",
" ,",
" <a class=\"drug drug_general\" href=\"UTD.htm?27/31/28151?
source=see_link\">",
" etanercept",
" </a>",
" , and",
" <a class=\"drug drug_general\" href=\"UTD.htm?28/6/28776?
source=see_link\">",
" infliximab",
" </a>",
" , have all been shown to modulate the Th17 pathway in psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/9,57,59-61\">",
" 9,57,59-61",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p>",
" Selective targeting of Th17 cells via inhibition of IL-23, the IL-23 receptor,
or IL-17A is a promising therapeutic approach for psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/62,63\">",
" 62,63",
" </a>",
" ].",
" <a class=\"drug drug_general\" href=\"UTD.htm?0/46/742?source=see_link\">",
" Ustekinumab",
" </a>",
" , a highly effective drug that is currently in use for psoriasis, is a
monoclonal antibody that binds to IL-23. Agents that interrupt",
" <span class=\"nowrap\">",
" JAK/STAT",
" </span>",
" signaling pathways (key intracellular events in Th17 cytokine production) are
also under investigation for the treatment of psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/64\">",
" 64",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219694\">",
" <span class=\"h4\">",
" T helper type 1 cells",
" </span>",
" &nbsp;&mdash;&nbsp;Th1 cells produce an array of proinflammatory cytokines,
including IFN-gamma, IL-2, and TNF-alpha [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/42\">",
" 42",
" </a>",
" ]. IFN-gamma, the prototypic cytokine produced by these cells, can promote
psoriasis-like changes in nonlesional psoriatic skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/65\">",
" 65",
" </a>",
" ]. Of note,",
" <a class=\"drug drug_general\" href=\"UTD.htm?28/6/28776?source=see_link\">",
" infliximab",
" </a>",
" , an effective anti-TNF therapy for psoriasis, is also capable of inhibiting
IFN-gamma production by Th1 cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/66\">",
" 66",
" </a>",
" ].",
" </p>",
" <p>",
" IL-12, a cytokine produced by activated myeloid dendritic cells, promotes the
differentiation of Th1 cells. The degree to which IL-12-mediated effects contribute
to psoriasis is uncertain [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/36\">",
" 36",
" </a>",
" ]. (See",
" <a class=\"local\" href=\"#H12219638\">",
" 'Dendritic cells'",
" </a>",
" above and",
" <a class=\"local\" href=\"#H12219659\">",
" 'Interleukin-12'",
" </a>",
" above.).",
" </p>",
" <p class=\"headingAnchor\" id=\"H1280083\">",
" <span class=\"h3\">",
" CD8 T cells",
" </span>",
" &nbsp;&mdash;&nbsp;Cytotoxic CD8+ T cells are found primarily in the epidermis
of psoriatic skin and are generally considered to play a less prominent role in
psoriasis than CD4+ T cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/67\">",
" 67",
" </a>",
" ]. Although they produce cytolytic enzymes, their role in psoriasis is
speculated to involve the elaboration of inflammatory cytokines [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/68-70\">",
" 68-70",
" </a>",
" ]. Interestingly, clonal restriction of psoriatic T cells seems limited to the
CD8+ compartment. This finding might suggest a link between viral or self antigens
in the epidermis and triggering of psoriasis, since these types of MHC class I-
restricted antigens are typically presented to CD8+ T cells, and not CD4+ T cells
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/71,72\">",
" 71,72",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H1280090\">",
" <span class=\"h3\">",
" Regulatory T cells",
" </span>",
" &nbsp;&mdash;&nbsp;CD18-knockout mice that are deficient in regulatory T cells
develop skin with features of psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/73\">",
" 73",
" </a>",
" ]. Additionally, defects in the suppressive function of regulatory T cells
have been found in psoriasis lesions [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/74\">",
" 74",
" </a>",
" ]. In the absence of properly functioning regulatory cells, downregulation of
immune responses is inadequate. This may contribute to unchecked inflammation in
psoriasis.",
" </p>",
" <p class=\"headingAnchor\" id=\"H1280183\">",
" <span class=\"h2\">",
" Cytokines",
" </span>",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219701\">",
" <span class=\"h3\">",
" Interleukin-17A",
" </span>",
" &nbsp;&mdash;&nbsp;IL-17A, a cytokine produced by Th17 cells, is elevated in
lesions of psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/34,75\">",
" 34,75",
" </a>",
" ]. IL-17A has many functions that are relevant to psoriasis, including the
activation, recruitment, and inhibition of apoptosis in neutrophils; the
enhancement of angiogenesis; the promotion of the release of other inflammatory
cytokines (TNF-alpha, IL-1, and IL-6); and the direct activation of keratinocytes
leading to increased production of chemokines [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/39,55,76-82\">",
" 39,55,76-82",
" </a>",
" ]. Therapeutic agents for psoriasis that block IL-17 production or the
downstream effects of IL-17 are in clinical trials [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/62\">",
" 62",
" </a>",
" ]. Phase II trials have demonstrated efficacy of an anti-IL-17 monoclonal
antibody (ixekizumab) and an anti-IL-17 receptor antibody (brodalumab) in moderate
to severe plaque psoriasis [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/83,84\">",
" 83,84",
" </a>",
" ]. &nbsp;",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219708\">",
" <span class=\"h3\">",
" Interleukin-22",
" </span>",
" &nbsp;&mdash;&nbsp;IL-22 levels are increased in the blood of patients with
psoriasis and in psoriatic plaques. Treatment of psoriasis decreases these levels
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/57,75,85\">",
" 57,75,85",
" </a>",
" ]. &nbsp;",
" </p>",
" <p>",
" IL-22 is produced by Th17 cells and Th22 cells. This cytokine stimulates the
growth and activation of keratinocytes and has little effect on immune cells. In
keratinocytes, IL-22-mediated signaling via STAT3 stimulates cell
hyperproliferation, secretion of antimicrobial peptides, and production of matrix
metalloproteinases that support increased cell mobility [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/40,85-88\">",
" 40,85-88",
" </a>",
" ]. Molecular therapies that target IL-22 are in clinical trials [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/89\">",
" 89",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219729\">",
" <span class=\"h1\">",
" KERATINOCYTES",
" </span>",
" &nbsp;&mdash;&nbsp;A role for epidermal keratinocytes as triggers for the
initiation of psoriasis is a subject of much debate. Keratinocyte-derived
antimicrobial peptides (AMPs), including beta-defensins, cathelicidins, and
psoriasin (S100A7), may be induced by trauma, and are upregulated in psoriatic
epidermis early in the course of lesion development [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/90\">",
" 90",
" </a>",
" ]. AMPs have both chemoattractant and immunomodulatory effects on dendritic
cells and T cells and may contribute to cutaneous inflammation. One theory on the
initiation of psoriasis involves the upregulation of the AMP cathelicidin LL-37 in
skin. LL-37 may bind self DNA and stimulate the production of IFN-alpha by
plasmacytoid dendritic cells through Toll-like receptor (TLR)-9 [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/91\">",
" 91",
" </a>",
" ].",
" </p>",
" <p>",
" Keratinocyte hyperplasia characteristic of psoriasis may develop as a result
of the effects of cytokines produced by immune cells. IL-22 is produced by Th17
cells and promotes many of the epidermal changes that occur in psoriatic lesions.
(See",
" <a class=\"local\" href=\"#H12219708\">",
" 'Interleukin-22'",
" </a>",
" above.) Additionally, IL-20 production by keratinocytes plays an important
synergistic role downstream of IL-22.",
" </p>",
" <p>",
" Both IL-22 and IL-20 are highly expressed in psoriatic skin and promote
alterations in epidermal thickness, maturation defects, and upregulation of AMPs
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/92,93\">",
" 92,93",
" </a>",
" ]. A role for IL-20 in psoriasis is supported by the observation that blocking
IL-20 in a SCID xenotransplant model of psoriasis induces resolution of psoriasis
and blocks initiation of disease [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/94\">",
" 94",
" </a>",
" ]. Therapeutics directed against both IL-22 and IL-20 have been tested in
early clinical trials [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/89\">",
" 89",
" </a>",
" ].",
" </p>",
" <p>",
" The cytokines and chemokines produced by activated keratinocytes contribute to
the sustainment of the inflammatory response in psoriasis via their effects on
innate and adaptive immune cells. Topical vitamin D analogs as well as topical and
oral retinoids primarily affect this pathway in psoriasis.",
" <a class=\"drug drug_general\" href=\"UTD.htm?23/38/24170?source=see_link\">",
" Methotrexate",
" </a>",
" was originally thought to modulate the epidermal component of psoriasis as
well, although current thinking suggests that its direct effects on the immune
system are more important. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/6/40042?
source=see_link&amp;anchor=H17#H17\">",
" \"Treatment of psoriasis\", section on 'Topical vitamin D analogs'",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/6/40042?
source=see_link&amp;anchor=H21#H21\">",
" \"Treatment of psoriasis\", section on 'Tazarotene'",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/6/40042?
source=see_link&amp;anchor=H31#H31\">",
" \"Treatment of psoriasis\", section on 'Methotrexate'",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219736\">",
" <span class=\"h1\">",
" VASCULAR CHANGES",
" </span>",
" &nbsp;&mdash;&nbsp;Endothelial cells within psoriatic plaques express elevated
levels of vascular endothelial growth factor (VEGF), prostaglandins, and nitric
oxide, all contributing to the characteristic leaky and tortuous vessels that are
abundant in psoriatic skin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/95,96\">",
" 95,96",
" </a>",
" ]. Transgenic mice overexpressing VEGF in the epidermis have been found to
develop psoriasiform skin changes [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/97\">",
" 97",
" </a>",
" ].",
" </p>",
" <p>",
" The activated vasculature promotes attraction and transmigration of the
leukocytes discussed above. Antiangiogenic agents have actually demonstrated some
success in psoriasis patients, but more investigation is needed [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/98\">",
" 98",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219743\">",
" <span class=\"h1\">",
" ENVIRONMENTAL FACTORS",
" </span>",
" &nbsp;&mdash;&nbsp;Medications, trauma, alcohol, cigarette smoking, stress,
and infections have all been linked to the onset of autoimmune inflammatory
conditions and are also known to trigger psoriasis. The current understanding of
this process is rudimentary.",
" </p>",
" <p>",
" A proposed pathogenic model highlights the possibility of innate recognition
of conserved sequences in microbes through TLR signaling as one possible
explanation for infectious triggers. The",
" <span class=\"nowrap\">",
" TLR-7/8",
" </span>",
" antagonist",
" <a class=\"drug drug_general\" href=\"UTD.htm?19/59/20406?source=see_link\">",
" imiquimod",
" </a>",
" can induce a psoriasis-like skin disease in mice through production of IFN-
alpha by plasmacytoid dendritic cells. This process is dependent on the Th17
pathway [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/729/abstract/20\">",
" 20",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H12219750\">",
" <span class=\"h1\">",
" SUMMARY",
" </span>",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Psoriasis is a complex immune-mediated disorder that presents as
inflammatory plaques in the skin (",
" <a class=\"graphic graphic_picture graphicRef54581 graphicRef78531 \"
href=\"UTD.htm?2/26/2473\">",
" picture 1A-B",
" </a>",
" ). Dysregulation or alteration of components of the innate and adaptive
immune systems, keratinocyte function, and vascular structure contribute to the
manifestations of this disease. (See",
" <a class=\"local\" href=\"#H12219617\">",
" 'Overview'",
" </a>",
" above.)",
" </li>",
" <li>",
" Plasmacytoid and myeloid dendritic cells are key contributors to development
of inflammation in psoriasis. IFN-alpha produced by plasmacytoid dendritic cells
stimulates the activation of myeloid dendritic cells, which contribute to the
adaptive immune response through the activation of T cells. (See",
" <a class=\"local\" href=\"#H481234\">",
" 'The innate immune response'",
" </a>",
" above.)",
" </li>",
" <li>",
" IL-23 and IL-12 produced by activated myeloid dendritic cells promote the
development of Th17 and Th1 cells, respectively. Th17 cells appear to play a major
role in the pathogenesis of psoriasis. (See",
" <a class=\"local\" href=\"#H12219673\">",
" 'The adaptive immune response'",
" </a>",
" above.)",
" </li>",
" <li>",
" Keratinocytes may contribute to the initiation of psoriasis via the
production of antimicrobial peptides. Epidermal hyperplasia is driven by cytokines
that stimulate keratinocyte activation and proliferation. (See",
" <a class=\"local\" href=\"#H12219729\">",
" 'Keratinocytes'",
" </a>",
" above.)",
" </li>",
" <li>",
" Knowledge of the pathophysiology of psoriasis is evolving. Advances in the
understanding of the mechanisms of disease will likely contribute to the
development of new therapeutic agents and improved patient outcomes. (See",
" <a class=\"local\" href=\"#H12219610\">",
" 'Introduction'",
" </a>",
" above and",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/6/40042?
source=see_link\">",
" \"Treatment of psoriasis\"",
" </a>",
" .)",
" </li>",
" </ul>",
" </p>",
" </div>",
" <div id=\"topicAgreement\">",
" Use of UpToDate is subject to the",
" <a class=\"licenseLink\" href=\"./license\" id=\"sla_in_page\"
target=\"_blank\">",
" Subscription and License Agreement",
" </a>",
" .",
" </div>",
" <div class=\"headingAnchor\" id=\"references\">",
" <h1>",
" REFERENCES",
" </h1>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/61\">",
" Zaba LC, Su&aacute;rez-Fari&ntilde;as M, Fuentes-Duculan J, et al. Effective
treatment of psoriasis with etanercept is linked to suppression of IL-17 signaling,
not immediate response TNF genes. J Allergy Clin Immunol 2009; 124:1022.",
" </a>",
" </li>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/62\">",
" Hueber W, Patel DD, Dryja T, et al. Effects of AIN457, a fully human
antibody to interleukin-17A, on psoriasis, rheumatoid arthritis, and uveitis. Sci
Transl Med 2010; 2:52ra72.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/63\">",
" Kurzeja M, Rudnicka L, Olszewska M. New interleukin-23 pathway inhibitors in
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" Kaminska B, Swiatek-Machado K. Targeting signaling pathways with small
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" Wei L, Debets R, Hegmans JJ, et al. IL-1 beta and IFN-gamma induce the
regenerative epidermal phenotype of psoriasis in the transwell skin organ culture
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" Lowes MA, Bowcock AM, Krueger JG. Pathogenesis and therapy of psoriasis.
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" Prinz JC, Vollmer S, Boehncke WH, et al. Selection of conserved TCR VDJ
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" Wilson NJ, Boniface K, Chan JR, et al. Development, cytokine profile and
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" Albanesi C, Scarponi C, Cavani A, et al. Interleukin-17 is produced by both
Th1 and Th2 lymphocytes, and modulates interferon-gamma- and interleukin-4-induced
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/77\">",
" Dragon S, Saffar AS, Shan L, Gounni AS. IL-17 attenuates the anti-apoptotic
effects of GM-CSF in human neutrophils. Mol Immunol 2008; 45:160.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/78\">",
" Homey B, Dieu-Nosjean MC, Wiesenborn A, et al. Up-regulation of macrophage
inflammatory protein-3 alpha/CCL20 and CC chemokine receptor 6 in psoriasis. J
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" Laan M, Cui ZH, Hoshino H, et al. Neutrophil recruitment by human IL-17 via
C-X-C chemokine release in the airways. J Immunol 1999; 162:2347.",
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" Numasaki M, Fukushi J, Ono M, et al. Interleukin-17 promotes angiogenesis
and tumor growth. Blood 2003; 101:2620.",
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" Ruddy MJ, Wong GC, Liu XK, et al. Functional cooperation between
interleukin-17 and tumor necrosis factor-alpha is mediated by CCAAT/enhancer-
binding protein family members. J Biol Chem 2004; 279:2559.",
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" Starnes T, Broxmeyer HE, Robertson MJ, Hromas R. Cutting edge: IL-17D, a
novel member of the IL-17 family, stimulates cytokine production and inhibits
hemopoiesis. J Immunol 2002; 169:642.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/83\">",
" Leonardi C, Matheson R, Zachariae C, et al. Anti-interleukin-17 monoclonal
antibody ixekizumab in chronic plaque psoriasis. N Engl J Med 2012; 366:1190.",
" </a>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/84\">",
" Papp KA, Leonardi C, Menter A, et al. Brodalumab, an anti-interleukin-17-
receptor antibody for psoriasis. N Engl J Med 2012; 366:1181.",
" </a>",
" </li>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/85\">",
" Wolk K, Witte E, Wallace E, et al. IL-22 regulates the expression of genes
responsible for antimicrobial defense, cellular differentiation, and mobility in
keratinocytes: a potential role in psoriasis. Eur J Immunol 2006; 36:1309.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/86\">",
" Boniface K, Bernard FX, Garcia M, et al. IL-22 inhibits epidermal
differentiation and induces proinflammatory gene expression and migration of human
keratinocytes. J Immunol 2005; 174:3695.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/87\">",
" Liang SC, Tan XY, Luxenberg DP, et al. Interleukin (IL)-22 and IL-17 are
coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial
peptides. J Exp Med 2006; 203:2271.",
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" </li>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/88\">",
" Wolk K, Kunz S, Witte E, et al. IL-22 increases the innate immunity of
tissues. Immunity 2004; 21:241.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/89\">",
" Nograles KE, Krueger JG. Anti-cytokine therapies for psoriasis. Exp Cell Res
2011; 317:1293.",
" </a>",
" </li>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/90\">",
" Hollox EJ, Huffmeier U, Zeeuwen PL, et al. Psoriasis is associated with
increased beta-defensin genomic copy number. Nat Genet 2008; 40:23.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/91\">",
" Lande R, Gregorio J, Facchinetti V, et al. Plasmacytoid dendritic cells
sense self-DNA coupled with antimicrobial peptide. Nature 2007; 449:564.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/92\">",
" Blumberg H, Conklin D, Xu WF, et al. Interleukin 20: discovery, receptor
identification, and role in epidermal function. Cell 2001; 104:9.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/93\">",
" Wolk K, Witte E, Warszawska K, et al. The Th17 cytokine IL-22 induces IL-20
production in keratinocytes: a novel immunological cascade with potential relevance
in psoriasis. Eur J Immunol 2009; 39:3570.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/94\">",
" Stenderup K, Rosada C, Worsaae A, et al. Interleukin-20 plays a critical
role in maintenance and development of psoriasis in the human xenograft
transplantation model. Br J Dermatol 2009; 160:284.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/95\">",
" Costa C, Incio J, Soares R. Angiogenesis and chronic inflammation: cause or
consequence? Angiogenesis 2007; 10:149.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/96\">",
" Detmar M, Brown LF, Claffey KP, et al. Overexpression of vascular
permeability factor/vascular endothelial growth factor and its receptors in
psoriasis. J Exp Med 1994; 180:1141.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/97\">",
" Xia YP, Li B, Hylton D, et al. Transgenic delivery of VEGF to mouse skin
leads to an inflammatory condition resembling human psoriasis. Blood 2003;
102:161.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/729/abstract/98\">",
" Ehrlich A, Booher S, Becerra Y, et al. Micellar paclitaxel improves severe
psoriasis in a prospective phase II pilot study. J Am Acad Dermatol 2004; 50:533.",
" </a>",
" </li>",
" </ol>",
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" INTRODUCTION",
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" OVERVIEW",
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" THE INNATE IMMUNE RESPONSE",
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" - Dendritic cells",
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" - CD4+ T cells",
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" T helper type 17 cells",
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" T helper type 1 cells",
" </a>",
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" - CD8 T cells",
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" - Regulatory T cells",
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" VASCULAR CHANGES",
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" ENVIRONMENTAL FACTORS",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H12219750\">",
" SUMMARY",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a href=\"#references\">",
" REFERENCES",
" </a>",
" </li>",
" </ul>",
" </div>",
" <h1>",
" <div class=\"openRelatedGraphics\" id=\"DERM/15277\" rel=\"outline_link\">",
" GRAPHICS",
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" View All",
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" <a href=\"#\" title=\"PICTURES\">",
" PICTURES",
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" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_picture\" href=\"UTD.htm?32/28/33219\"
title=\"picture 1A\">",
" Psoriasis plaque",
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title=\"picture 1B\">",
" Inverse psoriasis chest",
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" RELATED TOPICS",
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" <ul>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?26/62/27625?
source=related_link\">",
" Epidemiology, clinical manifestations, and diagnosis of psoriasis",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?22/54/23401?
source=related_link\">",
" Toll-like receptors: Roles in disease and therapy",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/6/40042?
source=related_link\">",
" Treatment of psoriasis",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?14/31/14842?
source=related_link\">",
" Treatment selection for moderate to severe plaque psoriasis in special
populations",
" </a>",
" </li>",
" </ul>",
" </div>",
" </div>"].join("\n");
var title_f0_45_730="Cushing's syndrome due to ACTH-independent macronodular
adrenal hyperplasia";
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" Cushing's syndrome due to ACTH-independent macronodular adrenal hyperplasia",
" </div>",
" <div id=\"topicContributors\">",
" <div>",
" <a id=\"authors\">",
" </a>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/45/730/contributors\">",
" Author",
" </a>",
" <br/>",
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0/45/730/contributors\">",
" Andre Lacroix, MD",
" </a>",
" <br/>",
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href=\"UTD.htm?0/45/730/contributors\">",
" Section Editor",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/45/730/contributors\">",
" Lynnette K Nieman, MD",
" </a>",
" <br/>",
" </div>",
" <div>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/45/730/contributors\">",
" Deputy Editor",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/45/730/contributors\">",
" Kathryn A Martin, MD",
" </a>",
" <br/>",
" </div>",
" </div>",
" <div id=\"disclosures\">",
" <a href=\"UTD.htm?0/45/730/contributor-disclosure\" target=\"_blank\">",
" Disclosures",
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" <span class=\"emphasis\">",
" Literature review current through:",
" </span>",
" Oct 2013.",
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" This topic last updated:",
" </span>",
" Oct 1, 2012.",
" </div>",
" <div id=\"topicText\">",
" <p class=\"headingAnchor\" id=\"H1\">",
" <span class=\"h1\">",
" INTRODUCTION",
" </span>",
" &nbsp;&mdash;&nbsp;Among the causes of Cushing's syndrome are three rare types
of nodular adrenocortical diseases that are usually bilateral:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Corticotropin (ACTH)-dependent bilateral macronodular hyperplasia secondary
to long-term adrenal stimulation in patients with Cushing's disease or ectopic ACTH
syndrome.",
" </li>",
" <li>",
" ACTH-independent micronodular adrenal hyperplasia and its most frequent
variant primary pigmented nodular adrenocortical disease (PPNAD), which may be
sporadic or familial (as part of the Carney complex).",
" </li>",
" <li>",
" ACTH-independent bilateral macronodular adrenal hyperplasia (AIMAH).",
" </li>",
" </ul>",
" </p>",
" <p>",
" ACTH-independent bilateral macronodular adrenal hyperplasia will be reviewed
here. Other causes of Cushing's syndrome, and primary pigmented nodular
adrenocortical disease are discussed separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?25/55/26489?
source=see_link\">",
" \"Causes and pathophysiology of Cushing's syndrome\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?21/35/22072?
source=see_link\">",
" \"Cushing's syndrome due to primary pigmented nodular adrenocortical
disease\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H2\">",
" <span class=\"h1\">",
" CLINICAL FEATURES",
" </span>",
" &nbsp;&mdash;&nbsp;ACTH-independent macronodular adrenal hyperplasia (AIMAH)
has been described by various terms, including massive macronodular adrenocortical
disease (MMAD), autonomous macronodular adrenal hyperplasia (AMAH), ACTH-
independent massive bilateral adrenal disease (AIMBAD), and \"giant\" or \"huge\"
macronodular adrenal disease. AIMAH results in hypercortisolism through a number of
mechanisms that are described below. (See",
" <a class=\"local\" href=\"#H4\">",
" 'Pathogenesis'",
" </a>",
" below.)",
" </p>",
" <p>",
" AIMAH is associated with adrenal glands weighing from 24 to 500 g that contain
multiple nonpigmented nodules greater than 5 mm in diameter [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/1-3\">",
" 1-3",
" </a>",
" ]. The nodules appear to be typical benign adrenal nodules, but the
internodular cortex may be either hyperplastic or atrophic.",
" </p>",
" <p>",
" Most patients with AIMAH and Cushing&rsquo;s syndrome present in the fifth and
sixth decades [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/1-4\">",
" 1-4",
" </a>",
" ], a later age of onset compared with unilateral cortisol-producing adenomas,
PPNAD or pituitary corticotroph adenomas (Cushing's disease). The majority of
patients with AIMAH have only subclinical cortisol production and present with
bilateral adrenal incidentalomas [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/5\">",
" 5",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H3\">",
" <span class=\"h2\">",
" Biochemical",
" </span>",
" &nbsp;&mdash;&nbsp;Laboratory findings in AIMAH with overt Cushing's syndrome
are the same as those seen in ACTH-independent Cushing's syndrome with unilateral
tumors and include the following:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Increased serum and urinary cortisol and undetectable plasma ACTH in the
basal state and after administration of corticotropin-releasing hormone [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/1-4\">",
" 1-4",
" </a>",
" ].",
" </li>",
" <li>",
" Cortisol production is not suppressed by low or high-dose",
" <a class=\"drug drug_general\" href=\"UTD.htm?33/4/33856?
source=see_link\">",
" dexamethasone",
" </a>",
" .",
" </li>",
" <li>",
" An exception to this general pattern occurs in patients with gastric
inhibitory polypeptide (GIP)-dependent Cushing's syndrome in whom cortisol
hypersecretion occurs in response to meals and serum cortisol may be low in the
fasting state [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/6,7\">",
" 6,7",
" </a>",
" ].",
" </li>",
" <li>",
" Steroid hormone synthesis is relatively inefficient in AIMAH, as a
consequence of decreased steroidogenic enzymatic activity resulting frequently in
elevated 17-hydroxyprogesterone levels after stimulation with ACTH [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/8,9\">",
" 8,9",
" </a>",
" ]. This probably explains why urinary 17-hydroxycorticosteroids (17-OHCS),
which also measure precursor steroids, are more often elevated than urinary free
cortisol levels in AIMAH [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/10\">",
" 10",
" </a>",
" ].",
" </li>",
" <li>",
" Serum aldosterone, 18-hydroxycorticosterone, corticosterone, and estrone may
cause hypertension or feminization in the rare patients in whom they are increased
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/11\">",
" 11",
" </a>",
" ].",
" </li>",
" <li>",
" A case of bilateral massive AIMAH in a male patient was found to produce
large amounts of adrenal androgens without any cortisol excess or clinical symptoms
and was detected only as bilateral incidentaloma [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/12\">",
" 12",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p>",
" AIMAH can be distinguished from ACTH-dependent macronodular hyperplasia by
measuring plasma ACTH. Plasma ACTH is suppressed by excess cortisol in AIMAH
(&lt;5",
" <span class=\"nowrap\">",
" pg/mL",
" </span>",
" [&lt;1.1",
" <span class=\"nowrap\">",
" pmol/L])",
" </span>",
" and is inappropriately normal or high in ACTH-dependent macronodular
hyperplasia (&ge;15",
" <span class=\"nowrap\">",
" pg/mL",
" </span>",
" [3.3",
" <span class=\"nowrap\">",
" pmol/L]).",
" </span>",
" </p>",
" <p>",
" Rare patients with ACTH-dependent hyperplasia have low, but consistently
detectable plasma ACTH concentrations (&le;10",
" <span class=\"nowrap\">",
" pg/mL",
" </span>",
" [2.8",
" <span class=\"nowrap\">",
" pmol/L]),",
" </span>",
" presumably due to its suppression by some of their adrenal nodules, which have
acquired the capacity to secrete cortisol \"autonomously\" or constitutively by
unidentified mechanisms [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/13,14\">",
" 13,14",
" </a>",
" ]. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?30/31/31225?
source=see_link\">",
" \"Establishing the cause of Cushing's syndrome\"",
" </a>",
" .)",
" </p>",
" <p>",
" The majority of patients with primary bilateral macronodular adrenal
hyperplasia have subclinical Cushing's syndrome and, therefore, their ACTH levels
may not be suppressed, particularly when urine free cortisol is still in the normal
range [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/8\">",
" 8",
" </a>",
" ]. In these patients, low or high dose",
" <a class=\"drug drug_general\" href=\"UTD.htm?33/4/33856?source=see_link\">",
" dexamethasone",
" </a>",
" will produce partial suppression of cortisol, but not to less than 1.8",
" <span class=\"nowrap\">",
" mcg/dL",
" </span>",
" (50",
" <span class=\"nowrap\">",
" nmol/L)",
" </span>",
" in the morning following night-time dexamethasone administration [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/8,15\">",
" 8,15",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H4\">",
" <span class=\"h1\">",
" PATHOGENESIS",
" </span>",
" &nbsp;&mdash;&nbsp;Both aberrant hormone receptors and genetic mutations have
been identified in the pathogenesis of ACTH-independent macronodular adrenal
hyperplasia.",
" </p>",
" <p class=\"headingAnchor\" id=\"H5\">",
" <span class=\"h2\">",
" Aberrant hormone receptors",
" </span>",
" &nbsp;&mdash;&nbsp;The most prevalent abnormality in patients with AIMAH
results from the aberrant adrenal expression of ectopic or increased activity of
eutopic peptide hormone receptors&nbsp;(",
" <a class=\"graphic graphic_table graphicRef65003 \" href=\"UTD.htm?
5/58/6061\">",
" table 1",
" </a>",
" ) [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/15,16\">",
" 15,16",
" </a>",
" ]. Cortisol secretion becomes driven by a hormone that escapes cortisol-
mediated feedback.",
" </p>",
" <p class=\"headingAnchor\" id=\"H596836211\">",
" <span class=\"h3\">",
" Receptor types",
" </span>",
" </p>",
" <p class=\"headingAnchor\" id=\"H6\">",
" <span class=\"h4\">",
" GIP",
" </span>",
" &nbsp;&mdash;&nbsp;The ectopic expression of glucose-dependent insulinotropic
peptide (also known as gastric inhibitory polypeptide or GIP) receptor in zona
fasciculata cells causes \"food-dependent\" cortisol production.",
" </p>",
" <p>",
" Plasma cortisol levels may be relatively low during fasting and increase
transiently following meals [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/6,7,17\">",
" 6,7,17",
" </a>",
" ]. GIP-dependent Cushing's syndrome has been identified in approximately 20
patients with AIMAH [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/6,7,17-21\">",
" 6,7,17-21",
" </a>",
" ]. GIP receptors are not expressed in the normal adult or fetal zona
fasciculata [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/17-20,22\">",
" 17-20,22",
" </a>",
" ].",
" </p>",
" <p>",
" Aberrant GIP receptor expression has also been identified in unilateral
adrenal adenomas causing Cushing's syndrome [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/6,7,17-20\">",
" 6,7,17-20",
" </a>",
" ] or primary aldosteronism [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/22\">",
" 22",
" </a>",
" ], although this is rare: only 1 of 16 adenomas in one series expressed the
receptor [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/18\">",
" 18",
" </a>",
" ]. The adrenal nodules in rare patients with AIMAH can progress
asynchronously, first in one adrenal, later in the other [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/20\">",
" 20",
" </a>",
" ]; in one report, the adrenal adjacent to the macronodules was not atrophic,
but showed diffuse adrenal hyperplasia with ectopic GIP receptor expression [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/20\">",
" 20",
" </a>",
" ], suggesting that larger nodules were the result of secondary clonal
proliferation events [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/23\">",
" 23",
" </a>",
" ].",
" </p>",
" <p>",
" Other reported cases include a patient with GIP-dependent androgen and
cortisol secretion in an adrenal adenoma [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/24\">",
" 24",
" </a>",
" ], and patients with combined aberrant expression of GIP receptor and",
" <span class=\"nowrap\">",
" LH/hCG",
" </span>",
" receptor [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/25,26\">",
" 25,26",
" </a>",
" ] or with leptin receptor [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/27\">",
" 27",
" </a>",
" ].",
" </p>",
" <p>",
" The factors responsible for overexpression of the GIP receptor (GIPR) are not
known. Thus far, GIPR gene mutations have not been identified [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/28\">",
" 28",
" </a>",
" ]. One study suggested that chronic stimulation by ACTH in Cushing's disease
could lead to increased GIPR expression [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/29\">",
" 29",
" </a>",
" ], but others did not [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/19,30,31\">",
" 19,30,31",
" </a>",
" ]. Several genes have been identified that are differentially expressed in
GIP-dependent AIMAH or unilateral adenomas, compared with normal adrenals, or those
in Cushing's disease, and form the basis to investigate which one is specifically
implicated in the ectopic expression of GIPR in the adrenal fasciculata [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/23,32\">",
" 23,32",
" </a>",
" ].",
" </p>",
" <p>",
" Hypercortisolism due to ectopic GIP receptor expression has also been
demonstrated in an animal model. Bovine adrenal cells transfected with the GIP
receptor and injected under the renal capsule of nude mice generate adrenal-like
hyperplastic nodules that produce glucocorticoid excess [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/33\">",
" 33",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H7\">",
" <span class=\"h4\">",
" Vasopressin",
" </span>",
" &nbsp;&mdash;&nbsp;Vasopressin-responsive Cushing's syndrome has been reported
in several patients with AIMAH or a unilateral adenoma. In these patients, cortisol
secretion increased with upright posture or other physiological stimuli of
endogenous vasopressin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/8,15,16,25,34-40\">",
" 8,15,16,25,34-40",
" </a>",
" ]. In most, cortisol secretion was regulated by the V1-vasopressin receptor,
expressed at either normal or high levels.",
" </p>",
" <p>",
" The V1-vasopressin receptor is normally expressed in the adrenal cortex but is
not a major regulator of steroidogenesis. In the patients with AIMAH, the
exaggerated steroidogenic responses to vasopressin are secondary to the increased
activity",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" expression of a \"eutopic\" receptor-effector system. One patient had
orthostatic hypotension that persisted after bilateral adrenalectomy, suggesting a
possible alteration in adrenal and vascular responses of the vasopressin signal
transduction pathway [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/35\">",
" 35",
" </a>",
" ].",
" </p>",
" <p>",
" Ectopic expression of V2- and V3-vasopressin receptors has been reported in
some AIMAH cases. The significance of this finding is unclear, because a cortisol
response was not observed when dDAVP, a preferential V2-vasopressin receptor
agonist, was administered to some of these patients [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/39,40\">",
" 39,40",
" </a>",
" ]. However, in vitro studies suggest that in some cases of AIMAH, vasopressin
hyper-responsiveness is mediated by V2-vasopressin receptor, while V1-vasopressin
receptor can be repressed [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/41\">",
" 41",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H8\">",
" <span class=\"h4\">",
" Beta adrenergic",
" </span>",
" &nbsp;&mdash;&nbsp;AIMAH and Cushing's syndrome have been reported in patients
with aberrant adrenal expression of beta-adrenergic receptors. In one patient,
plasma cortisol and aldosterone levels increased in response to an increase in
endogenous catecholamines (upright posture, insulin-induced hypoglycemia and
exercise) [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/42\">",
" 42",
" </a>",
" ].",
" <a class=\"drug drug_general\" href=\"UTD.htm?22/31/23029?source=see_link\">",
" Isoproterenol",
" </a>",
" infusion stimulated cortisol and aldosterone secretion in this patient, and",
" <a class=\"drug drug_general\" href=\"UTD.htm?8/49/8986?source=see_link\">",
" propranolol",
" </a>",
" blocked this effect and reduced basal cortisol secretion with long-term
control of hypercortisolism. These effects were not seen in normal subjects.",
" </p>",
" <p>",
" Similar findings have been reported in other patients with AIMAH [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/36,38,43\">",
" 36,38,43",
" </a>",
" ]. High affinity binding sites compatible with beta-1- or beta-2-adrenergic
receptors were efficiently coupled to steroidogenesis in the adrenal tissues in
these patients, but not in controls, indicating the ectopic nature of this receptor
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/38,42,43\">",
" 38,42,43",
" </a>",
" ].",
" </p>",
" <p>",
" The combined presence of adrenal beta-adrenergic receptor and V1-vasopressin
receptor has been observed in other patients with AIMAH [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/36,38,43\">",
" 36,38,43",
" </a>",
" ]; fluctuations of endogenous physiological levels of vasopressin (water and
hypertonic sodium loading) resulted in parallel changes of plasma cortisol levels
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/36\">",
" 36",
" </a>",
" ]. In one patient with AIMAH, the combined overexpression of beta-2-
adrenoreceptor, of serotonin 5HT4 receptor, and V1- vasopressin receptor was
demonstrated [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/44\">",
" 44",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H9\">",
" <span class=\"h4\">",
" LH/hCG",
" </span>",
" &nbsp;&mdash;&nbsp;Hypercortisolism due to aberrant",
" <span class=\"nowrap\">",
" LH/hCG",
" </span>",
" receptors was first identified in a woman with transient Cushing's syndrome
during sequential pregnancies. Persistent Cushing's syndrome and AIMAH developed
only after the postmenopausal sustained increase of LH secretion [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/45\">",
" 45",
" </a>",
" ]. Administration of the long-acting GnRH agonist,",
" <a class=\"drug drug_general\" href=\"UTD.htm?4/41/4760?source=see_link\">",
" leuprolide",
" </a>",
" acetate, resulted in suppression of endogenous LH and normalization of
cortisol production [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/45\">",
" 45",
" </a>",
" ].",
" </p>",
" <p>",
" A 59-year old virilized woman with androgen-secreting AIMAH regulated by hCG
was shown to express the",
" <span class=\"nowrap\">",
" LH/hCG",
" </span>",
" receptor in one resected adrenal; suppression of endogenous LH with",
" <a class=\"drug drug_general\" href=\"UTD.htm?4/41/4760?source=see_link\">",
" leuprolide",
" </a>",
" acetate normalized androgen secretion from the contralateral adrenal, avoiding
bilateral adrenalectomy [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/46\">",
" 46",
" </a>",
" ].",
" </p>",
" <p>",
" Other cases of aberrant receptors for",
" <span class=\"nowrap\">",
" LH/hCG",
" </span>",
" or serotonin either alone or in combination have been reported [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/8,25,47\">",
" 8,25,47",
" </a>",
" ]. In the patient described above [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/45\">",
" 45",
" </a>",
" ], serotonin 5-HT4 receptor agonists, cisapride and",
" <a class=\"drug drug_general\" href=\"UTD.htm?0/13/216?source=see_link\">",
" metoclopramide",
" </a>",
" , also stimulated plasma cortisol.",
" </p>",
" <p class=\"headingAnchor\" id=\"H10\">",
" <span class=\"h4\">",
" Serotonin",
" </span>",
" &nbsp;&mdash;&nbsp;Following the initial description of combined aberrant LH
and serotonin 5-HT4 receptors in AIMAH, several other patients were found to have
increased secretion of cortisol following stimulation with cisapride,",
" <a class=\"drug drug_general\" href=\"UTD.htm?0/13/216?source=see_link\">",
" metoclopramide",
" </a>",
" or",
" <a class=\"drug drug_general\" href=\"UTD.htm?4/4/4164?source=see_link\">",
" tegaserod",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/8,25,40,47-50\">",
" 8,25,40,47-50",
" </a>",
" ]. In most cases, a large overexpression of 5-HT4 receptor was found in the
adrenals [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/51-53\">",
" 51-53",
" </a>",
" ]. The ectopic expression and function of 5-HT7 receptor was identified in a
patient with serotonin-responsive AIMAH and Cushing's syndrome [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/50\">",
" 50",
" </a>",
" ] and in one patient with adrenal carcinoma who also secreted renin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/54\">",
" 54",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H11\">",
" <span class=\"h4\">",
" Angiotensin",
" </span>",
" &nbsp;&mdash;&nbsp;In a patient with AIMAH and a large increase in plasma
aldosterone and cortisol levels during upright posture, short-term oral
administration of the angiotensin-1 receptor antagonist",
" <a class=\"drug drug_general\" href=\"UTD.htm?37/48/38663?source=see_link\">",
" candesartan",
" </a>",
" completely inhibited the elevation in cortisol and aldosterone [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/55\">",
" 55",
" </a>",
" ]. In vitro stimulation of cortisol secretion by angiotensin-II was also found
in patients with AIMAH and Cushing's syndrome who had increases in cortisol levels
with upright posture [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/25\">",
" 25",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H428975\">",
" <span class=\"h3\">",
" Systematic screening for aberrant receptors",
" </span>",
" &nbsp;&mdash;&nbsp;In series of patients with AIMAH who underwent screening
for aberrant receptors, more than 85 percent were found to have at least one and
usually several aberrant responses; the most frequent were those to vasopressin,
serotonin-4 agonists (patients with Cushing&rsquo;s syndrome), and to",
" <a class=\"drug drug_general\" href=\"UTD.htm?24/32/25093?source=see_link\">",
" glucagon",
" </a>",
" (in subclinical cortisol secretion) [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/9,10,36\">",
" 9,10,36",
" </a>",
" ].",
" </p>",
" <p>",
" In a study that looked to identify novel abnormally expressed G protein-
coupled receptors (GPCRs) in patients with AIMAH, several new aberrant receptor
genes were identified, one of which (the a2A adrenergic receptor [ADRA2A], highly
expressed in 13 of 18 AIMAHs) may be a potential target for pharmacologic treatment
of Cushing&rsquo;s syndrome due to AIMAH [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/56\">",
" 56",
" </a>",
" ].",
" <a class=\"drug drug_general\" href=\"UTD.htm?18/53/19289?source=see_link\">",
" Clonidine",
" </a>",
" (an ADRA2A agonist) administration resulted in an increase in cortisol
production; the increase could be blocked by an ADRA2A antagonist, yohimbine.",
" </p>",
" <p class=\"headingAnchor\" id=\"H596836184\">",
" <span class=\"h2\">",
" Paracrine mechanisms in AIMAH",
" </span>",
" &nbsp;&mdash;&nbsp;Paracrine regulatory mechanisms were suggested in some
AIMAH cases after the demonstration of increased adrenocortical expression of",
" <span class=\"nowrap\">",
" pro-opiomelanocortin/ACTH,",
" </span>",
" serotonin or vasopressin in some affected AIMAH tissues [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/50,57\">",
" 50,57",
" </a>",
" ]. Thus, in addition to the aberrant expression of diversified hormone
receptors, the local adrenal (adrenal cortex, adrenal medulla, and adrenal",
" <span class=\"nowrap\">",
" tumor/hyperplasia)",
" </span>",
" production of ligands for these receptors could allow an important
contribution of paracrine or autocrine regulation in addition to the hormonal
regulation of circulating hormones for these receptors.",
" </p>",
" <p class=\"headingAnchor\" id=\"H12\">",
" <span class=\"h2\">",
" Genetic causes",
" </span>",
" &nbsp;&mdash;&nbsp;Several molecular causes have been identified in the
pathogenesis of ACTH-independent macronodular adrenal hyperplasia indicating that
it is a heterogeneous disease [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/10\">",
" 10",
" </a>",
" ].",
" </p>",
" <p>",
" Gs alpha-subunit mutations &mdash; Cushing's syndrome associated with McCune-
Albright syndrome (MAS) is a rare variant of AIMAH. MAS is a sporadic disease
characterized by polyostotic fibrous dysplasia with caf&eacute; au lait spots,
sexual precocity, and other endocrine and nonendocrine disorders [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/51,58\">",
" 51,58",
" </a>",
" ]. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?19/5/19546?
source=see_link&amp;anchor=H3989453#H3989453\">",
" \"Definition, etiology, and evaluation of precocious puberty\", section on
'McCune-Albright syndrome'",
" </a>",
" .)",
" </p>",
" <p>",
" During the blastocyst phase of embryogenesis, an activating somatic Arg201Cys
or Arg201His mutation of the gene coding for the alpha-subunit stimulatory guanine
nucleotide-binding protein, Gs, occurs in some adrenal cells in a mosaic pattern,
which leads to the formation of adrenal nodules. Constitutive activation of the
cAMP pathway in the nodules leads to excess cortisol secretion and ACTH suppression
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/59\">",
" 59",
" </a>",
" ]; the internodular adrenal cortex, where the Gsa mutation is not present,
becomes atrophic [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/59,60\">",
" 59,60",
" </a>",
" ].",
" </p>",
" <p>",
" Ten patients with Cushing's syndrome and MAS have been reported, five males
and five females, eight of whom were less than six months old. Activating mutations
of Gsa have been occasionally found in the AIMAH nodules of pediatric or adult
patients without any other features of McCune-Albright syndrome [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/60,61\">",
" 60,61",
" </a>",
" ].",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" MEN1 &mdash; Bilateral adrenal nodules have also been described as part of
multiple endocrine neoplasia syndrome type 1 (MEN1), which is caused by the tumor
suppressor gene menin. In a series of 33 MEN1 patients, bilateral adrenal
enlargement was found in 21 percent; more than half of the remaining patients also
had unilateral adenomas or carcinomas [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/62\">",
" 62",
" </a>",
" ]. Similarly, in 33 patients from a single kindred with MEN1, the overall
prevalence of adrenal disease was 36 percent; bilateral macronodular cortical
hyperplasia was present in 6 percent [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/52\">",
" 52",
" </a>",
" ]. In the vast majority of MEN1 patients with adrenal lesions, there was no
evidence of abnormal hormone secretion. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?42/14/43240?
source=see_link\">",
" \"Multiple endocrine neoplasia type 1: Clinical manifestations and
diagnosis\"",
" </a>",
" .) However, some cases of AIMAH with Cushing&rsquo;s syndrome were found to
have MEN1 or MEN1-like syndrome (hyperparathyroidism, insulinomas",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" pituitary tumors) with or without MEN1 mutations [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/10,63-65\">",
" 10,63-65",
" </a>",
" ].",
" </li>",
" <li>",
" MC2R gene &mdash; There are rare reports of activating mutations of the ACTH
receptor (MC2R) gene in adrenal tumors. In one case of AIMAH, a MC2R mutation
(F278C) was associated with elevated basal cAMP production when compared with wild-
type receptor-expressing cell lines. This mutation in the C-terminal tail of the
MC2R impaired desensitization and internalization of the receptor [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/53\">",
" 53",
" </a>",
" ].",
" <br/>",
" <br/>",
" Two mutations in the same allele of the MC2R associated with clinical
hypersensitivity to ACTH have been described in a single case report. The presence
of both C21R and S247G mutations in the same molecule leads to a receptor with a
highly significant elevation in constitutive activity; the co-expression of the
normal MC2R allele results in the retention of a normal dose response to ACTH
despite the presence of constitutive activity [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/66\">",
" 66",
" </a>",
" ]. In one case of AIMAH, an increase in mRNA for MC2R was suggested [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/67\">",
" 67",
" </a>",
" ], but in other series of patients with AIMAH, MC2R levels were decreased
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/23,68\">",
" 23,68",
" </a>",
" ].",
" </li>",
" <li>",
" Other genes &mdash; AIMAH or adrenal nodules have been reported in patients
with familial polyposis coli and a mutation in the adenomatous polyposis coli (APC)
gene [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/10,69\">",
" 10,69",
" </a>",
" ] and with hereditary leiomyomatosis and renal cell cancer disorders due to
mutations in the fumarate hydratase gene (FH) on chromosome 1q42.3-43 [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/70\">",
" 70",
" </a>",
" ]. Missense germline mutations in phosphodiesterase 11A isoform 4 gene
(PDE11A) located on chromosome 2q31-35 have been identified initially in kindreds
with non-pigmented micronodular hyperplasia but have now been found at higher
frequency in patients with various adrenocortical tumors including bilateral
macronodular adrenal hyperplasia [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/71\">",
" 71",
" </a>",
" ]. Differential expression of several microRNAs were identified in AIMAH
tissues and some appeared to be correlated with severity of disease and
hypercortisolism [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/72\">",
" 72",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p class=\"headingAnchor\" id=\"H14\">",
" <span class=\"h2\">",
" Familial forms",
" </span>",
" &nbsp;&mdash;&nbsp;Most initial cases of AIMAH appeared to be sporadic;
however, family screening was not performed systematically [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/1-4\">",
" 1-4",
" </a>",
" ]. There are now several reports of familial cases of AIMAH whose presentation
suggests autosomal dominant transmission [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/38-40,73-77\">",
" 38-40,73-77",
" </a>",
" ]. As noted above, AIMAH is probably genetically heterogeneous with occasional
cases that occur in association with other syndromes [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/10,52,62,69,70,78\">",
" 10,52,62,69,70,78",
" </a>",
" ]. (See",
" <a class=\"local\" href=\"#H12\">",
" 'Genetic causes'",
" </a>",
" above.)",
" </p>",
" <p>",
" In familial cases of isolated AIMAH, a number of aberrant hormone receptors
have been identified in individual families, including V1-V2- and V3-vasopressin
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/39\">",
" 39",
" </a>",
" ], beta-adrenergic [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/76\">",
" 76",
" </a>",
" ], combined V1-vasopressin and beta-adrenergic [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/38\">",
" 38",
" </a>",
" ], and combined 5HT4 and V1-V-2 vasopressin [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/40\">",
" 40",
" </a>",
" ]. The germline transmission of the same receptors' phenotype in all affected
family members support a primary role of aberrant receptors in the pathophysiology
of this type of AIMAH. The prevalence of familial forms of AIMAH are not known
yet.",
" </p>",
" <p class=\"headingAnchor\" id=\"H15\">",
" <span class=\"h1\">",
" DIAGNOSIS",
" </span>",
" &nbsp;&mdash;&nbsp;The clinical presentation and biochemical findings of
Cushing's syndrome in AIMAH are similar to that seen in other types of ACTH-
independent Cushing's syndrome, as described above (see",
" <a class=\"local\" href=\"#H2\">",
" 'Clinical features'",
" </a>",
" above).",
" </p>",
" <p>",
" AIMAH can be distinguished from ACTH-dependent macronodular hyperplasias by
measuring plasma ACTH. Plasma ACTH is suppressed by excess cortisol in AIMAH
(&lt;5",
" <span class=\"nowrap\">",
" pg/mL",
" </span>",
" [&lt;1.1",
" <span class=\"nowrap\">",
" pmol/L])",
" </span>",
" and is inappropriately normal or slightly high in ACTH-dependent macronodular
hyperplasia (&ge;15",
" <span class=\"nowrap\">",
" pg/mL",
" </span>",
" [3.3",
" <span class=\"nowrap\">",
" pmol/L]).",
" </span>",
" (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?30/31/31225?
source=see_link\">",
" \"Establishing the cause of Cushing's syndrome\"",
" </a>",
" .)",
" </p>",
" <p>",
" Among the ACTH-independent types of Cushing's syndrome, there are several
features that are suggestive of AIMAH:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Most patients with overt Cushing's syndrome due to AIMAH present in the
fifth and sixth decades [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/1-4\">",
" 1-4",
" </a>",
" ], a later age of onset compared with unilateral cortisol-producing
adenomas, or PPNAD.",
" </li>",
" <li>",
" While the typical laboratory findings of ACTH-independent Cushing's syndrome
include high serum and urinary cortisol and suppressed plasma ACTH concentrations
[",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/1-4\">",
" 1-4",
" </a>",
" ], an exception to this general pattern occurs in patients with GIP-
dependent Cushing's syndrome, in whom cortisol hypersecretion occurs in response to
meals [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/6,7\">",
" 6,7",
" </a>",
" ].",
" </li>",
" <li>",
" Serum aldosterone, 18-hydroxycorticosterone, corticosterone, and estrone may
cause hypertension or feminization in the rare AIMAH patients in whom they are
increased [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/11\">",
" 11",
" </a>",
" ].",
" </li>",
" <li>",
" Subclinical Cushing's syndrome in AIMAH with normal urinary free cortisol,
detectable ACTH levels still responsive to CRH, but with subnormal suppression of
plasma cortisol following",
" <a class=\"drug drug_general\" href=\"UTD.htm?33/4/33856?
source=see_link\">",
" dexamethasone",
" </a>",
" has become increasingly recognized [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/8,15,16\">",
" 8,15,16",
" </a>",
" ].",
" </li>",
" <li>",
" Steroid hormone synthesis is inefficient in AIMAH, as a consequence of
decreased steroidogenic enzymatic expression and activity [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/23,32,68,79\">",
" 23,32,68,79",
" </a>",
" ]. Furthermore, elevated 17-hydroxyprogesterone levels occur following
stimulation with ACTH providing in vivo evidence of altered adrenocortical
enzymatic activity [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/8,9\">",
" 8,9",
" </a>",
" ]. This inefficient steroidogenesis may explain the discrepancy between the
sometimes subtle changes in cortisol hypersecretion such as seen in subclinical
Cushing's syndrome and the massive adrenal enlargement.",
" </li>",
" </ul>",
" </p>",
" <p>",
" Despite these steroidogenic enzyme defects, the increase in cortisol following
administration of exogenous ACTH is larger than in normal adrenals and reflects the
large adrenal cell mass [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/36\">",
" 36",
" </a>",
" ].",
" </p>",
" <p>",
" This can be useful in distinguishing AIMAH from other causes of bilaterally
enlarged adrenals such as metastatic or infiltrative diseases, where steroidogenic
response to ACTH administration is decreased.",
" </p>",
" <p class=\"headingAnchor\" id=\"H16\">",
" <span class=\"h2\">",
" Imaging",
" </span>",
" &nbsp;&mdash;&nbsp;The results of adrenal CT and MR imaging are variable,
ranging from apparently unilateral nodules to massive bilateral enlargement [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/1-4,20,80\">",
" 1-4,20,80",
" </a>",
" ]. In one series of 12 patients, 11 had enlarged multinodular glands, with
nodules 0.1 to 5.5 cm in diameter. In nine patients who underwent pituitary CT or
MRI, all were normal. Adrenal scintigraphy with 131-I-labeled cholesterol showed
bilateral uptake in four of five patients.",
" </p>",
" <p class=\"headingAnchor\" id=\"H17\">",
" <span class=\"h2\">",
" Aberrant receptors",
" </span>",
" &nbsp;&mdash;&nbsp;Protocols have been developed to systematically evaluate
patients with adrenal CS for the presence of aberrant adrenal hormone receptors
that are frequently present in AIMAH with overt or sub-clinical Cushing's syndrome
(",
" <a class=\"graphic graphic_table graphicRef65003 \" href=\"UTD.htm?
5/58/6061\">",
" table 1",
" </a>",
" ) [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/9,10,15,16,25,36\">",
" 9,10,15,16,25,36",
" </a>",
" ]. The strategy is to examine whether cortisol or other steroids change in
response to physiological (upright posture, mixed meals) and pharmacological
(gonadotropin-releasing hormone, thyrotropin-releasing hormone, vasopressin,",
" <a class=\"drug drug_general\" href=\"UTD.htm?24/32/25093?source=see_link\">",
" glucagon",
" </a>",
" ,",
" <a class=\"drug drug_general\" href=\"UTD.htm?0/13/216?source=see_link\">",
" metoclopramide",
" </a>",
" ) tests that modulate the levels of ligands for the potential aberrant
receptors.",
" </p>",
" <p>",
" We recommend that all patients with AIMAH and clinical or subclinical CS
undergo screening for aberrant receptors, as this may change the therapeutic
strategy (",
" <a class=\"graphic graphic_table graphicRef65003 \" href=\"UTD.htm?
5/58/6061\">",
" table 1",
" </a>",
" ).",
" </p>",
" <p class=\"headingAnchor\" id=\"H18\">",
" <span class=\"h2\">",
" Screening family members",
" </span>",
" &nbsp;&mdash;&nbsp;Family members (over age 25 to 30 years) of patients with
AIMAH with aberrant receptors should undergo screening for subclinical or clinical
AIMAH. We suggest performing the 1 mg overnight",
" <a class=\"drug drug_general\" href=\"UTD.htm?33/4/33856?source=see_link\">",
" dexamethasone",
" </a>",
" tests; those who do not suppress their plasma cortisol on the following
morning below 1.8",
" <span class=\"nowrap\">",
" mcg/dL",
" </span>",
" (50",
" <span class=\"nowrap\">",
" nmol/L)",
" </span>",
" should have an adrenal CT scan. Family members who are found to have
hypercortisolism should also undergo evaluation for aberrant hormone receptors.
Patients with AIMAH associated with genetic causes such as MEN 1 or polyposis coli
have their familial screening for other purposes. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?21/25/21913?
source=see_link\">",
" \"Establishing the diagnosis of Cushing's syndrome\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H19\">",
" <span class=\"h1\">",
" TREATMENT",
" </span>",
" </p>",
" <p class=\"headingAnchor\" id=\"H20\">",
" <span class=\"h2\">",
" Surgery",
" </span>",
" &nbsp;&mdash;&nbsp;Surgical bilateral adrenalectomy is uniformly effective in
patients with AIMAH since this disorder is a primary adrenal disease [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/4,6,81\">",
" 4,6,81",
" </a>",
" ]. Surgical adrenalectomy is indicated in all patients with AIMAH and overt
Cushing's syndrome who have no evidence of aberrant hormone receptors, or who have
aberrant receptors that are not be amenable to medical therapy. (See",
" <a class=\"local\" href=\"#H21\">",
" 'Pharmacological therapy'",
" </a>",
" below.)",
" </p>",
" <p>",
" Post-adrenalectomy, these patients are not at risk for Nelson's syndrome
(corticotroph tumor progression) because the pituitary is intrinsically normal.
Therefore, pituitary radiation to prevent Nelson's syndrome is unnecessary. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?3/0/3081?
source=see_link\">",
" \"Medical therapy of hypercortisolism (Cushing&rsquo;s syndrome)\"",
" </a>",
" .)",
" </p>",
" <p>",
" Surgical adrenalectomy, including surgical approach and postoperative hormone
replacement, is discussed in greater detail separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?3/0/3081?
source=see_link\">",
" \"Medical therapy of hypercortisolism (Cushing&rsquo;s syndrome)\"",
" </a>",
" .)",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" In patients with moderately increased cortisol production (less than twofold
increase in urinary free cortisol levels), unilateral adrenalectomy often restores
urinary free cortisol levels to normal [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/82-84\">",
" 82-84",
" </a>",
" ]. However, as the cell mass subsequently increases in the contralateral
adrenal, a second adrenalectomy may become necessary [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/82-84\">",
" 82-84",
" </a>",
" ].",
" </li>",
" <li>",
" In patients with subclinical AIMAH and normal levels of urinary cortisol,
the decision for therapy should be based on manifestations of cortisol excess such
as hypertension, diabetes, osteoporosis, or neuropsychological manifestations. Many
of these are identified as incidentalomas initially.",
" </li>",
" </ul>",
" </p>",
" <p>",
" In patients who are being monitored without adrenal surgery, annual CT scan
and biochemical assessment are sufficient, as AIMAH is a benign process that has
not been shown to become malignant.",
" </p>",
" <p class=\"headingAnchor\" id=\"H21\">",
" <span class=\"h2\">",
" Pharmacological therapy",
" </span>",
" &nbsp;&mdash;&nbsp;Pharmacological therapy is used in two settings in AIMAH.
Adrenal enzyme inhibitors are sometimes given to patients with overt Cushing's
syndrome to control cortisol secretion before surgery [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/81\">",
" 81",
" </a>",
" ]. In patients in whom aberrant hormone receptors have been identified,
several potential therapies have been investigated as alternatives to
adrenalectomy, including the following:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Pharmacological blockade of postprandial release of GIP with",
" <a class=\"drug drug_general\" href=\"UTD.htm?42/7/43128?
source=see_link\">",
" octreotide",
" </a>",
" or",
" <a class=\"drug drug_general\" href=\"UTD.htm?27/21/27989?
source=see_link\">",
" pasireotide",
" </a>",
" led to clinical and biochemical improvement of Cushing's syndrome, but did
not persist in the long-term, probably because of eventual desensitization of
somatostatin receptors in GIP-secreting duodenal K cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/7,17,21\">",
" 7,17,21",
" </a>",
" ].",
" </li>",
" <li>",
" In catecholamine-dependent Cushing's syndrome and AIMAH, beta-adrenergic
receptor antagonists (",
" <a class=\"drug drug_general\" href=\"UTD.htm?8/49/8986?source=see_link\">",
" propranolol",
" </a>",
" ) were efficient in the long-term control of hypercortisolism [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/42,44\">",
" 42,44",
" </a>",
" ].",
" </li>",
" <li>",
" In",
" <span class=\"nowrap\">",
" LH/hCG-dependent",
" </span>",
" AIMAH and Cushing's syndrome, suppression of endogenous LH levels with long-
acting",
" <a class=\"drug drug_general\" href=\"UTD.htm?4/41/4760?source=see_link\">",
" leuprolide",
" </a>",
" acetate controlled steroid secretion and avoided bilateral adrenalectomy [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/45,46\">",
" 45,46",
" </a>",
" ].",
" </li>",
" <li>",
" When specific receptor antagonists for vasopressin, serotonin, GIP, or other
aberrant receptors become available, a broader range of pharmacological therapies
could become useful.",
" </li>",
" </ul>",
" </p>",
" <p>",
" However, it is possible that despite complete blockade of the aberrant
receptors, tumor regression does not occur, as other genetic events inducing
proliferative gain-of-function mutations (other than aberrant receptors) have
accumulated over time [",
" <a class=\"abstract\" href=\"UTD.htm?0/45/730/abstract/16,23,85\">",
" 16,23,85",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H22\">",
" <span class=\"h1\">",
" SUMMARY AND RECOMMENDATIONS",
" </span>",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" ACTH-independent macronodular adrenal hyperplasia (AIMAH) has been described
by various terms, including massive macronodular adrenocortical disease (MMAD),
autonomous macronodular adrenal hyperplasia (AMAH), ACTH-independent massive
bilateral adrenal disease (AIMBAD), and \"giant\" or \"huge\" macronodular adrenal
disease. AIMAH results in hypercortisolism through a number of mechanisms that are
described above. (See",
" <a class=\"local\" href=\"#H4\">",
" 'Pathogenesis'",
" </a>",
" above.)",
" </li>",
" <li>",
" The most prevalent abnormality in patients with AIMAH results from the
aberrant adrenal expression of ectopic or increased activity of eutopic peptide
hormone receptors. Cortisol secretion becomes driven by a hormone that escapes
cortisol-mediated feedback. Aberrant receptors that have been identified include
gastric inhibitory polypeptide (GIP), vasopressin, beta-adrenergic,",
" <span class=\"nowrap\">",
" LH/hCG,",
" </span>",
" serotonin,",
" <a class=\"drug drug_general\" href=\"UTD.htm?24/32/25093?
source=see_link\">",
" glucagon",
" </a>",
" , and angiotensin receptors. (See",
" <a class=\"local\" href=\"#H5\">",
" 'Aberrant hormone receptors'",
" </a>",
" above.)",
" </li>",
" <li>",
" The clinical presentation and biochemical findings of Cushing's syndrome in
AIMAH are similar to those seen in other types of ACTH-independent Cushing's
syndrome. However, patients with AIMAH typically have a later age of onset (fifth
and sixth decades), and patients with GIP-dependent Cushing's syndrome have a
unique pattern of cortisol hypersecretion (\"food-dependent\"). (See",
" <a class=\"local\" href=\"#H6\">",
" 'GIP'",
" </a>",
" above.)",
" </li>",
" <li>",
" We recommend that all patients with AIMAH and clinical or subclinical CS
undergo screening for aberrant receptors, as this may change the therapeutic
strategy. (See",
" <a class=\"local\" href=\"#H5\">",
" 'Aberrant hormone receptors'",
" </a>",
" above.)",
" </li>",
" <li>",
" In addition, we recommend screening of first degree relatives using 1 mg
overnight",
" <a class=\"drug drug_general\" href=\"UTD.htm?33/4/33856?
source=see_link\">",
" dexamethasone",
" </a>",
" suppression test for the presence of familial AIMAH. (See",
" <a class=\"local\" href=\"#H18\">",
" 'Screening family members'",
" </a>",
" above.)",
" </li>",
" </ul>",
" </p>",
" <p class=\"headingAnchor\" id=\"H23\">",
" <span class=\"h2\">",
" Management",
" </span>",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" We suggest treatment with beta-blockers for patients with AIMAH and aberrant
beta-adrenergic receptors (",
" <a class=\"grade\" href=\"._grade_6?title=Grade 2C\">",
" Grade 2C",
" </a>",
" ). (See",
" <a class=\"local\" href=\"#H21\">",
" 'Pharmacological therapy'",
" </a>",
" above.)",
" </li>",
" <li>",
" We suggest treatment with GnRH agonists (and sex steroid replacement) for
patients with AIMAH and",
" <span class=\"nowrap\">",
" LH/hCG",
" </span>",
" receptors (",
" <a class=\"grade\" href=\"._grade_6?title=Grade 2C\">",
" Grade 2C",
" </a>",
" ). (See",
" <a class=\"local\" href=\"#H21\">",
" 'Pharmacological therapy'",
" </a>",
" above.)",
" </li>",
" </ul>",
" </p>",
" <p>",
" In patients with AIMAH in whom aberrant hormone receptors are not present or
for which no specific pharmacological blockade is available or effective:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" We suggest bilateral adrenalectomy for severe Cushing's syndrome (",
" <a class=\"grade\" href=\"._grade_2?title=Grade 1B\">",
" Grade 1B",
" </a>",
" ). (See",
" <a class=\"local\" href=\"#H20\">",
" 'Surgery'",
" </a>",
" above.)",
" </li>",
" <li>",
" We suggest unilateral adrenalectomy in patients with moderately increased
cortisol production (less than twofold increase in urinary free cortisol levels)
(",
" <a class=\"grade\" href=\"._grade_6?title=Grade 2C\">",
" Grade 2C",
" </a>",
" ). (See",
" <a class=\"local\" href=\"#H20\">",
" 'Surgery'",
" </a>",
" above.)",
" </li>",
" </ul>",
" </p>",
" <p>",
" In patients with subclinical AIMAH and normal levels of urinary cortisol, the
decision for therapy should be based on manifestations of cortisol excess
(hypertension, diabetes, osteoporosis, or neuropsychological manifestations).",
" </p>",
" </div>",
" <div id=\"topicAgreement\">",
" Use of UpToDate is subject to the",
" <a class=\"licenseLink\" href=\"./license\" id=\"sla_in_page\"
target=\"_blank\">",
" Subscription and License Agreement",
" </a>",
" .",
" </div>",
" <div class=\"headingAnchor\" id=\"references\">",
" <h1>",
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" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/70\">",
" Matyakhina L, Freedman RJ, Bourdeau I, et al. Hereditary leiomyomatosis
associated with bilateral, massive, macronodular adrenocortical disease and
atypical cushing syndrome: a clinical and molecular genetic investigation. J Clin
Endocrinol Metab 2005; 90:3773.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/71\">",
" Lib&eacute; R, Fratticci A, Coste J, et al. Phosphodiesterase 11A (PDE11A)
and genetic predisposition to adrenocortical tumors. Clin Cancer Res 2008;
14:4016.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/72\">",
" Bimpaki EI, Iliopoulos D, Moraitis A, Stratakis CA. MicroRNA signature in
massive macronodular adrenocortical disease and implications for adrenocortical
tumourigenesis. Clin Endocrinol (Oxf) 2010; 72:744.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/73\">",
" Findlay JC, Sheeler LR, Engeland WC, Aron DC. Familial adrenocorticotropin-
independent Cushing's syndrome with bilateral macronodular adrenal hyperplasia. J
Clin Endocrinol Metab 1993; 76:189.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/74\">",
" Minami S, Sugihara H, Sato J, et al. ACTH independent Cushing's syndrome
occurring in siblings. Clin Endocrinol (Oxf) 1996; 44:483.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/75\">",
" Nies C, Bartsch DK, Ehlenz K, et al. Familial ACTH-independent Cushing's
syndrome with bilateral macronodular adrenal hyperplasia clinically affecting only
female family members. Exp Clin Endocrinol Diabetes 2002; 110:277.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/76\">",
" Im&ouml;hl M, K&ouml;ditz R, Stachon A, et al. [Catecholamine-dependent
hereditary Cushing's syndrome - follow-up after unilateral adrenalectomy]. Med Klin
(Munich) 2002; 97:747.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/77\">",
" Someya, T, et al. Folia Endocrinol 1996 72, 762, Watson TD et al Radiology
2007; 244: 923.",
" </a>",
" </li>",
" <li>",
" Oheda, T, et al. Folia Endocrinol 1995, 71:416.",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/79\">",
" Wada N, Kubo M, Kijima H, et al. Adrenocorticotropin-independent bilateral
macronodular adrenocortical hyperplasia: immunohistochemical studies of
steroidogenic enzymes and post-operative course in two men. Eur J Endocrinol 1996;
134:583.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/80\">",
" Doppman JL, Chrousos GP, Papanicolaou DA, et al. Adrenocorticotropin-
independent macronodular adrenal hyperplasia: an uncommon cause of primary adrenal
hypercortisolism. Radiology 2000; 216:797.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/81\">",
" Malchoff, CD, MacGillvray, D, Malchoff, DM. Adrenocortical hormone-
independent adrenal hyperplasia. Endocrinologist 1996; 6:79.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/82\">",
" Boronat M, Lucas T, Barcel&oacute; B, et al. Cushing's syndrome due to
autonomous macronodular adrenal hyperplasia: long-term follow-up after unilateral
adrenalectomy. Postgrad Med J 1996; 72:614.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/83\">",
" Lamas C, Alfaro JJ, Lucas T, et al. Is unilateral adrenalectomy an
alternative treatment for ACTH-independent macronodular adrenal hyperplasia?: Long-
term follow-up of four cases. Eur J Endocrinol 2002; 146:237.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/84\">",
" Iacobone M, Albiger N, Scaroni C, et al. The role of unilateral
adrenalectomy in ACTH-independent macronodular adrenal hyperplasia (AIMAH). World J
Surg 2008; 32:882.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/45/730/abstract/85\">",
" Almeida MQ, Harran M, Bimpaki EI, et al. Integrated genomic analysis of
nodular tissue in macronodular adrenocortical hyperplasia: progression of
tumorigenesis in a disorder associated with multiple benign lesions. J Clin
Endocrinol Metab 2011; 96:E728.",
" </a>",
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" TOPIC OUTLINE",
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" <ul>",
" <li>",
" <a class=\"sr_button\" href=\"#H22\" id=\"summRecButton\">",
" <span>",
" SUMMARY &amp; RECOMMENDATIONS",
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" </a>",
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" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H1\">",
" INTRODUCTION",
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" CLINICAL FEATURES",
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" Biochemical",
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" PATHOGENESIS",
" </a>",
" </li>",
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" Aberrant hormone receptors",
" </a>",
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" - Receptor types",
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" </li>",
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" GIP",
" </a>",
" </li>",
" <li class=\"bulletItem2\">",
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" Vasopressin",
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" Beta adrenergic",
" </a>",
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" LH/hCG",
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" Serotonin",
" </a>",
" </li>",
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" <a class=\"outlineLink\" href=\"#H11\">",
" Angiotensin",
" </a>",
" </li>",
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" <a class=\"outlineLink\" href=\"#H428975\">",
" - Systematic screening for aberrant receptors",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H596836184\">",
" Paracrine mechanisms in AIMAH",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H12\">",
" Genetic causes",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H14\">",
" Familial forms",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H15\">",
" DIAGNOSIS",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H16\">",
" Imaging",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H17\">",
" Aberrant receptors",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H18\">",
" Screening family members",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H19\">",
" TREATMENT",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H20\">",
" Surgery",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H21\">",
" Pharmacological therapy",
" </a>",
" </li>",
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" <a class=\"outlineLink\" href=\"#H22\">",
" SUMMARY AND RECOMMENDATIONS",
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" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H23\">",
" Management",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a href=\"#references\">",
" REFERENCES",
" </a>",
" </li>",
" </ul>",
" </div>",
" <h1>",
" <div class=\"openRelatedGraphics\" id=\"ENDO/148\" rel=\"outline_link\">",
" GRAPHICS",
" <a class=\"graphics_icon\" href=\"#\" title=\"View All Related Graphics\">",
" View All",
" </a>",
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" </h1>",
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1\">",
" Aberrant receptor screen",
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" <h1>",
" RELATED TOPICS",
" </h1>",
" <div id=\"relatedTopics\">",
" <ul>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?25/55/26489?
source=related_link\">",
" Causes and pathophysiology of Cushing's syndrome",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?21/35/22072?
source=related_link\">",
" Cushing's syndrome due to primary pigmented nodular adrenocortical disease",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?19/5/19546?
source=related_link\">",
" Definition, etiology, and evaluation of precocious puberty",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?30/31/31225?
source=related_link\">",
" Establishing the cause of Cushing's syndrome",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?21/25/21913?
source=related_link\">",
" Establishing the diagnosis of Cushing's syndrome",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?3/0/3081?
source=related_link\">",
" Medical therapy of hypercortisolism (Cushing&rsquo;s syndrome)",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?42/14/43240?
source=related_link\">",
" Multiple endocrine neoplasia type 1: Clinical manifestations and diagnosis",
" </a>",
" </li>",
" </ul>",
" </div>",
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" <tr>",
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" </td>",
" <td>",
" 2587 to 6828",
" </td>",
" </tr>",
" <tr>",
" <td>",
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" <td>",
" 1500",
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" <tr>",
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" 4329",
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" 7000",
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" 9756",
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" 11,300",
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" <tr>",
" <td>",
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" <td>",
" 16,239",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Treatment of mild hypertension (DBP 90 to 110 mmHg)",
" </td>",
" <td>",
" 24,408",
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" <tr>",
" <td>",
" Breast cancer screening",
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" <td>",
" 26,800",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Treatment of cholesterol &gt;265 mg/dL (6.9 mmol/L) with cholestyramine",
" </td>",
" <td>",
" 36,000 to &gt;1,000,000",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Dialysis",
" </td>",
" <td>",
" 37,000",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Streptokinase for acute MI in patients &ge;65 years old",
" </td>",
" <td>",
" 55,000",
" </td>",
" </tr>",
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" </div>",
" <div class=\"lgnd\">",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Adapted from: Croghan IT, Offord KP, Evans RW, et al, Mayo Clin Proc 1997;
72:917.",
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" * Parenteral prophylactic antimicrobials can be given as a single IV dose
begun within 60 minutes before the procedure. For prolonged procedures (&gt;3
hours) or those with major blood loss, or in patients with extensive burns,
additional intraoperative doses should be given at intervals one to two times the
half-life of the drug (ampicillin-sulbactam every 2 hours, cefazolin every 4 hours,
cefuroxime every 4 hours, cefoxitin every 2 hours, clindamycin every 6 hours,
vancomycin every 12 hours) for the duration of the procedure in patients with
normal renal function. If vancomycin or a fluoroquinolone is used, the infusion
should be started within 60 to 120 minutes before the initial incision to have
adequate tissue levels at the time of incision and to minimize the possibility of
an infusion reaction close to the time of induction of anesthesia.",
" <br/>",
" <span class=\"bullet\">",
" &bull;",
" </span>",
" Urine culture positive or unavailable, preoperative catheter, transrectal
prostatic biopsy, or placement of prosthetic material.",
" <br/>",
" &Delta; Due to increasing resistance of E. coli to fluoroquinolones and
ampicillin-sulbactam, local sensitivity profiles should be reviewed prior to use.",
" <br/>",
" <span class=\"lozenge\">",
" &loz;",
" </span>",
" Shock wave lithotripsy, ureteroscopy.",
" <br/>",
" &sect; Including percutaneous renal surgery, procedures with entry into the
urinary tract, and those involving implantation of a prosthesis. If manipulation of
bowel is involved, prophylaxis is given according to colorectal guidelines.",
" <br/>",
" &yen; For patients allergic to penicillins and cephalosporins, clindamycin or
vancomycin with either gentamicin, ciprofloxacin, levofloxacin, or aztreonam is a
reasonable alternative. Fluoroquinolones should not be used for prophylaxis in
cesarean section.",
" </div>",
" <div class=\"reference\">",
" Reprinted with special permission from: Treatment Guidelines from The Medical
Letter, October 2012; Vol. 10 (122):73.",
" <a href=\"file://www.medicalletter.org\" target=\"_blank\">",
" www.medicalletter.org",
" </a>",
" .",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
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var title_f0_45_734="Outcome surgery vs surveillance";
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" <div id=\"graphicsCopy\">",
" &copy;2013 UpToDate",
" ^{",
" &reg;",
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" Print",
" </a>",
" <a class=\"etacLink\" href=\"#\">",
" <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
title=\"Email graphic(s)\"/>",
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" <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
" Email",
" </a>",
" </div>",
" </div>",
" <div class=\"graphic\">",
" <div class=\"figure\" style=\"width: 470px\">",
" <div class=\"ttl\">",
" Patients undergoing elective repair of an abdominal aortic aneurysm do better
at eight years",
" </div>",
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" </div>",
" <div class=\"lgnd\">",
" In the UK Small Aneurysm trial of 1090 patients with a medium-sized abdominal
aortic aneurysm, there is no difference in survival with early elective surgery
compared with initial surveillance. However, by eight years patients undergoing
early surgery have a significantly better outcome than those in the surveillance
group (P=0.05 ). I bars represent the 95 percent confidence intervals for the point
estimates.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Data from: The United Kingdom Small Aneurysm Trial Participants. N Engl J Med
2002; 346:1445.",
" </div>",
" </div>",
" </div>",
" </div>",
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var title_f0_45_735="Renal stones in primary oxaluria";
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" </div>",
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" <div class=\"figure\" style=\"width: 524px\">",
" <div class=\"ttl\">",
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" </div>",
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" </div>",
" <div class=\"lgnd\">",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
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