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var outline_f0_0_0=null;
var title_f0_0_1="Antibiotics for suspected shigellosis in developing settings";
var content_f0_0_1=[" <div id=\"graphicsToolbar\">",
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" &copy;2013 UpToDate",
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" Antibiotics for suspected shigellosis in developing settings",
" </div>",
" <div class=\"cntnt\">",
" <table cellspacing=\"0\">",
" <tbody>",
" <tr>",
" <td class=\"subtitle1\">",
" Antibiotic",
" </td>",
" <td class=\"subtitle1\">",
" Route",
" </td>",
" <td class=\"subtitle1\">",
" Typical pediatric dose",
" </td>",
" <td class=\"subtitle1\">",
" Comment(s)",
" </td>",
" </tr>",
" <tr>",
" <td class=\"subtitle2_left\" colspan=\"4\">",
" Preferred agents",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Ciprofloxacin",
" </td>",
" <td>",
" Oral",
" </td>",
" <td>",
" 30 mg/kg/day (divided twice daily) for 3 days",
" </td>",
" <td>",
" Multi-dose therapy is preferred.",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Azithromycin",
" </td>",
" <td>",
" Oral",
" </td>",
" <td>",
" <p>",
" 15 mg/kg initial dose (day 1)",
" </p>",
" <p>",
" 10 mg/kg/day (daily, day 2-5)",
" </p>",
" </td>",
" <td>",
" &nbsp;",
" </td>",
" </tr>",
" <tr>",
" <td class=\"subtitle2_left\" colspan=\"4\">",
" Alternative agents",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Ceftriaxone",
" </td>",
" <td>",
" IM/IV",
" </td>",
" <td>",
" 50-100 mg/kg/day (divided four times daily) for 2-5 days",
" </td>",
" <td rowspan=\"2\">",
" Ceftriaxone is the preferred empiric therapy for severe infections and
infections refractory to other therapies.",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Pivmecillinam",
" </td>",
" <td>",
" PO",
" </td>",
" <td>",
" 80 mg/kg/day (divided four times daily) for 5 days",
" </td>",
" </tr>",
" </tbody>",
" </table>",
" </div>",
" <div class=\"lgnd\">",
" Resistance to amoxicillin, trimethoprim-sulfamethoxazole, and chloramphenicol
(original first-line therapies) is too widespread to justify their empiric use for
invasive diarrhea in developing countries.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Modified from: World Health Organization. Guidelines for the control of
shigellosis, incuding epidemics due to Shigella dysenteriae 1. World Health
Organization, Geneva 2005.",
" </div>",
" </div>",
" </div>",
" </div>",
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var title_f0_0_10="Severe combined immunodeficiency (SCID): Specific defects";
var content_f0_0_10=[" <noscript>",
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" Official reprint from UpToDate",
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" www.uptodate.com",
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" <div id=\"topicContent\">",
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" Severe combined immunodeficiency (SCID): Specific defects",
" </div>",
" <div id=\"topicContributors\">",
" <div>",
" <a id=\"authors\">",
" </a>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/0/10/contributors\">",
" Author",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/10/contributors\">",
" Francisco A Bonilla, MD, PhD",
" </a>",
" <br/>",
" </div>",
" <div>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/0/10/contributors\">",
" Section Editor",
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" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/10/contributors\">",
" E Richard Stiehm, MD",
" </a>",
" <br/>",
" </div>",
" <div>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/0/10/contributors\">",
" Deputy Editor",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/10/contributors\">",
" Elizabeth TePas, MD, MS",
" </a>",
" <br/>",
" </div>",
" </div>",
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" is complete.",
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" Literature review current through:",
" </span>",
" Oct 2013.",
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" <span class=\"emphasis\">",
" This topic last updated:",
" </span>",
" Aug 1, 2012.",
" </div>",
" <div id=\"topicText\">",
" <p class=\"headingAnchor\" id=\"H1\">",
" <span class=\"h1\">",
" INTRODUCTION",
" </span>",
" &nbsp;&mdash;&nbsp;Combined immunodeficiency syndromes are a heterogeneous
group of disorders arising from a disturbance in the development and function of
both T and B cells (cellular and humoral immunity) (",
" <a class=\"graphic graphic_figure graphicRef77023 \" href=\"UTD.htm?
43/6/44137\">",
" figure 1",
" </a>",
" and",
" <a class=\"graphic graphic_table graphicRef64286 \" href=\"UTD.htm?
14/41/15006\">",
" table 1",
" </a>",
" and",
" <a class=\"graphic graphic_table graphicRef77724 \" href=\"UTD.htm?
17/53/18268\">",
" table 2",
" </a>",
" and",
" <a class=\"graphic graphic_table graphicRef82391 \" href=\"UTD.htm?
26/2/26668\">",
" table 3",
" </a>",
" ) [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/10/abstract/1\">",
" 1",
" </a>",
" ]. These disorders are termed \"severe\" (eg, severe combined immune
deficiency, SCID) when they lead to early death from overwhelming infection,
typically in the first year of life. Mutations of a particular gene may lead to
SCID or to milder immunodeficiency, depending upon whether the defect is complete
or partial. Gene defects that lead to partial function of the gene product are
called \"hypomorphic\", whereas complete defects are called \"null\"
or \"amorphic\".",
" </p>",
" <p>",
" Brief synopses are given for the molecular types of SCID that are discussed in
detail separately:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" X-linked SCID (see",
" <a class=\"medical medical_review\" href=\"UTD.htm?1/18/1316?
source=see_link\">",
" \"X-linked severe combined immunodeficiency (SCID)\"",
" </a>",
" )",
" </li>",
" <li>",
" Adenosine deaminase (ADA) deficiency (see",
" <a class=\"medical medical_review\" href=\"UTD.htm?2/27/2488?
source=see_link\">",
" \"Adenosine deaminase deficiency: Pathogenesis, clinical manifestations,
and diagnosis\"",
" </a>",
" )",
" </li>",
" <li>",
" Artemis, RAG-1, RAG-2, and DNA protein kinase catalytic subunit (DNA-PKcs)
deficiencies (see",
" <a class=\"medical medical_review\" href=\"UTD.htm?19/56/20362?
source=see_link\">",
" \"T cell negative, B cell negative, NK cell positive severe combined
immunodeficiency\"",
" </a>",
" )",
" </li>",
" <li>",
" Janus kinase 3 (JAK-3) deficiency (see",
" <a class=\"medical medical_review\" href=\"UTD.htm?14/52/15176?
source=see_link\">",
" \"Severe combined immunodeficiency (SCID) with JAK3 deficiency\"",
" </a>",
" )",
" </li>",
" <li>",
" Deficiencies in CD3 complex components (see",
" <a class=\"medical medical_review\" href=\"UTD.htm?27/42/28329?
source=see_link\">",
" \"CD3/T cell receptor complex disorders causing immunodeficiency\"",
" </a>",
" )",
" </li>",
" <li>",
" Reticular dysgenesis (see",
" <a class=\"local\" href=\"#H13\">",
" 'Reticular dysgenesis'",
" </a>",
" below)",
" </li>",
" </ul>",
" </p>",
" <p>",
" A general overview of SCID is also presented separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?41/30/42471?
source=see_link\">",
" \"Severe combined immunodeficiency (SCID): An overview\"",
" </a>",
" .)",
" </p>",
" <p>",
" Combined immune deficiencies that are not considered \"severe\" are discussed
separately (",
" <a class=\"graphic graphic_table graphicRef64286 \" href=\"UTD.htm?
14/41/15006\">",
" table 1",
" </a>",
" ). (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/58/40873?
source=see_link\">",
" \"Combined immunodeficiencies\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?27/42/28329?
source=see_link\">",
" \"CD3/T cell receptor complex disorders causing immunodeficiency\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?2/27/2488?
source=see_link\">",
" \"Adenosine deaminase deficiency: Pathogenesis, clinical manifestations, and
diagnosis\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?25/2/25637?
source=see_link\">",
" \"Purine nucleoside phosphorylase deficiency\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?41/2/42022?
source=see_link\">",
" \"ZAP-70 deficiency\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?19/56/20362?
source=see_link\">",
" \"T cell negative, B cell negative, NK cell positive severe combined
immunodeficiency\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H2\">",
" <span class=\"h1\">",
" T-B+NK+ SCID",
" </span>",
" &nbsp;&mdash;&nbsp;The T cell negative, B cell positive, NK cell positive (T-
B+NK+) SCID syndromes (MIM 608971) include defects in interleukin-7 receptor alpha
chain (IL7RA; also called CD127), CD45 (also called protein-tyrosine phosphatase,
receptor-type, C; PTPRC), and the CD3 chains: CD3 delta (CD3D), CD3 epsilon (CD3E),
and CD3 zeta (CD3Z).",
" </p>",
" <p class=\"headingAnchor\" id=\"H3\">",
" <span class=\"h2\">",
" Interleukin-7 receptor alpha chain (CD127) deficiency",
" </span>",
" &nbsp;&mdash;&nbsp;The IL-7 receptor alpha chain (IL7RA, encoded on chromosome
5p13) plays a critical role in cytokine signaling that it is necessary for T cell
development. Many patients with a classic SCID phenotype who lack the IL-7R alpha
chain have been identified [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/10/abstract/2-4\">",
" 2-4",
" </a>",
" ]. This defect is the third most common type of SCID. Mutations in the IL7R
gene can also present with an Omenn syndrome phenotype [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/10/abstract/5\">",
" 5",
" </a>",
" ]. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?19/56/20362?
source=see_link\">",
" \"T cell negative, B cell negative, NK cell positive severe combined
immunodeficiency\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H4\">",
" <span class=\"h2\">",
" Actin-regulating protein coronin 1A deficiency",
" </span>",
" &nbsp;&mdash;&nbsp;Coronin 1 (CORO1A, encoded on chromosome 16p11.2) is
involved in actin cytoskeleton regulation and is essential for T cell egress from
the thymus. Defects in CORO1A lead to absence of normal peripheral T cells and a
classic SCID phenotype [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/10/abstract/6\">",
" 6",
" </a>",
" ]. The thymus is present, unlike most other forms of SCID.",
" </p>",
" <p class=\"headingAnchor\" id=\"H5\">",
" <span class=\"h2\">",
" CD45 deficiency",
" </span>",
" &nbsp;&mdash;&nbsp;CD45, the leukocyte common antigen, is encoded on
chromosome 1q31-q32. CD45 is a transmembrane tyrosine phosphatase involved in T
cell receptor (TCR) signaling and T cell development in the thymus. Only a few
patients with classic SCID due to CD45 deficiency have been described [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/10/abstract/7-9\">",
" 7-9",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H6\">",
" <span class=\"h2\">",
" CD3 complex component deficiencies",
" </span>",
" &nbsp;&mdash;&nbsp;The CD3 complex plays a major role in signaling through the
TCR. Mutations in the genes encoding CD3 chains (CD3 delta, CD3 epsilon, and CD3
zeta) lead to SCID. CD3 chain deficiencies are discussed in greater detail
separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?27/42/28329?
source=see_link&amp;anchor=H17#H17\">",
" \"CD3/T cell receptor complex disorders causing immunodeficiency\", section
on 'CD3 deficiency'",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H7\">",
" <span class=\"h1\">",
" T-B+NK- SCID",
" </span>",
" &nbsp;&mdash;&nbsp;Gene mutations affecting the integrity of the gamma",
" <span class=\"nowrap\">",
" c/JAK-3",
" </span>",
" signaling pathway result in the most common form of inherited SCID: T cell
negative, B cell positive, NK cell negative (T-B+NK-) SCID.",
" </p>",
" <p class=\"headingAnchor\" id=\"H8\">",
" <span class=\"h2\">",
" X-linked SCID",
" </span>",
" &nbsp;&mdash;&nbsp;X-linked severe combined immunodeficiency (SCID) is due to
defects in the common gamma chain (gamma-c, interleukin-2 receptor gamma). X-linked
SCID (SCIDX1 or X-SCID, MIM 300400) is the most common form of SCID. These male
patients usually have the classic clinical SCID phenotype, presenting in the
newborn period with recurrent severe infections, chronic diarrhea, and failure to
thrive. This SCID is discussed in greater detail separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?1/18/1316?
source=see_link\">",
" \"X-linked severe combined immunodeficiency (SCID)\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H9\">",
" <span class=\"h2\">",
" JAK-3 deficiency",
" </span>",
" &nbsp;&mdash;&nbsp;Janus kinase 3 (JAK3, encoded on chromosome 19p12-13.1)
mediates cytokine signal transduction. This autosomal recessive form of T-B+NK-
SCID (MIM 600802) is identical to X-linked SCID in cellular and clinical
phenotypes. Rarely, partial JAK3 defects associated with low amounts of functional
protein can present with mild immunodeficiency. SCID due to JAK3 deficiency is
discussed in greater detail separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?14/52/15176?
source=see_link\">",
" \"Severe combined immunodeficiency (SCID) with JAK3 deficiency\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H10\">",
" <span class=\"h1\">",
" T-B-NK+ SCID",
" </span>",
" &nbsp;&mdash;&nbsp;The T cell negative, B cell negative, NK cell positive (T-
B-NK+) SCID syndromes include defects in recombinase activating genes 1 and 2
(RAG1, RAG2), Artemis (ARTEMIS or DCLRE1C), and DNA protein kinase catalytic
subunit (DNA-PKcs).",
" </p>",
" <p>",
" Mutations in the genes for Artemis and DNA-PKcs lead to increased sensitivity
to ionizing radiation, since these gene products are important in the process of
non-homologous end joining required for repair of double-strand DNA breaks caused
by radiation. Mutations in RAG1 and RAG2 are not associated with radiation
sensitivity. These genes are expressed exclusively in lymphocytes and mediate the
creation of double strand DNA breaks at the sites of recombination and signal
sequences during T and B cells receptor gene rearrangement. Non-homologous end
joining is normal in individuals with RAG1 or RAG2 defects. Artemis deficiency is
also known as Athabascan SCID (SCIDA), since a founder mutation in ARTEMIS is found
with increased frequency in Native Americans speaking one of the Athabascan family
languages (eg, Apache, Navajo). (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?19/56/20362?
source=see_link\">",
" \"T cell negative, B cell negative, NK cell positive severe combined
immunodeficiency\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H11\">",
" <span class=\"h1\">",
" T-B-NK- SCID",
" </span>",
" &nbsp;&mdash;&nbsp;The two identified T cell negative, B cell negative, NK
cell negative (T-B-NK-) SCID are adenosine deaminase (ADA) deficiency and reticular
dysgenesis.",
" </p>",
" <p class=\"headingAnchor\" id=\"H12\">",
" <span class=\"h2\">",
" Adenosine deaminase deficiency",
" </span>",
" &nbsp;&mdash;&nbsp;With an incidence of 1 in 200,000 live births, adenosine
deaminase deficiency (ADAD) accounts for approximately 15 percent of SCID.
Approximately 90 percent of ADA deficient individuals have a classic severe SCID
phenotype and they develop severe infections in the first months of life. Most of
the remainder have a \"delayed\" or \"late onset\" form that presents in late
infancy or early childhood.",
" </p>",
" <p>",
" The definitive treatment of choice is hematopoietic cell transplantation from
an HLA identical sibling or other appropriate donor. PEG-ADA is an effective
alternative therapeutic agent, which is sometimes preferred in patients without an
HLA-identical sibling. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?2/27/2488?
source=see_link\">",
" \"Adenosine deaminase deficiency: Pathogenesis, clinical manifestations, and
diagnosis\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H13\">",
" <span class=\"h2\">",
" Reticular dysgenesis",
" </span>",
" &nbsp;&mdash;&nbsp;Reticular dysgenesis (MIM 267500) is one of the rarest and
most severe forms of SCID. Severe infections occur earlier than in other forms of
SCID due to profound neutropenia in addition to markedly decreased T and NK cells.
B cells are absent to low normal. This autosomal recessive SCID is caused by
mutations in the mitochondrial adenylate kinase 2 (AK2) gene.",
" </p>",
" <p class=\"headingAnchor\" id=\"H14\">",
" <span class=\"h1\">",
" SUMMARY",
" </span>",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Combined immunodeficiency syndromes are a heterogeneous group of disorders
arising from mutations in genes whose products are essential for the normal
development and function of T and B cells (cellular and humoral immunity) (",
" <a class=\"graphic graphic_figure graphicRef77023 \" href=\"UTD.htm?
43/6/44137\">",
" figure 1",
" </a>",
" and",
" <a class=\"graphic graphic_table graphicRef64286 \" href=\"UTD.htm?
14/41/15006\">",
" table 1",
" </a>",
" and",
" <a class=\"graphic graphic_table graphicRef77724 \" href=\"UTD.htm?
17/53/18268\">",
" table 2",
" </a>",
" ). These disorders are termed \"severe\" (eg, severe combined immune
deficiency, SCID) when they typically lead to death from overwhelming infection in
the first year or so of life. (See",
" <a class=\"local\" href=\"#H1\">",
" 'Introduction'",
" </a>",
" above.)",
" </li>",
" <li>",
" A useful paradigm that can be used until a genetic diagnosis is established
is to classify SCID syndromes as T-B+NK+, T-B+NK-, T-B-NK+, or T-B-NK- based upon
the presence of molecular defects affecting T cells and presence or absence of
defects affecting B",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" NK cells, regardless of the functional status of these cells (",
" <a class=\"graphic graphic_table graphicRef77724 \" href=\"UTD.htm?
17/53/18268\">",
" table 2",
" </a>",
" and",
" <a class=\"graphic graphic_table graphicRef82391 \" href=\"UTD.htm?
26/2/26668\">",
" table 3",
" </a>",
" ). (See",
" <a class=\"local\" href=\"#H2\">",
" 'T-B+NK+ SCID'",
" </a>",
" above and",
" <a class=\"local\" href=\"#H7\">",
" 'T-B+NK- SCID'",
" </a>",
" above and",
" <a class=\"local\" href=\"#H10\">",
" 'T-B-NK+ SCID'",
" </a>",
" above and",
" <a class=\"local\" href=\"#H11\">",
" 'T-B-NK- SCID'",
" </a>",
" above.)",
" </li>",
" <li>",
" SCID can also be categorized based upon cellular function of the protein
encoded by the defective gene: cytokine signaling, antigen presentation, V(D)J
recombination, T cell receptor signaling, and basic cellular processes (",
" <a class=\"graphic graphic_figure graphicRef77023 \" href=\"UTD.htm?
43/6/44137\">",
" figure 1",
" </a>",
" ). However, it is more appropriate to refer to SCID according to the
specific molecular defect once it is identified, since the mutated genes
responsible for the majority of cases of SCID are known.",
" </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>",
" <ol id=\"reference\">",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/10/abstract/1\">",
" International Union of Immunological Societies Expert Committee on Primary
Immunodeficiencies, Notarangelo LD, Fischer A, et al. Primary immunodeficiencies:
2009 update. J Allergy Clin Immunol 2009; 124:1161.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/10/abstract/2\">",
" Roifman CM, Zhang J, Chitayat D, Sharfe N. A partial deficiency of
interleukin-7R alpha is sufficient to abrogate T-cell development and cause severe
combined immunodeficiency. Blood 2000; 96:2803.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/10/abstract/3\">",
" Puel A, Leonard WJ. Mutations in the gene for the IL-7 receptor result in
T(-)B(+)NK(+) severe combined immunodeficiency disease. Curr Opin Immunol 2000;
12:468.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/10/abstract/4\">",
" Puel A, Ziegler SF, Buckley RH, Leonard WJ. Defective IL7R expression in
T(-)B(+)NK(+) severe combined immunodeficiency. Nat Genet 1998; 20:394.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/10/abstract/5\">",
" Villa A, Notarangelo LD, Roifman CM. Omenn syndrome: inflammation in leaky
severe combined immunodeficiency. J Allergy Clin Immunol 2008; 122:1082.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/10/abstract/6\">",
" Shiow LR, Roadcap DW, Paris K, et al. The actin regulator coronin 1A is
mutant in a thymic egress-deficient mouse strain and in a patient with severe
combined immunodeficiency. Nat Immunol 2008; 9:1307.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/10/abstract/7\">",
" Kung C, Pingel JT, Heikinheimo M, et al. Mutations in the tyrosine
phosphatase CD45 gene in a child with severe combined immunodeficiency disease. Nat
Med 2000; 6:343.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/10/abstract/8\">",
" Tchilian EZ, Wallace DL, Wells RS, et al. A deletion in the gene encoding
the CD45 antigen in a patient with SCID. J Immunol 2001; 166:1308.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/10/abstract/9\">",
" Roberts JL, Buckley RH, Luo B, et al. CD45-deficient severe combined
immunodeficiency caused by uniparental disomy. Proc Natl Acad Sci U S A 2012;
109:10456.",
" </a>",
" </li>",
" </ol>",
" </div>",
" <div id=\"topicVersionRevision\">",
" Topic 3912 Version 5.0",
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" </a>",
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" <div id=\"innerOutline\">",
" <h1>",
" TOPIC OUTLINE",
" </h1>",
" <div id=\"outline\">",
" <ul>",
" <li>",
" <a class=\"sr_button\" href=\"#H14\" id=\"summRecButton\">",
" <span>",
" SUMMARY",
" </span>",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H1\">",
" INTRODUCTION",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H2\">",
" T-B+NK+ SCID",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H3\">",
" Interleukin-7 receptor alpha chain (CD127) deficiency",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H4\">",
" Actin-regulating protein coronin 1A deficiency",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H5\">",
" CD45 deficiency",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H6\">",
" CD3 complex component deficiencies",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H7\">",
" T-B+NK- SCID",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H8\">",
" X-linked SCID",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H9\">",
" JAK-3 deficiency",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H10\">",
" T-B-NK+ SCID",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H11\">",
" T-B-NK- SCID",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H12\">",
" Adenosine deaminase deficiency",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H13\">",
" Reticular dysgenesis",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H14\">",
" SUMMARY",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a href=\"#references\">",
" REFERENCES",
" </a>",
" </li>",
" </ul>",
" </div>",
" <h1>",
" <div class=\"openRelatedGraphics\" id=\"ALLRG/3912\" rel=\"outline_link\">",
" GRAPHICS",
" <a class=\"graphics_icon\" href=\"#\" title=\"View All Related Graphics\">",
" View All",
" </a>",
" </div>",
" </h1>",
" <div id=\"relatedGraphics\">",
" <ul>",
" <li class=\"plainItem\">",
" <div class=\"openRelatedGraphics\" id=\"ALLRG/3912|FIG\">",
" <a href=\"#\" title=\"FIGURES\">",
" FIGURES",
" </a>",
" </div>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_figure\" href=\"UTD.htm?43/6/44137\"
title=\"figure 1\">",
" Combined immunodeficiency gene defects and functional categories",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <div class=\"openRelatedGraphics\" id=\"ALLRG/3912|TAB\">",
" <a href=\"#\" title=\"TABLES\">",
" TABLES",
" </a>",
" </div>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_table\" href=\"UTD.htm?14/41/15006\" title=\"table
1\">",
" Syndromes combined immunodef",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_table\" href=\"UTD.htm?17/53/18268\" title=\"table
2\">",
" SCID classification and gene defects",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_table\" href=\"UTD.htm?26/2/26668\" title=\"table
3\">",
" Alterations of periph blood lymphocyte populations in SCID",
" </a>",
" </li>",
" </ul>",
" </div>",
" <h1>",
" RELATED TOPICS",
" </h1>",
" <div id=\"relatedTopics\">",
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//Z);\">",
" </div>",
" <div class=\"lgnd\">",
" Ulcerated, erythematous nodules in polyarteritis nodosa.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Reproduced with permission from: www.visualdx.com. Copyright Logical Images,
Inc.",
" </div>",
" </div>",
" </div>",
" </div>",
" <div class=\"graphic\">",
" <div class=\"figure\" style=\"width: 470px\">",
" <div class=\"ttl\">",
" Livedo racemosa in polyarteritis nodosa",
" </div>",
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" </div>",
" <div class=\"lgnd\">",
" An irregular, branched, vascular pattern (livedo racemosa) and a few healing
ulcerations are present on the skin.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Reproduced with permission from: www.visualdx.com. Copyright Logical Images,
Inc.",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
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var outline_f0_0_11=null;
var title_f0_0_12="Steroid hormone metabolism in polycystic ovary syndrome";
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" Steroid hormone metabolism in polycystic ovary syndrome",
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" Author",
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" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/12/contributors\">",
" Robert L Barbieri, MD",
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href=\"UTD.htm?0/0/12/contributors\">",
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0/0/12/contributors\">",
" Peter J Snyder, MD",
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" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/12/contributors\">",
" William F Crowley, Jr, MD",
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" Deputy Editor",
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" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/12/contributors\">",
" Kathryn A Martin, MD",
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" Jun 19, 2012.",
" </div>",
" <div id=\"topicText\">",
" <p class=\"headingAnchor\" id=\"H1\">",
" <span class=\"h1\">",
" INTRODUCTION",
" </span>",
" &nbsp;&mdash;&nbsp;The polycystic ovary syndrome (PCOS) is characterized
clinically by menstrual dysfunction, including oligo- or anovulation and signs of
hyperandrogenism [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/1\">",
" 1",
" </a>",
" ]. This review will describe the abnormalities in steroid hormones that are
present in this disorder, including the factors responsible for the increase in
androgen production. The clinical manifestations of the PCOS are discussed
separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?16/6/16490?
source=see_link\">",
" \"Clinical manifestations of polycystic ovary syndrome in adults\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H2\">",
" <span class=\"h1\">",
" ANDROGEN METABOLISM",
" </span>",
" &nbsp;&mdash;&nbsp;As a group, women with PCOS have serum concentrations of
testosterone, free testosterone, androstenedione, dehydroepiandrosterone (DHEA),
and DHEA sulfate (DHEA-S) that are significantly elevated compared to ovulatory,
non-hirsute women (",
" <a class=\"graphic graphic_figure graphicRef72842 \" href=\"UTD.htm?
21/25/21918\">",
" figure 1",
" </a>",
" )&nbsp;[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/1,2\">",
" 1,2",
" </a>",
" ]. There is, however, significant individual variation, and some women with
PCOS may have normal androgen levels when assayed in a single blood specimen [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/1\">",
" 1",
" </a>",
" ]. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?38/36/39495?
source=see_link\">",
" \"Diagnosis of polycystic ovary syndrome in adults\"",
" </a>",
" .)",
" </p>",
" <p>",
" In women, androgens are produced by the adrenal glands and the ovaries, as
well as by conversion of less potent androgens to more potent androgens in the
periphery. The source of the major androgens in PCOS is shown in the table (",
" <a class=\"graphic graphic_table graphicRef60049 \" href=\"UTD.htm?
19/41/20123\">",
" table 1",
" </a>",
" ). In PCOS, androstenedione is secreted primarily by the ovaries and to a
lesser degree the adrenals. This pattern differs from that in normal premenopausal
women who have about equal androstenedione and testosterone production from the
ovaries and the adrenals [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/3\">",
" 3",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H3\">",
" <span class=\"h2\">",
" Testosterone",
" </span>",
" &nbsp;&mdash;&nbsp;Testosterone is the most potent circulating androgen. Its
biologic activity is determined by the amount of binding to sex hormone binding
globulin (SHBG), as only the free fraction is active. Serum SHBG concentrations are
controlled by androgens (decrease), estrogens (increase), and insulin (decrease)
[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/4\">",
" 4",
" </a>",
" ]. Thus, hyperandrogenic women with PCOS tend to have low serum SHBG
concentrations. This decrease tends to mask the degree of testosterone excess if
only serum total testosterone concentration is measured. Thus, a higher proportion
of women with PCOS have elevated serum free testosterone concentrations than have
elevated serum total testosterone concentrations.",
" </p>",
" <p>",
" Body mass index (BMI) is positively correlated with serum total testosterone
and inversely correlated with SHBG concentrations in women of all reproductive
ages.",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" In a cohort study of 1526 Scandinavian premenopausal women (mean age 31
years), increasing BMI was associated with increased serum testosterone and
decreased serum SHBG concentrations in both ovulatory and oligo-ovulatory women [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/5\">",
" 5",
" </a>",
" ].",
" </li>",
" <li>",
" Similar associations were observed in the Study of Women's Health Across the
Nation (SWAN), of 2930 perimenopausal women (mean age 46 years) [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/6\">",
" 6",
" </a>",
" ], and in a study of menopausal women [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/7\">",
" 7",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p>",
" Cigarette smoking is associated with increased serum testosterone
concentrations in premenopausal women [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/6,8\">",
" 6,8",
" </a>",
" ]. It is not known if discontinuing smoking is associated with a subsequent
decrease in serum testosterone.",
" <br/>",
" </p>",
" <p class=\"headingAnchor\" id=\"H4\">",
" <span class=\"h2\">",
" Androstenedione",
" </span>",
" &nbsp;&mdash;&nbsp;Androstenedione is the immediate precursor to testosterone.
Androstenedione is converted to testosterone by the 17beta-hydroxysteroid
dehydrogenase (17-ketosteroid reductase) enzyme, which is present in most tissues.
In the ovary of ovulatory women, the theca cells secrete significant quantities of
androstenedione, which enters the granulosa cells and is converted to estrone and
estradiol. LH directly stimulates thecal secretion of androstenedione. In PCOS, LH
levels are elevated so the theca secretes increased quantities of androstenedione.
The androstenedione secreted into the circulation by the ovary and adrenal can be
converted to the potent androgen, testosterone, by most peripheral tissues.",
" </p>",
" <p class=\"headingAnchor\" id=\"H5\">",
" <span class=\"h2\">",
" Dehydroepiandrosterone sulfate",
" </span>",
" &nbsp;&mdash;&nbsp;The majority of DHEA-S derives from the adrenal glands and
there is little, if any, sulfotransferase (sulfokinase) activity in the periphery
to convert DHEA to DHEA-S. As a result, the serum concentration of DHEA-S is a good
marker of adrenal androgen hypersecretion. In addition, since DHEA-S has a long
serum half-life, with minimal pulsatile or diurnal variation a single measurement
of serum DHEAS correlates well with integrated measures of DHEAS secretion.",
" </p>",
" <p>",
" However, some adrenocortical carcinomas have no sulfotransferase activity and
some patients with congenital adrenal hyperplasia have normal DHEA-S levels. Thus,
normal serum DHEA-S concentrations do not necessarily exclude a pathologic adrenal
source of excess androgens.",
" </p>",
" <p>",
" Although DHEA and DHEA-S are markers of adrenal androgen production, they have
little if any intrinsic androgenic activity. Small amounts are converted to
androstenedione and then to testosterone (and to estrogen) in both the adrenal
glands and peripheral tissues, including hair follicles and external genitalia.
Thus, the hirsutism and virilization that may occur in patients with adrenal
hyperandrogenism are caused by androstenedione and testosterone. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/8/40071?
source=see_link\">",
" \"Adrenal hyperandrogenism\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H6\">",
" <span class=\"h2\">",
" Dihydrotestosterone",
" </span>",
" &nbsp;&mdash;&nbsp;Testosterone binds to the intracellular androgen receptor
with modest affinity. In androgen responsive tissues, intracellular 5-alpha
reductase converts testosterone to dihydrotestosterone. Dihydrotestosterone binds
to the androgen receptor with an affinity 10 times greater than testosterone. There
are multiple subtypes of 5-alpha reductase. In a tissue such as the prostate the
type II isoenzyme predominates, while in the pilosebaceous unit both the type I and
II isoforms are present. Women with PCOS have increased 5-alpha reductase activity
[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/9\">",
" 9",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H7\">",
" <span class=\"h2\">",
" Androstanediol",
" </span>",
" &nbsp;&mdash;&nbsp;3-Alpha-androstanediol-glucuronide (3aA-G) is derived from
the metabolism of the potent intracellular androgen dihydrotestosterone (DHT). It
can therefore be used as a marker of peripheral androgen metabolism. Serum
concentrations of 3aA-G are almost uniformly high in women with hirsutism. Except
for research purposes, however, it is probably unnecessary to measure 3aA-G as the
presence of hirsutism by definition indicates that androgen activity in the skin is
increased.",
" </p>",
" <p class=\"headingAnchor\" id=\"H8\">",
" <span class=\"h1\">",
" ESTROGEN METABOLISM",
" </span>",
" &nbsp;&mdash;&nbsp;Most women with PCOS have serum estradiol concentrations
similar to the early follicular phase of ovulatory women, and elevated serum
estrone concentrations (",
" <a class=\"graphic graphic_figure graphicRef52544 \" href=\"UTD.htm?
32/4/32845\">",
" figure 2",
" </a>",
" )&nbsp;[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/1,2\">",
" 1,2",
" </a>",
" ]. The serum estrogens in women with PCOS come partly from the multiple small
follicles in the polycystic ovaries and partly from aromatization of androgens to
estrogens in fat cells.",
" </p>",
" <p>",
" The net effect is that PCOS is a normoestrogenic state, and estrogen
replacement is not required, even in amenorrheic women with PCOS. Women with PCOS
are oligo- or anovulatory and do not produce normal quantities of progesterone.
Consequently, they are at an increased risk of endometrial hyperplasia and heavy
menstrual bleeding. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?16/6/16490?
source=see_link\">",
" \"Clinical manifestations of polycystic ovary syndrome in adults\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H9\">",
" <span class=\"h1\">",
" CONTROL OF ANDROGEN PRODUCTION",
" </span>",
" &nbsp;&mdash;&nbsp;The control of androgen production in women is complex
because the androgens are produced in multiple sites. In both the ovaries and
adrenal glands, androgen secretion requires the activity of multiple steroidogenic
enzymes (",
" <a class=\"graphic graphic_figure graphicRef70372 \" href=\"UTD.htm?
0/7/123\">",
" figure 3",
" </a>",
" ), including:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Cholesterol synthesis &ndash; All gonadal steroid synthesis begins with
synthesis of cholesterol and its transport to steroidogenic tissues in
lipoproteins. In placebo-controlled trials, the cholesterol synthesis inhibitor",
" <a class=\"drug drug_general\" href=\"UTD.htm?34/37/35417?
source=see_link\">",
" atorvastatin",
" </a>",
" (20",
" <span class=\"nowrap\">",
" mg/day)",
" </span>",
" reduced hyperandrogenemia when administered to women with PCOS [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/10\">",
" 10",
" </a>",
" ].",
" </li>",
" <li>",
" P450scc (side-chain cleavage) that converts cholesterol to pregnenolone.",
" </li>",
" <li>",
" 3-Beta-hydroxysteroid dehydrogenase that converts steroids such as
pregnenolone, 17-hydroxypregnenolone, and DHEA to progesterone, 17-
hydroxyprogesterone, and androstenedione.",
" </li>",
" <li>",
" P450c17 that has both 17-hydroxylation and 17,20 lyase functions and which,
therefore, converts pregnenolone to 17-hydroxypregnenolone and 17-OH pregnenolone
to DHEA, and progesterone to 17-hydroxyprogesterone and 17-hydroxyprogesterone to
androstenedione.",
" </li>",
" </ul>",
" </p>",
" <p class=\"headingAnchor\" id=\"H10\">",
" <span class=\"h2\">",
" Ovarian androgen secretion",
" </span>",
" &nbsp;&mdash;&nbsp;Ovarian androgens are produced in the theca cells which
respond to luteinizing hormone (LH) [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/11\">",
" 11",
" </a>",
" ]. Theca cells synthesize mostly androstenedione and some testosterone, which
diffuse across the basement membrane to the granulosa cells. The granulosa cells,
in response to stimulation by follicle-stimulating hormone (FSH), produce aromatase
which converts the androgen precursors to estrone and estradiol&nbsp;(",
" <a class=\"graphic graphic_figure graphicRef76006 \" href=\"UTD.htm?
9/16/9487\">",
" figure 4",
" </a>",
" ) [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/11\">",
" 11",
" </a>",
" ].",
" </p>",
" <p>",
" In women with PCOS, ovarian androgen production may increase as a result of
one or more of the following:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" An increased volume of theca cells.",
" </li>",
" <li>",
" Increased LH stimulation of the theca cells. Indirect support for
the \"excess LH drive\" hypothesis derives from transgenic animal studies.
Overexpression of human chorionic gonadotropin (which binds and activates the same
receptor as LH) resulted in mice with large cystic ovaries [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/12\">",
" 12",
" </a>",
" ].",
" </li>",
" <li>",
" Potentiation of the action of LH by hyperinsulinemia.",
" </li>",
" <li>",
" Production of beta subunits of LH that have different biological activity as
a result of polymorphism of the gene for the subunit [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/13\">",
" 13",
" </a>",
" ]. The more active LH need not be more immunoreactive, so serum LH
concentrations as routinely measured might be normal (and often are normal) in
these women.",
" </li>",
" <li>",
" Increased expression of LH receptor, StAR, CYP11A, and CYP17 mRNAs in thecal
cells from PCOS follicles versus size-matched control follicles [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/14\">",
" 14",
" </a>",
" ]. In addition theca cells from the ovaries of women with PCOS demonstrate
increased CYP17 and 3-beta HSD enzyme activity [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/15\">",
" 15",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p class=\"headingAnchor\" id=\"H11\">",
" <span class=\"h3\">",
" Role of insulin",
" </span>",
" &nbsp;&mdash;&nbsp;In vitro experiments with human theca cells have
demonstrated a synergistic effect of LH and insulin to increase androgen secretion
[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/16\">",
" 16",
" </a>",
" ]. Several studies in obese women with PCOS are compatible with a contributory
role of insulin. As an example, reducing the degree of insulin resistance with",
" <a class=\"drug drug_general\" href=\"UTD.htm?7/48/7944?source=see_link\">",
" metformin",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/17\">",
" 17",
" </a>",
" ] or reducing insulin secretion with",
" <a class=\"drug drug_general\" href=\"UTD.htm?13/38/13924?source=see_link\">",
" diazoxide",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/18\">",
" 18",
" </a>",
" ] results in a fall in serum androgen concentrations.",
" </p>",
" <p>",
" The association of insulin resistance with hyperinsulinemia in women with PCOS
results in the \"insulin paradox,\" since a resistant organ should not be able to
hyperrespond. Several hypotheses have been proposed to explain this paradox:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" The high serum insulin concentrations may activate the homologous receptors
for insulin-like growth factors-1 and -2 (IGF-1 and IGF-2). This argument is
tenable for women with extreme insulin resistance syndromes who have very high
serum insulin concentrations. However, women with PCOS usually have only mildly
elevated serum insulin concentrations.",
" </li>",
" <li>",
" There may be hybrid receptors in which a half-insulin receptor dimerizes
with a half-IGF-1 receptor (",
" <a class=\"graphic graphic_figure graphicRef61896 \" href=\"UTD.htm?
38/60/39886\">",
" figure 5",
" </a>",
" ). This hypothesis has not yet been demonstrated in women with PCOS.",
" </li>",
" </ul>",
" </p>",
" <p>",
" Regardless of the mechanism, it appears that some women with PCOS have insulin
resistance in muscle, adipose tissue, and liver but demonstrate insulin sensitivity
in the ovary. A 1995 report described a woman with PCOS and severe insulin
resistance (in terms of glucose metabolism) in whom ovarian insulin sensitivity was
normal [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/19\">",
" 19",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H12\">",
" <span class=\"h3\">",
" Other factors",
" </span>",
" &nbsp;&mdash;&nbsp;Other factors that can increase ovarian androgen secretion
in women with PCOS include:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Decreased aromatase activity due to decreased FSH secretion.",
" </li>",
" <li>",
" A decreased number of maturing follicles to \"deactivate\" the androgens to
estrogens. However, the granulosa cells from the small follicles of PCOS ovaries
usually maintain the ability to aromatize androgens to estrogens in response to FSH
[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/20\">",
" 20",
" </a>",
" ].",
" </li>",
" <li>",
" Dysregulated ovarian androgen secretion. An increased serum 17-
hydroxyprogesterone response to gonadotropins in hyperandrogenic women suggests
that there is dysregulated function of the P450c17 enzyme in the ovaries [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/21\">",
" 21",
" </a>",
" ]; the dysfunction may be intrinsic to the thecal cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/22\">",
" 22",
" </a>",
" ]. In theca cells from women with PCOS, mRNA transcripts for P450c17 have an
increased half-life [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/23\">",
" 23",
" </a>",
" ]. In addition, these cells appear to have alterations in pathways of
mitogen-activated protein kinase and extracellular regulated kinase signaling that
enhance P450c17 activity [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/24\">",
" 24",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p>",
" As noted above, P450c17 catalyzes both 17-hydroxylation and 17,20-lyase
reactions; however, it can be selectively induced to increase its 17,20-lyase
activity (thereby producing more androgens) by serine phosphorylation [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/25\">",
" 25",
" </a>",
" ].",
" </p>",
" <p>",
" In theca cells from women with PCOS, GATA6, a transcription factor that
increases expression of multiple steroidogenic enzymes, has increased activity [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/26\">",
" 26",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H13\">",
" <span class=\"h2\">",
" Adrenal androgen secretion",
" </span>",
" &nbsp;&mdash;&nbsp;Adrenal steroidogenesis is a complex process under the
control of ACTH, as well as other factors (",
" <a class=\"graphic graphic_figure graphicRef70372 \" href=\"UTD.htm?
0/7/123\">",
" figure 3",
" </a>",
" ). Corticotropin (ACTH) has a primary role in controlling the rate-limiting
step of adrenal steroidogenesis, the cholesterol side-chain cleavage enzyme,
leading to increased secretion of adrenal androgens as well as glucocorticoids and
mineralocorticoids.",
" </p>",
" <p>",
" Over 50 percent of women with PCOS have evidence of increased adrenal and
androgen secretion including hyper-responsivity of adrenal steroidogenesis to
exogenous ACTH administration [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/27\">",
" 27",
" </a>",
" ]. This increased adrenal androgen secretion is not due to subtle defects in
CYP21 [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/28\">",
" 28",
" </a>",
" ]. During the normal aging process in men and women, adrenal androgen
secretion decreases. Based on the results from one small study, women with PCOS
demonstrate excess adrenal androgen secretion with no age-related decrease into the
onset of menopause [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/29\">",
" 29",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H14\">",
" <span class=\"h2\">",
" Other",
" </span>",
" &nbsp;&mdash;&nbsp;There is evidence that other factors can contribute to the
regulation of androgen synthesis in PCOS. One important factor may be genetic
predisposition. Familial cases of PCOS have been described, although the underlying
defect is not known [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/30,31\">",
" 30,31",
" </a>",
" ]. In addition, there is evidence for abnormalities of steroidogenic enzyme
function, which may be related to feedback from intraglandular steroid levels,
modification of cofactor function, or unknown mechanisms [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/21,32-35\">",
" 21,32-35",
" </a>",
" ].",
" </p>",
" <p>",
" In women with PCOS, steroid hormone concentrations may be influenced by
genetic traits. For example, the SNP rs182420 in the DHEA sulfotransferase enzyme
(SULT2A1, which converts DHEA to DHEAS) is associated with increased circulating
levels of DHEAS and the promoter variant 1C in the enzyme CYP3A7, which degrades
DHEAS through 16-hydroxylation, is associated with reduced levels of circulating
DHEAS [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/12/abstract/36,37\">",
" 36,37",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H3109666\">",
" <span class=\"h1\">",
" SUMMARY",
" </span>",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" The polycystic ovary syndrome is characterized by excessive secretion of
androgens from the ovary and, in many cases, the adrenal gland. Approximately 75
percent of women with PCOS have an elevated concentration of circulating free
testosterone, total testosterone, or DHEA-S.",
" </li>",
" <li>",
" Women with PCOS typically have elevated pituitary secretion of LH, which
stimulates the ovarian theca cells to secrete excess quantities of androstenedione,
an androgen precursor that can be metabolized to testosterone, a potent circulating
androgen. Circulating testosterone is converted to DHT, the most potent
intracellular androgen, in target tissues.",
" </li>",
" <li>",
" Sex hormone binding globulin is the major high affinity circulating binding
protein for testosterone. Testosterone bound to SHBG is believed to not be
bioavailable to tissues. Free testosterone and testosterone weakly bound to albumin
are thought to be available to stimulate androgen activity in target tissues such
as the hair follicle. In PCOS, hyperandrogenism and hyperinsulinemia due to insulin
resistance reduce hepatic production of SHBG and decrease circulating SHBG levels.
The decrease in SHBG results in a proportionate increase in free testosterone,
increasing testosterone bioactivity and, at the same time, decreasing total
testosterone levels.",
" </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>",
" <ol id=\"reference\">",
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" Nelson VL, Qin KN, Rosenfield RL, et al. The biochemical basis for increased
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" Nestler JE, Jakubowicz DJ. Decreases in ovarian cytochrome P450c17 alpha
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" Nestler JE, Barlascini CO, Matt DW, et al. Suppression of serum insulin by
diazoxide reduces serum testosterone levels in obese women with polycystic ovary
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/12/abstract/19\">",
" Willis D, Franks S. Insulin action in human granulosa cells from normal and
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like growth factor receptor. J Clin Endocrinol Metab 1995; 80:3788.",
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" Mason HD, Willis DS, Beard RW, et al. Estradiol production by granulosa
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/12/abstract/21\">",
" Barnes RB, Rosenfield RL, Burstein S, Ehrmann DA. Pituitary-ovarian
responses to nafarelin testing in the polycystic ovary syndrome. N Engl J Med 1989;
320:559.",
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" Gilling-Smith C, Story H, Rogers V, Franks S. Evidence for a primary
abnormality of thecal cell steroidogenesis in the polycystic ovary syndrome. Clin
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" Wickenheisser JK, Nelson-Degrave VL, McAllister JM. Dysregulation of
cytochrome P450 17alpha-hydroxylase messenger ribonucleic acid stability in theca
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" </a>",
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" Nelson-Degrave VL, Wickenheisser JK, Hendricks KL, et al. Alterations in
mitogen-activated protein kinase kinase and extracellular regulated kinase
signaling in theca cells contribute to excessive androgen production in polycystic
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" </a>",
" </li>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/12/abstract/25\">",
" Zhang LH, Rodriguez H, Ohno S, Miller WL. Serine phosphorylation of human
P450c17 increases 17,20-lyase activity: implications for adrenarche and the
polycystic ovary syndrome. Proc Natl Acad Sci U S A 1995; 92:10619.",
" </a>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/12/abstract/26\">",
" Ho CK, Wood JR, Stewart DR, et al. Increased transcription and increased
messenger ribonucleic acid (mRNA) stability contribute to increased GATA6 mRNA
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90:6596.",
" </a>",
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" Azziz R, Black V, Hines GA, et al. Adrenal androgen excess in the polycystic
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" Glintborg D, Hermann AP, Brusgaard K, et al. Significantly higher
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" Puurunen J, Piltonen T, Jaakkola P, et al. Adrenal androgen production
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" Hague WM, Adams J, Reeders ST, et al. Familial polycystic ovaries: a genetic
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" Givens JR. Familial polycystic ovarian disease. Endocrinol Metab Clin North
Am 1988; 17:771.",
" </a>",
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" Lucky AW, Rosenfield RL, McGuire J, et al. Adrenal androgen
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" </a>",
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" Toscano V, Balducci R, Bianchi P, et al. Ovarian 17-ketosteroid reductase
deficiency as a possible cause of polycystic ovarian disease. J Clin Endocrinol
Metab 1990; 71:288.",
" </a>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/12/abstract/34\">",
" Vermesh M, Silva PD, Rosen GF, et al. Effect of androgen on adrenal
steroidogenesis in normal women. J Clin Endocrinol Metab 1988; 66:128.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/12/abstract/35\">",
" Ehrmann DA, Rosenfield RL, Barnes RB, et al. Detection of functional ovarian
hyperandrogenism in women with androgen excess. N Engl J Med 1992; 327:157.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/12/abstract/36\">",
" Goodarzi MO, Antoine HJ, Azziz R. Genes for enzymes regulating
dehydroepiandrosterone sulfonation are associated with levels of
dehydroepiandrosterone sulfate in polycystic ovary syndrome. J Clin Endocrinol
Metab 2007; 92:2659.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/12/abstract/37\">",
" Goodarzi MO, Xu N, Azziz R. Association of CYP3A7*1C and serum
dehydroepiandrosterone sulfate levels in women with polycystic ovary syndrome. J
Clin Endocrinol Metab 2008; 93:2909.",
" </a>",
" </li>",
" </ol>",
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" <div id=\"innerOutline\">",
" <h1>",
" TOPIC OUTLINE",
" </h1>",
" <div id=\"outline\">",
" <ul>",
" <li>",
" <a class=\"sr_button\" href=\"#H3109666\" id=\"summRecButton\">",
" <span>",
" SUMMARY",
" </span>",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H1\">",
" INTRODUCTION",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H2\">",
" ANDROGEN METABOLISM",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H3\">",
" Testosterone",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H4\">",
" Androstenedione",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H5\">",
" Dehydroepiandrosterone sulfate",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H6\">",
" Dihydrotestosterone",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H7\">",
" Androstanediol",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H8\">",
" ESTROGEN METABOLISM",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H9\">",
" CONTROL OF ANDROGEN PRODUCTION",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H10\">",
" Ovarian androgen secretion",
" </a>",
" </li>",
" <li class=\"dashItem\">",
" <a class=\"outlineLink\" href=\"#H11\">",
" - Role of insulin",
" </a>",
" </li>",
" <li class=\"dashItem\">",
" <a class=\"outlineLink\" href=\"#H12\">",
" - Other factors",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H13\">",
" Adrenal androgen secretion",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"outlineLink\" href=\"#H14\">",
" Other",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"outlineLink\" href=\"#H3109666\">",
" SUMMARY",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a href=\"#references\">",
" REFERENCES",
" </a>",
" </li>",
" </ul>",
" </div>",
" <h1>",
" <div class=\"openRelatedGraphics\" id=\"ENDO/7442\" rel=\"outline_link\">",
" GRAPHICS",
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" View All",
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" <ul>",
" <li class=\"plainItem\">",
" <div class=\"openRelatedGraphics\" id=\"ENDO/7442|FIG\">",
" <a href=\"#\" title=\"FIGURES\">",
" FIGURES",
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" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_figure\" href=\"UTD.htm?21/25/21918\"
title=\"figure 1\">",
" Androgen levels in PCOS",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_figure\" href=\"UTD.htm?32/4/32845\"
title=\"figure 2\">",
" Estrogen levels in PCOS",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_figure\" href=\"UTD.htm?0/7/123\" title=\"figure
3\">",
" Adrenal steroid synthesis",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_figure\" href=\"UTD.htm?9/16/9487\" title=\"figure
4\">",
" Theca cell androgen production",
" </a>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_figure\" href=\"UTD.htm?38/60/39886\"
title=\"figure 5\">",
" IGF receptors in insulin resistance",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <div class=\"openRelatedGraphics\" id=\"ENDO/7442|TAB\">",
" <a href=\"#\" title=\"TABLES\">",
" TABLES",
" </a>",
" </div>",
" </li>",
" <li class=\"bulletItem\">",
" <a class=\"graphic graphic_table\" href=\"UTD.htm?19/41/20123\" title=\"table
1\">",
" Androgens in PCOS",
" </a>",
" </li>",
" </ul>",
" </div>",
" <h1>",
" RELATED TOPICS",
" </h1>",
" <div id=\"relatedTopics\">",
" <ul>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?39/8/40071?
source=related_link\">",
" Adrenal hyperandrogenism",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?16/6/16490?
source=related_link\">",
" Clinical manifestations of polycystic ovary syndrome in adults",
" </a>",
" </li>",
" <li class=\"plainItem\">",
" <a class=\"medical medical_review\" href=\"UTD.htm?38/36/39495?
source=related_link\">",
" Diagnosis of polycystic ovary syndrome in adults",
" </a>",
" </li>",
" </ul>",
" </div>",
" </div>"].join("\n");
var title_f0_0_13="Treatment of neonatal seizures";
var content_f0_0_13=[" <noscript>",
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" Treatment of neonatal seizures",
" </div>",
" <div id=\"topicContributors\">",
" <div>",
" <a id=\"authors\">",
" </a>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/0/13/contributors\">",
" Author",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/13/contributors\">",
" Eli M Mizrahi, MD",
" </a>",
" <br/>",
" </div>",
" <div>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/0/13/contributors\">",
" Section Editors",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/13/contributors\">",
" Douglas R Nordli, Jr, MD",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/13/contributors\">",
" Joseph A Garcia-Prats, MD",
" </a>",
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" </div>",
" <div>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/0/13/contributors\">",
" Deputy Editor",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/13/contributors\">",
" April F Eichler, MD, MPH",
" </a>",
" <br/>",
" </div>",
" </div>",
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" Literature review current through:",
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" Oct 2013.",
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" This topic last updated:",
" </span>",
" Feb 28, 2013.",
" </div>",
" <div id=\"topicText\">",
" <p class=\"headingAnchor\" id=\"H1\">",
" <span class=\"h1\">",
" INTRODUCTION",
" </span>",
" &nbsp;&mdash;&nbsp;The occurrence of neonatal seizures may be the first, and
perhaps the only, clinical sign of a central nervous system (CNS) disorder in the
newborn infant. Seizures may indicate the presence of a potentially treatable
etiology and should prompt an immediate evaluation to determine cause and to
institute etiology-specific therapy. In addition, seizures themselves may require
emergent therapy, since they can adversely affect the infant's homeostasis or they
may contribute to further brain injury. Some types of neonatal seizures are
associated with a relatively high incidence of early death and, in survivors, a
high incidence of neurologic impairment, developmental delay, and postneonatal
epilepsy.",
" </p>",
" <p>",
" This topic will discuss the approach to treatment of neonatal seizures. The
etiology, clinical features and diagnosis of neonatal seizures are discussed
separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?40/23/41335?
source=see_link\">",
" \"Etiology and prognosis of neonatal seizures\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?34/60/35783?
source=see_link\">",
" \"Neonatal epileptic syndromes\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?6/11/6328?
source=see_link\">",
" \"Clinical features and electrodiagnosis of neonatal seizures\"",
" </a>",
" .)",
" </p>",
" <p>",
" Both seizures and their subsequent therapy may be associated with changes in
respiration, heart rate, and blood pressure. An adequate airway and access to the
circulatory system must be insured early in the course of treatment.",
" </p>",
" <p class=\"headingAnchor\" id=\"H2\">",
" <span class=\"h1\">",
" ETIOLOGIC-SPECIFIC THERAPY",
" </span>",
" &nbsp;&mdash;&nbsp;Etiologic specific therapy is critical since it may prevent
further brain injury. This is particularly true for seizures associated with some
metabolic disorders (eg, hypoglycemia, hypocalcemia, and hypomagnesemia) and with
central nervous system (CNS) or systemic infections. Furthermore, neonatal seizures
may not be effectively controlled with antiepileptic drugs (AEDs) unless their
underlying cause is treated.",
" </p>",
" <p>",
" The most common etiologies of neonatal seizures are reviewed in the Table (",
" <a class=\"graphic graphic_table graphicRef73867 \" href=\"UTD.htm?
7/34/7724\">",
" table 1",
" </a>",
" ).",
" </p>",
" <p class=\"headingAnchor\" id=\"H3\">",
" <span class=\"h2\">",
" Neonatal encephalopathy",
" </span>",
" &nbsp;&mdash;&nbsp;Neonatal encephalopathy (and associated hypoxic-ischemic
encephalopathy) is the most common cause of neonatal seizures. The treatment of
neonatal encephalopathy is discussed separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?2/24/2442?
source=see_link\">",
" \"Clinical features, diagnosis, and treatment of neonatal encephalopathy\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H4\">",
" <span class=\"h2\">",
" CNS infection",
" </span>",
" &nbsp;&mdash;&nbsp;Infection of the central nervous system is a relatively
common cause of neonatal seizures and should be treated with broad spectrum
antibiotics at doses sufficient to treat meningitis.",
" </p>",
" <p>",
" Treatment of infection and meningitis in neonates is discussed separately.
(See",
" <a class=\"medical medical_review\" href=\"UTD.htm?27/26/28074?
source=see_link\">",
" \"Evaluation and management of fever in the neonate and young infant (less
than three months of age)\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?15/47/16121?
source=see_link\">",
" \"Treatment and outcome of bacterial meningitis in the neonate\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?18/16/18698?
source=see_link&amp;anchor=H25#H25\">",
" \"Group B streptococcal infection in neonates and young infants\", section on
'Management'",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H5\">",
" <span class=\"h2\">",
" Metabolic disturbances",
" </span>",
" &nbsp;&mdash;&nbsp;Metabolic disturbance are a treatable common cause of
neonatal seizures. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?34/23/35188?
source=see_link\">",
" \"Metabolic emergencies at birth\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H6\">",
" <span class=\"h3\">",
" Hypoglycemia",
" </span>",
" &nbsp;&mdash;&nbsp;Hypoglycemia should be corrected immediately with a 10
percent glucose solution given intravenously at 2",
" <span class=\"nowrap\">",
" mL/kg.",
" </span>",
" Maintenance glucose infusion can be given to a maximum of 8",
" <span class=\"nowrap\">",
" mg/kg",
" </span>",
" per minute. A detailed review of the evaluation and treatment of hypoglycemia
in infants is discussed separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?8/0/8201?
source=see_link\">",
" \"Approach to hypoglycemia in infants and children\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H7\">",
" <span class=\"h3\">",
" Hypocalcemia",
" </span>",
" &nbsp;&mdash;&nbsp;Hypocalcemia associated with severe neuromuscular
irritability or seizures is treated with 10 percent",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?40/13/41175?
source=see_link\">",
" calcium gluconate",
" </a>",
" (100",
" <span class=\"nowrap\">",
" mg/kg",
" </span>",
" or 1",
" <span class=\"nowrap\">",
" mL/kg",
" </span>",
" IV). The solution is infused over 5 to 10 minutes while the heart rate and
infusion site are monitored. The dose can be repeated in 10 minutes if no response
occurs. Alternatively,",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?18/63/19446?
source=see_link\">",
" calcium chloride",
" </a>",
" (20",
" <span class=\"nowrap\">",
" mg/kg",
" </span>",
" or 0.2",
" <span class=\"nowrap\">",
" ml/kg)",
" </span>",
" can be given. After acute treatment, maintenance calcium gluconate should be
added to the intravenous solution. The etiology, evaluation and treatment of
hypocalcemia in neonates are discussed in detail separately. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?26/23/26999?
source=see_link\">",
" \"Neonatal hypocalcemia\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H8\">",
" <span class=\"h3\">",
" Hypomagnesemia",
" </span>",
" &nbsp;&mdash;&nbsp;Neonatal hypomagnesemia is often associated with
hypocalcemia, although it can occur alone. The treatment is 50 percent solution
of",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?33/29/34262?
source=see_link\">",
" magnesium sulfate",
" </a>",
" given by intramuscular injection at 0.25",
" <span class=\"nowrap\">",
" mL/kg",
" </span>",
" or 125",
" <span class=\"nowrap\">",
" mg/kg.",
" </span>",
" The same dose can be repeated every 12 hours until normomagnesemia is
achieved.",
" </p>",
" <p class=\"headingAnchor\" id=\"H9\">",
" <span class=\"h2\">",
" Pyridoxine dependency",
" </span>",
" &nbsp;&mdash;&nbsp;Pyridoxine (100 mg IV) or pyridoxal phosphate (the active
form of pyridoxine [vitamin B6]) 10",
" <span class=\"nowrap\">",
" mg/kg",
" </span>",
" IV [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/1\">",
" 1",
" </a>",
" ] should be given to neonates with seizures unresponsive to conventional
anticonvulsants. If there is no response to pyridoxine, folinic acid (",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?3/56/3974?source=see_link\">",
" leucovorin",
" </a>",
" , 2.5 mg IV) may be administered for possible folinic acid responsive seizures
[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/2\">",
" 2",
" </a>",
" ].",
" </p>",
" <p>",
" A registry review of 63 cases (ranging in age from one day to nine years, with
most in the neonatal time period) revealed that seizures attributed to pyridoxine
dependency can be partial, generalized, or myoclonic; some patients have infantile
spasms [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/3\">",
" 3",
" </a>",
" ]. In one case series, frequent multifocal and generalized myoclonic jerks
intermixed with tonic symptoms were features common in infants with pyridoxine
dependency and rare in infants with seizures of other causes [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/4\">",
" 4",
" </a>",
" ]. Most children have excellent seizure control with pyridoxine
supplementation, but have a wide variety of neurodevelopmental problems [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/5,6\">",
" 5,6",
" </a>",
" ].",
" </p>",
" <p>",
" The results of one case series caution that EEG-response alone to pyridoxine
IV does not definitively identify (nor does lack of initial response exclude)
pyridoxine-dependent epilepsy [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/7,8\">",
" 7,8",
" </a>",
" ]. Individuals with pyridoxine or folinic acid responsive seizures and other
neonates with treatment-resistant epilepsy should undergo further evaluation
including measurement of urine or plasma alpha-aminoadipic semialdehyde (alpha-
AASA) [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/6\">",
" 6",
" </a>",
" ]. These tests are informative in both treated and untreated states. Most
cases of pyridoxine-dependent epilepsy are due to alpha-aminoadipic semialdehyde
dehydrogenase (also known as antiquitin, or ATQ) deficiency, an autosomal recessive
inborn error of metabolism caused by defects in the",
" <em>",
" ALDH7A1",
" </em>",
" gene that lead to accumulation of alpha-AASA [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/9,10\">",
" 9,10",
" </a>",
" ]. Mutation analysis of the",
" <em>",
" ALDH7A1",
" </em>",
" gene is recommended in patients with abnormal biochemical screening",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" clear evidence of pyridoxine or folinic acid responsiveness. Patients with ATQ
deficiency should receive chronic supplementation with pyridoxine",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" folinic acid [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/6,11\">",
" 6,11",
" </a>",
" ]. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?10/0/10250?
source=see_link\">",
" \"Inborn errors of metabolism: Metabolic emergencies\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H10\">",
" <span class=\"h1\">",
" ANTIEPILEPTIC THERAPY",
" </span>",
" &nbsp;&mdash;&nbsp;The use of antiepileptic drug (AED) therapy in neonates
will be reviewed. Initiating therapy, selecting appropriate agents, and stopping or
continuing therapy are the main decisions involved. Evidence of effectiveness is
limited [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/12\">",
" 12",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H11\">",
" <span class=\"h2\">",
" Decision to institute AED therapy",
" </span>",
" &nbsp;&mdash;&nbsp;After initial management of airway and cardiovascular
support and the identification and institution of etiologic-specific therapy, the
physician must decide whether to initiate antiepileptic drug therapy and then
decide what AEDs to use. Factors that must be considered in deciding whether to
initiate AED therapy include seizure type (epileptic versus nonepileptic in origin)
and, if epileptic in origin, seizure duration and severity.",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Antiepileptic drugs are utilized to treat neonatal seizures of epileptic
origin but not those of nonepileptic origin.",
" </li>",
" <li>",
" It is not necessary to treat all neonatal seizures of epileptic origin,
since some are brief, infrequent, and self-limited (occurring only in reaction to
an acute CNS insult). In these instances, no AEDs may be warranted, and the infant
need not be exposed to acute and chronic AED therapy.",
" </li>",
" <li>",
" On the other hand, some neonatal epileptic seizures are long in duration,
frequent, and are not self-limited. These are treated acutely and vigorously with
AEDs.",
" </li>",
" </ul>",
" </p>",
" <p>",
" The main clinical difficulty arises in the management of those infants whose
seizures have characteristics that fall between these two extremes. Currently,
almost all neonatal epileptic seizures within this intermediate category are
treated with AEDs.",
" </p>",
" <p class=\"headingAnchor\" id=\"H12\">",
" <span class=\"h2\">",
" Selection and administration of AEDs",
" </span>",
" &nbsp;&mdash;&nbsp;First-line AEDs and dosing schedules are listed in the
Table (",
" <a class=\"graphic graphic_table graphicRef79489 \" href=\"UTD.htm?
40/22/41323\">",
" table 2",
" </a>",
" ). The traditional strategy is to acutely treat seizures with an AED that can
be subsequently given as maintenance therapy.",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/63/29689?
source=see_link\">",
" Phenobarbital",
" </a>",
" is most frequently used as the initial drug. The next most frequently used
is",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?32/19/33082?
source=see_link\">",
" phenytoin",
" </a>",
" . However, neither agent appears to be more effective than the other and
neither is as effective as previously thought [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/13\">",
" 13",
" </a>",
" ].",
" </p>",
" <p>",
" As an alternative to",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?32/19/33082?
source=see_link\">",
" phenytoin",
" </a>",
" ,",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?22/45/23258?
source=see_link\">",
" fosphenytoin",
" </a>",
" is often used because of reports of reduced adverse effects with acute
administration [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/14\">",
" 14",
" </a>",
" ]. An alternative strategy of seizure management is acute treatment with
repeated doses of short acting benzodiazepines until seizures are controlled, thus
avoiding chronic AED therapy.",
" </p>",
" <p>",
" The use of",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/63/29689?
source=see_link\">",
" phenobarbital",
" </a>",
" and",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?32/19/33082?
source=see_link\">",
" phenytoin",
" </a>",
" in the neonate requires additional knowledge concerning their pharmacologic
characteristics [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/15-18\">",
" 15-18",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H13\">",
" <span class=\"h3\">",
" Phenobarbital",
" </span>",
" &nbsp;&mdash;&nbsp;",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/63/29689?
source=see_link\">",
" Phenobarbital",
" </a>",
" is eliminated by the liver and kidney; thus, infants with impaired hepatic or
renal function, such as those with HIE, will have a reduced rate of elimination and
potential for toxicity with standard dosing. The half-life of phenobarbital is
greater in premature compared with term infants, and longer in the first month of
life compared with older ages in term infants.",
" </p>",
" <p>",
" Thus, standard",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/63/29689?
source=see_link\">",
" phenobarbital",
" </a>",
" dosing in premature infants has the potential for higher serum levels and
resultant toxicity. As the infant becomes older, identical daily maintenance doses
may result in lower serum levels and create the potential for breakthrough seizures
with no other change in the infant's clinical condition. Overall, monitoring trends
of serum levels rather than day-to-day fluctuations are more useful in management
of phenobarbital therapy [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/19-21\">",
" 19-21",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H14\">",
" <span class=\"h3\">",
" Phenytoin",
" </span>",
" &nbsp;&mdash;&nbsp;Pharmacologic characteristics of",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?32/19/33082?
source=see_link\">",
" phenytoin",
" </a>",
" include its nonlinear pharmacokinetics, variable rate of hepatic metabolism, a
decrease in elimination rates during the first weeks of life, and a variable
bioavailability of the drug with various generic preparations [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/22,23\">",
" 22,23",
" </a>",
" ]. In addition, a redistribution of phenytoin results in a drop in brain
concentrations after the first dose. Thus, phenytoin use requires individualization
of dosing after initiation of therapy.",
" </p>",
" <p class=\"headingAnchor\" id=\"H15\">",
" <span class=\"h3\">",
" Other AEDs",
" </span>",
" &nbsp;&mdash;&nbsp;Some studies have reported limited success with second
line, alternative, or adjuvant AEDs for the control of medically refractory
neonatal seizures [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/12\">",
" 12",
" </a>",
" ]. A number of intravenous AEDs have been used including",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?11/7/11383?
source=see_link\">",
" clonazepam",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/24\">",
" 24",
" </a>",
" ],",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?36/57/37776?
source=see_link\">",
" lidocaine",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/25,26\">",
" 25,26",
" </a>",
" ],",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?0/46/746?source=see_link\">",
" midazolam",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/27-29\">",
" 27-29",
" </a>",
" ],",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?25/0/25608?
source=see_link\">",
" levetiracetam",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/30,31\">",
" 30,31",
" </a>",
" ], and",
" <a class=\"drug drug_general\" href=\"UTD.htm?23/35/24117?source=see_link\">",
" paraldehyde",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/32\">",
" 32",
" </a>",
" ]. Oral AEDs have also been employed including",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?5/36/5706?source=see_link\">",
" carbamazepine",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/33\">",
" 33",
" </a>",
" ],",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?41/11/42167?
source=see_link\">",
" primidone",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/34\">",
" 34",
" </a>",
" ],",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?26/54/27497?
source=see_link\">",
" valproate",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/35\">",
" 35",
" </a>",
" ],",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?24/27/25015?
source=see_link\">",
" vigabatrin",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/36\">",
" 36",
" </a>",
" ],",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?3/34/3626?source=see_link\">",
" lamotrigine",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/37\">",
" 37",
" </a>",
" ],",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?20/60/21448?
source=see_link\">",
" topiramate",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/38,39\">",
" 38,39",
" </a>",
" ], and levetiracetam [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/40,41\">",
" 40,41",
" </a>",
" ].",
" </p>",
" <p>",
" Newer AEDs are increasingly prescribed for neonatal seizures, despite the fact
this is an off-label indication [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/12\">",
" 12",
" </a>",
" ]. This trend has been driven by incomplete efficacy of more standard agents
and concerns about their potential neurotoxicity. However, there is little
supporting evidence, and none from randomized controlled trials, that support a
greater efficacy and lower adverse event rate with these agents in neonates.",
" </p>",
" <p class=\"headingAnchor\" id=\"H16\">",
" <span class=\"h2\">",
" Effectiveness",
" </span>",
" &nbsp;&mdash;&nbsp;There are little data from high quality clinical trials
regarding the effectiveness of AEDs for the treatment of neonatal seizures [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/42,43\">",
" 42,43",
" </a>",
" ]. Systematic reviews have identified only two randomized controlled trials
[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/13,44\">",
" 13,44",
" </a>",
" ], and the results of these are summarized as follows:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/63/29689?
source=see_link\">",
" Phenobarbital",
" </a>",
" and",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?32/19/33082?
source=see_link\">",
" phenytoin",
" </a>",
" appear to have comparable but limited efficacy. In a trial of 59 infants
with neonatal seizures, both drugs controlled seizures in less than half of the
infants [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/13\">",
" 13",
" </a>",
" ]. Seizure severity was a better predictor of treatment success of treatment
than the assigned treatment.",
" </li>",
" <li>",
" Neonatal seizures refractory to",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/63/29689?
source=see_link\">",
" phenobarbital",
" </a>",
" appear to respond poorly to second line AEDs. This observation is
illustrated by results of a small trial that randomly assigned neonates with
seizures who failed to respond to phenobarbital (11 of 22) to second line therapy
with either",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?11/7/11383?
source=see_link\">",
" clonazepam",
" </a>",
" (n=3),",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?0/46/746?
source=see_link\">",
" midazolam",
" </a>",
" (n=3), or",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?36/57/37776?
source=see_link\">",
" lidocaine",
" </a>",
" (n=5) [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/44\">",
" 44",
" </a>",
" ]. No response was seen in the neonates treated with clonazepam or
midazolam. Three of five responded to lidocaine; two neonates became seizure-free
with 4",
" <span class=\"nowrap\">",
" mg/kg",
" </span>",
" per hour of lidocaine, and one had an 80 percent reduction in seizure
burden. All of the 11 neonates whose seizures failed to respond to phenobarbital
had a poor neurodevelopmental outcome at one year.",
" </li>",
" </ul>",
" </p>",
" <p>",
" In contrast to the above data, a subsequent nonrandomized retrospective study
found that",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?0/46/746?source=see_link\">",
" midazolam",
" </a>",
" was rapidly effective in 13 neonates (10 with status epilepticus [SE]) who had
electrographic seizures refractory to",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/63/29689?
source=see_link\">",
" phenobarbital",
" </a>",
" and",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?32/19/33082?
source=see_link\">",
" phenytoin",
" </a>",
" [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/28\">",
" 28",
" </a>",
" ]. Midazolam was given as a bolus of 0.15",
" <span class=\"nowrap\">",
" mg/kg",
" </span>",
" followed by continuous infusion beginning at 1",
" <span class=\"nowrap\">",
" mcg/kg",
" </span>",
" per minute and increasing by 0.5 to 1",
" <span class=\"nowrap\">",
" mcg/kg",
" </span>",
" per minute every two minutes to electrographic seizure control or to a maximum
of 18",
" <span class=\"nowrap\">",
" mcg/kg",
" </span>",
" per minute. Neonates with SE were given a repeat bolus of midazolam 0.10 to
0.15",
" <span class=\"nowrap\">",
" mg/kg",
" </span>",
" if SE persisted 15 to 30 minutes after the initial bolus.",
" </p>",
" <p>",
" While these results appear promising, randomized clinical trial data are
needed to confirm that",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?0/46/746?source=see_link\">",
" midazolam",
" </a>",
" is effective for neonatal seizures, especially since midazolam was ineffective
in the randomized clinical trial discussed above [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/44\">",
" 44",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H17\">",
" <span class=\"h2\">",
" End point of acute AED therapy",
" </span>",
" &nbsp;&mdash;&nbsp;With the decision to initiate acute therapy, there should
come a predefined, expected end point of treatment. The ideal result in the acute
treatment of electroclinical seizures is the cessation of both the clinical and the
electrical seizures. However, a typical response by electroclinical seizures to
acute AED therapy is the initial control of the clinical seizures with the
persistence of the electrical seizure activity [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/45,46\">",
" 45,46",
" </a>",
" ]. With additional doses, the electrical seizures may be controlled. However,
there are also instances in which the EEG seizures cannot be controlled despite
increasing doses of the initial AED and addition of others.",
" </p>",
" <p>",
" The role of continuous EEG monitoring in directing treatment is also debated.
(See",
" <a class=\"medical medical_review\" href=\"UTD.htm?6/11/6328?
source=see_link&amp;anchor=H26#H26\">",
" \"Clinical features and electrodiagnosis of neonatal seizures\", section on
'EEG monitoring'",
" </a>",
" .) In one small study, 33 infants were randomized to treatment using amplitude
integrated EEG (aEEG) monitoring results versus treatment blinded to aEEG
monitoring results, ie, focusing on clinical seizures only [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/47\">",
" 47",
" </a>",
" ]. There was a nonsignificant trend for a reduction in clinical seizure
duration in patients for whom the aEEG monitoring data was available.",
" </p>",
" <p>",
" Current practice consists of acute AED therapy until clinical seizures are
controlled, with the first AED given in doses to achieve serum levels in the high
therapeutic range or to the maximum tolerated dose. This is followed by the second
AED. A benzodiazepine may also be given if needed. If EEG is recorded during acute
treatment, the same AED strategy is followed to treat the clinical seizures.
However, if the clinical seizures are controlled and the electrical seizures
persist, the AEDs are only given to high therapeutic range, since the electrical
seizure discharges are most often resistant to further AED therapy. Additional
drugs are not given, since they are likely to provide very limited additional
benefit while increasing the chances of the occurrence of adverse effects.",
" </p>",
" <p class=\"headingAnchor\" id=\"H18\">",
" <span class=\"h2\">",
" Chronic AED therapy",
" </span>",
" &nbsp;&mdash;&nbsp;There are no well-defined criteria to determine which
neonates require chronic AED therapy after acute seizures are controlled or the
duration of such treatment. When chronic therapy is considered, maintenance doses
of either",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?28/63/29689?
source=see_link\">",
" phenobarbital",
" </a>",
" or",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?32/19/33082?
source=see_link\">",
" phenytoin",
" </a>",
" are given (3 to 4",
" <span class=\"nowrap\">",
" mg/kg",
" </span>",
" per day for both drugs), and serum levels are monitored. Reported schedules
for chronic AED treatment range from one week up to 12 months after the last
seizure [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/48\">",
" 48",
" </a>",
" ], although a currently utilized schedule is to withdraw AEDs two weeks after
the infant's last seizure [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/13/abstract/49\">",
" 49",
" </a>",
" ]. This is often done just prior to the recording of an EEG that demonstrates
no electrical seizure activity.",
" </p>",
" <p class=\"headingAnchor\" id=\"H7764638\">",
" <span class=\"h1\">",
" SUMMARY AND RECOMMENDATIONS",
" </span>",
" &nbsp;&mdash;&nbsp;In the neonate, seizures may indicate the presence of a
potentially treatable etiology and should prompt an immediate evaluation to
determine cause and to institute etiology-specific therapy.",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Etiologic specific therapy (for metabolic disorders, central nervous system
or systemic infection) is critical since it may prevent further brain injury. Also,
neonatal seizures may not be effectively controlled with antiepileptic drugs (AEDs)
unless their underlying cause is treated. (See",
" <a class=\"local\" href=\"#H2\">",
" 'Etiologic-specific therapy'",
" </a>",
" above.)",
" </li>",
" <li>",
" Factors that must be considered in deciding whether to initiate AED therapy
include seizure type (epileptic versus nonepileptic in origin) and, if epileptic in
origin, seizure duration and severity. (See",
" <a class=\"local\" href=\"#H11\">",
" 'Decision to institute AED therapy'",
" </a>",
" above.)",
" </li>",
" <li>",
" First-line AEDs and dosing schedules are listed in the Table (",
" <a class=\"graphic graphic_table graphicRef79489 \" href=\"UTD.htm?
40/22/41323\">",
" table 2",
" </a>",
" ). (See",
" <a class=\"local\" href=\"#H12\">",
" 'Selection and administration of AEDs'",
" </a>",
" above.)",
" </li>",
" <li>",
" Pyridoxine (100 mg IV) or pyridoxal phosphate (10",
" <span class=\"nowrap\">",
" mg/kg",
" </span>",
" IV) should be given to neonates with seizures unresponsive to conventional
anticonvulsants. If there is no response to pyridoxine, folinic acid (",
" <a class=\"drug drug_pediatric\" href=\"UTD.htm?3/56/3974?
source=see_link\">",
" leucovorin",
" </a>",
" , 2.5 mg IV) may be administered for possible folinic acid responsive
seizures. (See",
" <a class=\"local\" href=\"#H9\">",
" 'Pyridoxine dependency'",
" </a>",
" above.)",
" </li>",
" <li>",
" Current practice consists of continuing acute AED therapy until clinical
seizures are controlled, with the first AED given in doses to achieve serum levels
in the high therapeutic range or to the maximum tolerated dose. This is followed by
the second AED or a benzodiazepine. (See",
" <a class=\"local\" href=\"#H12\">",
" 'Selection and administration of AEDs'",
" </a>",
" above and",
" <a class=\"local\" href=\"#H17\">",
" 'End point of acute AED therapy'",
" </a>",
" above.)",
" </li>",
" <li>",
" If the clinical seizures are controlled and the electrical seizures persist,
the AEDs are only given to high therapeutic range, since the electrical seizure
discharges are most often resistant to further AED therapy. (See",
" <a class=\"local\" href=\"#H17\">",
" 'End point of acute AED therapy'",
" </a>",
" above.)",
" </li>",
" <li>",
" AEDs are typically withdrawn two weeks after the infant's last seizure.
There are no well defined criteria that predict which neonates will require chronic
AED therapy. (See",
" <a class=\"local\" href=\"#H18\">",
" 'Chronic AED therapy'",
" </a>",
" above.)",
" </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>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/36\">",
" Aicardi J, Mumford JP, Dumas C, Wood S. Vigabatrin as initial therapy for
infantile spasms: a European retrospective survey. Sabril IS Investigator and Peer
Review Groups. Epilepsia 1996; 37:638.",
" </a>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/37\">",
" Barr PA, Buettiker VE, Antony JH. Efficacy of lamotrigine in refractory
neonatal seizures. Pediatr Neurol 1999; 20:161.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/38\">",
" Silverstein FS, Ferriero DM. Off-label use of antiepileptic drugs for the
treatment of neonatal seizures. Pediatr Neurol 2008; 39:77.",
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" Glass HC, Poulin C, Shevell MI. Topiramate for the treatment of neonatal
seizures. Pediatr Neurol 2011; 44:439.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/40\">",
" Shoemaker MT, Rotenberg JS. Levetiracetam for the treatment of neonatal
seizures. J Child Neurol 2007; 22:95.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/41\">",
" Hmaimess G, Kadhim H, Nassogne MC, et al. Levetiracetam in a neonate with
malignant migrating partial seizures. Pediatr Neurol 2006; 34:55.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/42\">",
" Booth D, Evans DJ. Anticonvulsants for neonates with seizures. Cochrane
Database Syst Rev 2004; :CD004218.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/43\">",
" Slaughter LA, Patel AD, Slaughter JL. Pharmacological treatment of neonatal
seizures: a systematic review. J Child Neurol 2013; 28:351.",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/44\">",
" Boylan GB, Rennie JM, Chorley G, et al. Second-line anticonvulsant treatment
of neonatal seizures: a video-EEG monitoring study. Neurology 2004; 62:486.",
" </a>",
" </li>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/45\">",
" Mizrahi EM, Kellaway P. Characterization and classification of neonatal
seizures. Neurology 1987; 37:1837.",
" </a>",
" </li>",
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" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/46\">",
" Mizrahi, EM, Kellaway, P. The response of electroclinical neonatal seizures
to antiepileptic drug therapy. Epilepsia 1992; 33:114.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/47\">",
" van Rooij LG, Toet MC, van Huffelen AC, et al. Effect of treatment of
subclinical neonatal seizures detected with aEEG: randomized, controlled trial.
Pediatrics 2010; 125:e358.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/13/abstract/48\">",
" Boer HR, Gal P. Neonatal seizures: a survey of current practice. Clin
Pediatr (Phila) 1982; 21:453.",
" </a>",
" </li>",
" <li>",
" Fenichel, GM. Paroxysmal disorders. In: Clinical Pediatric Neurology, 3rd ed,
WB Saunders, Philadelphia 1997. p.1.",
" </li>",
" </ol>",
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" SUMMARY &amp; RECOMMENDATIONS",
" </span>",
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" </li>",
" <li class=\"plainItem\">",
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" INTRODUCTION",
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" ETIOLOGIC-SPECIFIC THERAPY",
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var title_f0_0_14="Paget disease of the breast";
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" Paget disease of the breast",
" </div>",
" <div id=\"topicContributors\">",
" <div>",
" <a id=\"authors\">",
" </a>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/0/14/contributors\">",
" Authors",
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" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/14/contributors\">",
" Michael S Sabel, MD",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/14/contributors\">",
" Donald L Weaver, MD",
" </a>",
" <br/>",
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" <div>",
" <a class=\"contributor contributor_credentials contributorType\"
href=\"UTD.htm?0/0/14/contributors\">",
" Section Editors",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/14/contributors\">",
" Anees B Chagpar, MD, MSc, MA, MPH, FACS, FRCS(C)",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/14/contributors\">",
" Daniel F Hayes, MD",
" </a>",
" <br/>",
" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/14/contributors\">",
" Lori J Pierce, MD",
" </a>",
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" Deputy Editor",
" </a>",
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" <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
0/0/14/contributors\">",
" Rosemary B Duda, MD, MPH, FACS",
" </a>",
" <br/>",
" </div>",
" </div>",
" <div id=\"disclosures\">",
" <a href=\"UTD.htm?0/0/14/contributor-disclosure\" target=\"_blank\">",
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" <span class=\"emphasis\">",
" Literature review current through:",
" </span>",
" Oct 2013.",
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" </span>",
" Nov 27, 2012.",
" </div>",
" <div id=\"topicText\">",
" <p class=\"headingAnchor\" id=\"H1\">",
" <span class=\"h1\">",
" INTRODUCTION",
" </span>",
" &nbsp;&mdash;&nbsp;In 1874, Sir James Paget described 15 women with chronic
nipple ulceration who all went on to develop cancer of the involved breast within
two years [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/1\">",
" 1",
" </a>",
" ]. The ulceration was described as an eczema-like eruption on the nipple and
areola with a copious clear yellowish exudate. Ultimately this would become known
as Paget disease of the breast (PDB) or mammary Paget disease. While Paget believed
that the nipple changes were themselves benign, it was subsequently discovered that
the characteristic cells within the epidermis of the nipple (Paget cells) were in
fact malignant [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/2\">",
" 2",
" </a>",
" ].",
" </p>",
" <p>",
" This topic review will discuss the clinical presentation, pathogenesis,
pathology, diagnosis and management of mammary Paget disease.",
" </p>",
" <p class=\"headingAnchor\" id=\"H2\">",
" <span class=\"h1\">",
" EPIDEMIOLOGY",
" </span>",
" &nbsp;&mdash;&nbsp;PDB is much less common than other presentations of breast
cancer, accounting for only 1 to 3 percent of new cases of female breast cancer
that are diagnosed annually in the United States [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/3-7\">",
" 3-7",
" </a>",
" ]. PDB can occur in men; however, this is an extremely rare finding. Although
cases have been described in patients ranging in age from 26 to 88, the peak
incidence is between 50 and 60 [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/8-11\">",
" 8-11",
" </a>",
" ].",
" </p>",
" <p>",
" Histologic (subclinical) evidence of PDB may be more frequent. In a series of
3000 consecutive mastectomy specimens, the incidence of clinical Paget disease was
0.7 percent, but histologic evidence of the disease was present in 4.9 percent of
the mastectomies [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/12\">",
" 12",
" </a>",
" ].",
" </p>",
" <p>",
" At least some epidemiologic data suggest that the incidence of PDB is
decreasing over time [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/13\">",
" 13",
" </a>",
" ]. In a report of 1738 cases of PDB reported to the SEER database, the
incidence of PDB decreased by 45 percent between 1988 and 2002, while the overall
incidence of breast cancer increased over this same time period.",
" </p>",
" <p>",
" Although PDB is a less common presentation of breast cancer than is a palpable
mass or mammographic abnormality, it is an important consideration in the
differential diagnosis of a chronic persistent abnormality of the nipple.",
" </p>",
" <p class=\"headingAnchor\" id=\"H3\">",
" <span class=\"h1\">",
" CLINICAL PRESENTATION",
" </span>",
" &nbsp;&mdash;&nbsp;The hallmark of PDB is a scaly, raw, vesicular, or
ulcerated lesion that begins on the nipple and then spreads to the areola (",
" <a class=\"graphic graphic_picture graphicRef60575 \" href=\"UTD.htm?
2/23/2423\">",
" picture 1",
" </a>",
" ). Occasionally, a bloody discharge is present. PDB is usually unilateral,
although bilateral cases have been described [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/14\">",
" 14",
" </a>",
" ]. Nipple retraction is also a rare finding, but may occur with more advanced
disease.",
" </p>",
" <p>",
" Pain, burning",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" pruritus are commonly associated with PDB and may be present before the
development of clinically apparent disease. Thus, any patient complaining of these
symptoms but without an obvious lesion should be followed closely with further
investigation if the symptoms persist. Despite the superficial nature of the
findings, the median duration of signs and symptoms prior to histologic diagnosis
is between six and eight months [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/8,9\">",
" 8,9",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H4\">",
" <span class=\"h1\">",
" DIAGNOSTIC WORK UP",
" </span>",
" &nbsp;&mdash;&nbsp;The diagnostic work up of suspected PDB focuses on both
establishing the diagnosis and identifying an underlying breast cancer. An
underlying breast cancer (in situ or invasive) is present in 85 to 88 percent of
cases, although often without an associated breast mass or mammographic abnormality
[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/13\">",
" 13",
" </a>",
" ].",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" A palpable breast mass is present in 50 percent of cases of PDB; the mass is
often located more than 2 cm from the nipple-areolar complex [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/3,5\">",
" 3,5",
" </a>",
" ].",
" </li>",
" <li>",
" In 20 percent of cases, a mammographic abnormality is present without a
palpable mass [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/15\">",
" 15",
" </a>",
" ].",
" </li>",
" <li>",
" In 25 percent of cases, there is neither an underlying mass nor a
mammographic abnormality, but an occult ductal carcinoma is present.",
" </li>",
" <li>",
" About 12 to 15 percent of cases are not associated with a palpable mass,
mammographic abnormality, or parenchymal breast cancer [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/13\">",
" 13",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p>",
" Patients with either a palpable mass or a mammographic abnormality are more
likely to have an underlying invasive cancer, while intraductal cancer is found
more often in the absence of a palpable mass or mammographic abnormality [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/16\">",
" 16",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H5\">",
" <span class=\"h2\">",
" History and physical examination",
" </span>",
" &nbsp;&mdash;&nbsp;A detailed history should document the length of time the
lesion has been present and any associated symptoms, including pain, nipple
discharge, bleeding, burning, and pruritus. The history should also cover the
patient's individual risk profile for breast cancer, including any risk factors for
hereditary breast cancer. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?28/17/28954?
source=see_link\">",
" \"Factors that modify breast cancer risk in women\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?42/63/44025?
source=see_link\">",
" \"Characteristics of hereditary breast and ovarian cancer syndromes\"",
" </a>",
" .)",
" </p>",
" <p>",
" Bilateral breast examination should be performed, focusing on associated
breast abnormalities. An underlying breast malignancy is present in 85 to 88
percent of cases, and a palpable mass is present in approximately one-half.",
" </p>",
" <p class=\"headingAnchor\" id=\"H6\">",
" <span class=\"h2\">",
" Differential diagnosis",
" </span>",
" &nbsp;&mdash;&nbsp;The differential diagnosis includes both benign etiologies
(eczema, contact as well as radiation dermatitis, nipple adenoma) and malignant
conditions (Bowen's disease (squamous carcinoma of the epidermis), basal cell
carcinoma, superficial spreading malignant melanoma) [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/17-21\">",
" 17-21",
" </a>",
" ]. Spontaneous improvement or healing of the nipple dermatitis can occur and
should not be taken as an indication that PDB is not present or has resolved [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/4\">",
" 4",
" </a>",
" ].",
" </p>",
" <p>",
" Given the differential diagnosis, a short course of topical steroids is often
considered if eczema is strongly suspected. However, transient improvement in the
eczematous changes may occur even in the presence of PDB. In order to avoid undue
delay in definitive diagnosis, any persistent nipple abnormality should be
considered an indication for biopsy.",
" </p>",
" <p class=\"headingAnchor\" id=\"H7\">",
" <span class=\"h2\">",
" Skin biopsy and histology",
" </span>",
" &nbsp;&mdash;&nbsp;Nipple scrape cytology can accurately diagnose PDB [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/22,23\">",
" 22,23",
" </a>",
" ], but the diagnosis is usually established by full-thickness wedge or punch
biopsy of the nipple. Wedge biopsy has the advantage of frequently containing
lactiferous ducts, which may disclose the ductal etiology of PDB.",
" </p>",
" <p>",
" Histologically, the hallmark of PDB is the presence of malignant,
intraepithelial adenocarcinoma cells (Paget cells) occurring singly or in small
groups within the epidermis of the nipple (",
" <a class=\"graphic graphic_picture graphicRef81226 \" href=\"UTD.htm?
42/18/43304\">",
" picture 2",
" </a>",
" ). The cells are often large but may be similar in size to keratinocytes. The
cytoplasm is pale to clear, and nuclei are usually high grade with prominent
nucleoli. In many instances, the Paget cells retract from the surrounding
keratinocytes and appear to be within a vacuole.",
" </p>",
" <p>",
" Histologically, PDB can mimic malignant melanoma, particularly if the cells
have incorporated melanin from the adjacent epidermis. The presence of cytoplasmic
mucin vacuoles can aid in the diagnosis, as can special stains such as mucicarmine,
which may highlight the vacuoles. Immunohistochemistry (IHC) may also be helpful in
diagnostically difficult cases (",
" <a class=\"graphic graphic_table graphicRef74830 \" href=\"UTD.htm?
30/30/31212\">",
" table 1",
" </a>",
" ). PDB can be distinguished from malignant melanoma by positive IHC for CEA
(polyclonal) and negative IHC for S-100 protein; however, some cases of PDB are S-
100 positive [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/24\">",
" 24",
" </a>",
" ] and CEA may not always be expressed.",
" </p>",
" <p>",
" If present, estrogen",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" progesterone receptor positivity is extremely helpful. Unfortunately, about
one-half of PDB cases do not express hormone receptors; a finding that is not
surprising considering the frequent association with high-grade invasive ductal
carcinomas that are also likely to be hormone receptor negative.",
" </p>",
" <p>",
" Paget cells are positive for low molecular weight cytokeratins, a feature that
can help distinguish PDB from squamous carcinoma of the epidermis (Bowen's
disease), which typically expresses high molecular weight cytokeratins. CK7 is
probably the most useful marker, but caution must be exercised in interpreting CK 7
stains in the absence of other typical histologic features of PDB. Although
positive in PDB, CK 7 may also be expressed in benign Toker cell hyperplasia [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/25,26\">",
" 25,26",
" </a>",
" ], and some breast carcinomas may not express CK7 [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/27\">",
" 27",
" </a>",
" ]. Toker cells in the nipple may be derived from or related to lactiferous
duct epithelium, and malignant transformation of these cells may explain some cases
of PDB without associated ductal carcinoma [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/28\">",
" 28",
" </a>",
" ].",
" </p>",
" <p>",
" Between 84 and 91 percent of cases of PDB overexpress HER2. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?29/22/30058?
source=see_link\">",
" \"HER2 and predicting response to therapy in breast cancer\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H8\">",
" <span class=\"h2\">",
" Mammography",
" </span>",
" &nbsp;&mdash;&nbsp;Bilateral mammography is mandatory to identify an
associated mass as well as rule out synchronous cancers or widespread
calcifications that might preclude breast conservation therapy. Approximately one-
half of cases of PDB have an associated mammographic abnormality [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/15,29\">",
" 15,29",
" </a>",
" ]. The mammographic findings in 17 women in one study included suspicious
microcalcifications, a mass, architectural distortion, nipple retraction and
asymmetric thickening of the nipple-areolar complex [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/15\">",
" 15",
" </a>",
" ]. In seven cases, the mammographic abnormalities were located distant from
the nipple-areolar complex.",
" </p>",
" <p>",
" As noted above, while women with a negative mammogram in the setting of PDB
appear to have a low likelihood of underlying invasive breast cancer (particularly
in the absence of a palpable mass [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/16,30\">",
" 16,30",
" </a>",
" ]), an occult associated intraductal carcinoma may be present and quite
extensive. In the above noted series, all of the 17 women with negative mammograms
had ductal carcinoma in situ (DCIS), five with extensive multicentric disease [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/15\">",
" 15",
" </a>",
" ]. In another series, mammography failed to identify 64 percent of cases of
multifocal underlying breast cancer (both in situ and invasive cancer) in women
with PDB and no palpable mass [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/31\">",
" 31",
" </a>",
" ]. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?38/35/39482?
source=see_link\">",
" \"Breast imaging: Mammography and ultrasonography\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H9\">",
" <span class=\"h2\">",
" Magnetic resonance imaging",
" </span>",
" &nbsp;&mdash;&nbsp;Magnetic resonance imaging (MRI) is a sensitive imaging
tool for invasive breast cancer, particularly mammographically occult disease,
although its sensitivity for DCIS is less clear. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?6/33/6680?
source=see_link&amp;anchor=H100033269#H100033269\">",
" \"Breast ductal carcinoma in situ: Epidemiology, clinical manifestations, and
diagnosis\", section on 'Role of magnetic resonance imaging'",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?9/49/10009?
source=see_link\">",
" \"Clinical features, diagnosis, and staging of newly diagnosed breast
cancer\"",
" </a>",
" .)",
" </p>",
" <p>",
" There are few data addressing the utility of breast MRI in women with PDB and
a negative mammogram [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/32-36\">",
" 32-36",
" </a>",
" ]. The largest series included 34 women with PDB, 32 of whom had a
histologically confirmed breast cancer (seven invasive, 25 DCIS) [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/32\">",
" 32",
" </a>",
" ]. All patients underwent preoperative mammography, while 13 had an
ipsilateral breast MRI. Among the 23 women with biopsy proven PDB and negative
mammography, eight underwent MRI which detected otherwise occult disease in four
women (three DCIS, one invasive cancer), three of whom required mastectomy because
of extensive disease. However, MRI did not detect three cancers (two unifocal DCIS,
one invasive cancer) in the other four patients.",
" </p>",
" <p>",
" Thus, MRI may disclose occult cancer in some women with PDB and no findings on
mammography or physical examination, potentially allowing directed treatment of the
ipsilateral breast. However, a negative preoperative study cannot reliably exclude
an underlying cancer.",
" </p>",
" <p>",
" In addition, because MRI is highly sensitive but not highly specific, MRI may
reveal abnormalities that might lead to the overuse of mastectomy rather than
breast conserving therapy. Thus, if MRI is to be performed, it should only be
undertaken at an institution that has the capability of performing MRI-guided
biopsies, and the patient should be counseled regarding the high false positive
rate of breast MRI and the possible need for additional biopsies.",
" </p>",
" <p class=\"headingAnchor\" id=\"H10\">",
" <span class=\"h2\">",
" Biopsy of underlying abnormalities",
" </span>",
" &nbsp;&mdash;&nbsp;In addition to nipple biopsy, any underlying masses or
mammographic abnormalities must be biopsied to assist in decisions about local
treatment of the breast and the need for evaluation of the axilla.",
" </p>",
" <p class=\"headingAnchor\" id=\"H11\">",
" <span class=\"h1\">",
" PATHOGENESIS",
" </span>",
" &nbsp;&mdash;&nbsp;Two theories have been proposed to explain the pathogenesis
of PDB: the epidermotrophic theory, which is by far the more widely accepted, and
the transformation theory.",
" </p>",
" <p class=\"headingAnchor\" id=\"H12\">",
" <span class=\"h2\">",
" Epidermotrophic theory",
" </span>",
" &nbsp;&mdash;&nbsp;According to the prevailing epidermotrophic theory, the
Paget cell arises from an underlying mammary adenocarcinoma, with the neoplastic
ductal epithelial cells migrating through the ductal system of the breast into the
epidermis of the nipple.",
" </p>",
" <p>",
" In many series, immunohistochemical staining (IHC) is concordant in Paget
cells and the ductal epithelial cells, but discordant in Paget cells and the
epidermal keratinocytes of the surrounding nipple tissue (",
" <a class=\"graphic graphic_table graphicRef74830 \" href=\"UTD.htm?
30/30/31212\">",
" table 1",
" </a>",
" )&nbsp;[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/9,37-42\">",
" 9,37-42",
" </a>",
" ].",
" </p>",
" <p>",
" Similarly, expression of several molecular markers is concordant in PDB and
underlying parenchymal breast tumors [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/37,43\">",
" 37,43",
" </a>",
" ]. Over 80 percent of PDB have overexpression or amplification of the gene for
HER2 [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/17,18,43,44\">",
" 17,18,43,44",
" </a>",
" ]. In one report, all 23 cases of PDB stained with an anti-HER2 monoclonal
antibody; staining was also positive in all the underlying ductal carcinomas, but
never in normal nipple epidermis [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/8\">",
" 8",
" </a>",
" ]. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?29/22/30058?
source=see_link\">",
" \"HER2 and predicting response to therapy in breast cancer\"",
" </a>",
" .)",
" </p>",
" <p>",
" It is hypothesized that the spread of Paget cells to the nipple epidermis from
the duct system may be mediated through a motility factor that exerts its effect
via the HER2 receptor (",
" <a class=\"graphic graphic_figure graphicRef61409 \" href=\"UTD.htm?
3/35/3633\">",
" figure 1",
" </a>",
" )&nbsp;[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/45\">",
" 45",
" </a>",
" ].",
" </p>",
" <p>",
" Taken together, these data lend support to a common genetic alteration",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" possibly a common progenitor cell for both the Paget cells and the underlying
ductal carcinoma.",
" </p>",
" <p class=\"headingAnchor\" id=\"H13\">",
" <span class=\"h2\">",
" Transformation theory",
" </span>",
" &nbsp;&mdash;&nbsp;In contrast, the transformation theory proposes that
epidermal keratinocytes within the nipple transform into malignant Paget cells, and
that PDB in fact represents an epidermal carcinoma in situ that is independent of
any underlying ductal carcinoma [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/19\">",
" 19",
" </a>",
" ]. George Thin proposed this theory in 1881, believing that secretions from
the breast ducts damaged the epithelium, transforming normal keratinocytes to
cancer cells [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/2\">",
" 2",
" </a>",
" ].",
" </p>",
" <p>",
" The transformation theory was bolstered by the following observations:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" In a small percentage of cases, no parenchymal cancer can be identified in
association with PDB.",
" </li>",
" <li>",
" When an underlying parenchymal carcinoma is present, it is often located
peripheral to the nipple, suggesting two independent neoplastic processes. As an
example, in one series of 80 women with breast cancer and PDB, 29 of the underlying
breast tumors were located more than 2 cm from the areolar margin [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/10\">",
" 10",
" </a>",
" ].",
" </li>",
" <li>",
" Desmosomal attachments have been identified between Paget cells and adjacent
epidermal keratinocytes [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/46\">",
" 46",
" </a>",
" ]. These authors describe a \"pre-Paget cell\" with an appearance
intermediate between that of a keratinocyte and a Paget cell, suggesting that
epidermal cells can acquire the characteristics of ductal cells as they undergo
malignant transformation. Others suggest the presence of a unique precursor, the
Toker cell, to explain cases of PDB with no contiguous ductal carcinoma [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/28,47\">",
" 28,47",
" </a>",
" ].",
" </li>",
" </ul>",
" </p>",
" <p>",
" The transformation theory has fallen out of favor, in part because if enough
tissue sections are studied, involvement of the large (lactiferous) ducts
immediately beneath the nipple can usually be demonstrated.",
" </p>",
" <p class=\"headingAnchor\" id=\"H14\">",
" <span class=\"h1\">",
" STAGING",
" </span>",
" &nbsp;&mdash;&nbsp;The presence of Paget disease of the nipple does not change
the stage of an underlying breast cancer. If an associated breast cancer is not
identified, Paget disease is classified as Tis (Paget) disease. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?23/45/24278?
source=see_link\">",
" \"Tumor node metastasis (TNM) staging classification for breast cancer\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H15\">",
" <span class=\"h1\">",
" TREATMENT",
" </span>",
" &nbsp;&mdash;&nbsp;The most important aspect of presentation that influences
the treatment decision is the presence or absence of an ipsilateral palpable breast
mass or mammographic abnormality. The prognosis of PDB is based upon the underlying
breast cancer, and treatment should be guided by the stage of the tumor and other
prognostic",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" predictive factors.",
" </p>",
" <p>",
" Simple mastectomy has been the historic standard treatment for PDB. However,
the widespread use of breast conserving treatment (BCT) for invasive and in-situ
breast carcinoma has led to its use for PDB. In contrast to invasive breast cancer,
treatment recommendations are limited by the lack of prospective, randomized trials
comparing mastectomy to BCT or comparing various BCT options in patients with PDB.
Most reported series are small, and patient selection, treatment techniques and
median follow-up vary from study to study. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?30/42/31402?
source=see_link\">",
" \"Breast conserving therapy\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?12/18/12586?
source=see_link\">",
" \"Mastectomy\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?36/43/37561?
source=see_link\">",
" \"Ductal carcinoma in situ: Treatment and prognosis\"",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H16\">",
" <span class=\"h2\">",
" PDB with a palpable mass or abnormal imaging",
" </span>",
" &nbsp;&mdash;&nbsp;When PDB is present in association with a palpable mass or
defined mammographic abnormality, the associated breast cancer tends to be a more
advanced stage (ie, larger size, multifocal, more frequent presence of invasive
disease and axillary node positivity) than if a mass is absent [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/10,16,31\">",
" 10,16,31",
" </a>",
" ]. The incidence of axillary metastases in women who present with PDB with and
without a palpable mass is shown in the following table (",
" <a class=\"graphic graphic_table graphicRef67429 \" href=\"UTD.htm?
6/63/7163\">",
" table 2",
" </a>",
" ).",
" </p>",
" <p>",
" Both the nipple-areolar complex and the underlying cancer must be excised.
Many patients will require a mastectomy. However, if nipple-areolar resection and
wide local excision of the palpable mass or area of mammographic abnormality can be
performed with an acceptable cosmetic result and negative margins, breast-
conserving surgery followed by whole breast radiotherapy (RT) is an appropriate
local treatment option. If the breasts are large, resection of the palpable mass
and nipple-areolar complex with nipple reconstruction and contralateral breast
reduction can be combined with definitive breast RT to achieve an adequate
oncologic outcome with acceptable breast contour and symmetry.",
" </p>",
" <p>",
" Women with multicentric cancer or diffuse calcifications should be treated by
mastectomy. Many women with PDB and a palpable mass are not amenable to BCT because
of the distance between the primary tumor and the nipple-areolar complex [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/10\">",
" 10",
" </a>",
" ]. If resection of both the nipple-areolar complex and the palpable mass with
a negative margin would result in an unacceptable cosmetic result, women may be
better served by simple mastectomy with or without breast reconstruction. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?30/42/31402?
source=see_link&amp;anchor=H7#H7\">",
" \"Breast conserving therapy\", section on 'Patient selection for BCT'",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?12/18/12586?
source=see_link&amp;anchor=H1378592045#H1378592045\">",
" \"Mastectomy\", section on 'Selection criteria for mastectomy'",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H17\">",
" <span class=\"h2\">",
" PDB with no palpable mass or imaging abnormality",
" </span>",
" &nbsp;&mdash;&nbsp;Underlying carcinoma is present in most of these patients
despite the absence of a palpable mass or mammographic abnormality [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/31\">",
" 31",
" </a>",
" ]. The majority will have DCIS but invasive cancer is present in one-fourth to
one-third of cases [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/3,5,48\">",
" 3,5,48",
" </a>",
" ]. Standard treatment options include mastectomy or breast conserving therapy
(resection of the nipple-areola complex followed by whole breast irradiation) (",
" <a class=\"graphic graphic_picture graphicRef75416 \" href=\"UTD.htm?
1/35/1593\">",
" picture 3",
" </a>",
" ).",
" </p>",
" <p>",
" Simple mastectomy with or without breast reconstruction is an effective option
[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/4,49\">",
" 4,49",
" </a>",
" ]. In a series of 37 patients treated by simple mastectomy alone, the local
recurrence rate was only 5 percent, with a median follow-up of 40 months [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/4\">",
" 4",
" </a>",
" ].",
" </p>",
" <p>",
" Several reports describe the use of limited surgery or nipple-areolar
resection followed by breast RT for treatment of PDB in women without a palpable
breast mass (",
" <a class=\"graphic graphic_table graphicRef80724 \" href=\"UTD.htm?
27/24/28043\">",
" table 3",
" </a>",
" )&nbsp;[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/8,30,50-53\">",
" 8,30,50-53",
" </a>",
" ]. Rates of local recurrence, successful salvage, and distant disease-free
survival seem comparable to those seen with DCIS [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/54\">",
" 54",
" </a>",
" ]. The following represents the range of findings:",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" A study of 36 patients with PDB and no underlying palpable mass or
mammographic abnormality who underwent complete or partial resection of the nipple-
areola complex followed by RT demonstrated a local recurrence rate of 11 percent at
a median follow-up of 112 months [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/8\">",
" 8",
" </a>",
" ]. Of the 22 patients undergoing complete nipple-areolar resection followed
by whole breast RT with a boost (total dose 61.5 Gy), three (14 percent) developed
a local recurrence. In contrast, two of six women (33 percent) treated with the
same dose of RT but only a partial nipple-areolar resection recurred locally, one
with distant metastases. All four women with an isolated local recurrence were
successfully salvaged with mastectomy and remained disease-free at the time of last
follow-up.",
" </li>",
" <li>",
" The European Organization for Research and Treatment of Cancer (EORTC)
conducted a prospective study of BCT for PDB [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/30\">",
" 30",
" </a>",
" ]. This study excluded women with invasive cancer. Of the 61 women enrolled
in the study with histologically proven PDB, 97 percent had no associated palpable
mass, and 84 percent had a normal mammogram. Associated DCIS was present in 93
percent, and the remainder had no underlying parenchymal carcinoma. Treatment
consisted of complete nipple-areolar resection followed by whole breast RT (median
dose 50 Gy). There were four local recurrences (6.5 percent), with a median follow-
up of 6.4 years. Three recurrences were invasive, and one was DCIS; one patient
with an invasive recurrence subsequently died of metastatic disease.",
" </li>",
" </ul>",
" </p>",
" <p>",
" Taken together, these data suggest that central lumpectomy or complete
resection of the nipple-areola complex followed by whole breast RT is a reasonable
alternative to mastectomy for women with PDB and no palpable mass or mammographic
abnormality as long as a good cosmetic outcome and negative margins can be
achieved. A variety of techniques can be used to reconstruct the nipple areolar
complex, and cosmesis has been assessed as good to excellent in the majority of
patients so treated.",
" </p>",
" <p class=\"headingAnchor\" id=\"H18\">",
" <span class=\"h2\">",
" Management of the axilla",
" </span>",
" &nbsp;&mdash;&nbsp;The risk of axillary metastases in series of patients with
PDB is higher in women with invasive cancer and a palpable mass (",
" <a class=\"graphic graphic_table graphicRef67429 \" href=\"UTD.htm?
6/63/7163\">",
" table 2",
" </a>",
" )&nbsp;[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/9,10,48,49,55,56\">",
" 9,10,48,49,55,56",
" </a>",
" ].",
" </p>",
" <p>",
" Evaluation and treatment of the axilla in PDB are the same as for any breast
cancer, depending on the underlying cancer: (see",
" <a class=\"medical medical_review\" href=\"UTD.htm?41/52/42825?
source=see_link\">",
" \"Management of the regional lymph nodes in breast cancer\"",
" </a>",
" )",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Patients with in situ disease do not require axillary investigation unless
the disease is extensive enough to merit mastectomy. If mastectomy is planned, SLN
biopsy is often (and appropriately) done preemptively in order to avoid complete
axillary lymph node dissection in case an invasive component is identified at final
pathology. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?35/47/36602?
source=see_link\">",
" \"Sentinel lymph node dissection for breast cancer: Indications and
outcomes\"",
" </a>",
" .)",
" </li>",
" <li>",
" If invasive disease has been identified, patients with clinically node-
negative disease should undergo SLN biopsy at the time of wide excision. An SLN can
be successfully identified in 97 percent of patients with PDB [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/56\">",
" 56",
" </a>",
" ]. Management of a positive SLN is discussed in detail elsewhere. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?35/47/36602?
source=see_link&amp;anchor=H5456194#H5456194\">",
" \"Sentinel lymph node dissection for breast cancer: Indications and
outcomes\", section on 'When should completion axillary dissection be performed?'",
" </a>",
" .)",
" </li>",
" <li>",
" Patients with a clinically positive axilla should undergo an initial
ultrasound-guided fine needle or core needle aspiration of the palpable axillary
nodes; if disease is confirmed histologically, full axillary lymph node dissection
(ALND) is needed. In contrast, if the FNA or core biopsy is negative, sentinel
lymph node (SLN) biopsy should be performed.",
" </li>",
" <li>",
" For patients with pure PDB, no underlying palpable mass and clinically
negative axillary nodes, there is some controversy as to the need for axillary
evaluation. Given the high incidence of DCIS alone in patients with PDB and no
evidence of an underlying breast mass, SLN biopsy is recommended only if invasive
disease is identified or mastectomy is planned [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/56\">",
" 56",
" </a>",
" ]. However, some consider the likelihood of invasive disease high enough to
recommend a SLN biopsy, regardless of the type of surgery that is planned. In a
series of 19 patients with PDB only, an invasive component was found in 27 percent
and positive SLNs in 11 percent [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/48\">",
" 48",
" </a>",
" ]. As most patients prefer to avoid a procedure that is not necessary, it is
best to recommend SLN only if indicated, but the potential need for a second
operation for SLN biopsy if an invasive component is identified should be
discussed. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?35/47/36602?
source=see_link\">",
" \"Sentinel lymph node dissection for breast cancer: Indications and
outcomes\"",
" </a>",
" .)",
" </li>",
" </ul>",
" </p>",
" <p class=\"headingAnchor\" id=\"H19\">",
" <span class=\"h2\">",
" Alternative approaches",
" </span>",
" &nbsp;&mdash;&nbsp;Mastectomy and breast conserving therapy (surgery plus
whole-breast RT) represent standard approaches to treatment of PDB without an
underlying mass or mammographic abnormality. While less aggressive approaches have
been examined (ipsilateral breast RT following only a diagnostic nipple biopsy [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/50-53\">",
" 50-53",
" </a>",
" ], breast-conserving surgery alone (",
" <a class=\"graphic graphic_table graphicRef60782 \" href=\"UTD.htm?
31/44/32460\">",
" table 4",
" </a>",
" )&nbsp;[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/4,49,57,58\">",
" 4,49,57,58",
" </a>",
" ]), only small number of patients have been studied, and reported results are
variable. Thus, neither of these approaches can be considered a standard treatment
for most patients with PDB in the absence of an underlying mass.",
" </p>",
" <p>",
" Few areas in breast cancer treatment are as contentious as the need for RT as
a component of BCT in women with DCIS. Proponents of RT for all women with DCIS
argue that local recurrence rates are substantially higher when RT is withheld and
that one-half of all local recurrences are invasive. Others contend that RT
represents overly aggressive therapy for many women with DCIS and that by weighing
factors of prognostic importance (ie, grade, size, age, and distance to margins), a
sizable subset can be identified who have excellent recurrence-free survival with
excision alone. These issues are all discussed in detail elsewhere. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?36/43/37561?
source=see_link&amp;anchor=H562651883#H562651883\">",
" \"Ductal carcinoma in situ: Treatment and prognosis\", section on 'Radiation
therapy'",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H20\">",
" <span class=\"h2\">",
" Use of tamoxifen",
" </span>",
" &nbsp;&mdash;&nbsp;There are no data addressing the efficacy of",
" <a class=\"drug drug_general\" href=\"UTD.htm?32/27/33208?source=see_link\">",
" tamoxifen",
" </a>",
" in reducing the risk for local recurrence in patients with PDB and no
underlying invasive ductal carcinoma who are treated with breast conserving
therapy. Recommendations regarding tamoxifen (as well as other forms of adjuvant
systemic therapy such as aromatase inhibitors, chemotherapy, and",
" <a class=\"drug drug_general\" href=\"UTD.htm?6/39/6776?source=see_link\">",
" trastuzumab",
" </a>",
" ) should be based solely upon the characteristics of any associated ductal
carcinoma. (See",
" <a class=\"medical medical_review\" href=\"UTD.htm?19/40/20106?
source=see_link\">",
" \"Adjuvant endocrine therapy for hormone receptor-positive breast cancer\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?37/4/37961?
source=see_link\">",
" \"Adjuvant chemotherapy for hormone receptor-positive or negative, HER2-
negative breast cancer\"",
" </a>",
" and",
" <a class=\"medical medical_review\" href=\"UTD.htm?36/43/37561?
source=see_link&amp;anchor=H562652190#H562652190\">",
" \"Ductal carcinoma in situ: Treatment and prognosis\", section on 'Systemic
treatment'",
" </a>",
" .)",
" </p>",
" <p class=\"headingAnchor\" id=\"H21\">",
" <span class=\"h1\">",
" PROGNOSIS",
" </span>",
" &nbsp;&mdash;&nbsp;The prognosis of Paget disease of the breast (PDB) is
dependent upon the presence of an underlying invasive ductal carcinoma or axillary
node metastases. Tumor stage is a better indicator of prognosis than the presence
of Paget disease per se.",
" </p>",
" <p>",
" As noted above, PDB presenting with a palpable mass is usually associated with
more advanced disease than cases without a palpable mass; because of this, five-
year survival rates are also lower (",
" <a class=\"graphic graphic_table graphicRef57584 \" href=\"UTD.htm?
15/4/15436\">",
" table 5",
" </a>",
" )&nbsp;[",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/9,10,49,55\">",
" 9,10,49,55",
" </a>",
" ]. In general, for women with PDB associated with a palpable mass, five-year
survival ranges from 20 to 60 percent, while for women without a palpable mass,
they are between 75 and 100 percent [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/10,19,49,55\">",
" 10,19,49,55",
" </a>",
" ].",
" </p>",
" <p>",
" For patients with a palpable mass and invasive ductal carcinoma, five-year
cause-specific survival ranges from 37 to 43 percent, while in patients without a
mass and with ductal carcinoma in situ (DCIS) only, the five-year cause-specific
survival is 90 to 100 percent [",
" <a class=\"abstract\" href=\"UTD.htm?0/0/14/abstract/3-5,8\">",
" 3-5,8",
" </a>",
" ].",
" </p>",
" <p class=\"headingAnchor\" id=\"H22\">",
" <span class=\"h1\">",
" SUMMARY AND RECOMMENDATIONS",
" </span>",
" </p>",
" <p>",
" <ul class=\"bullet-block\">",
" <li>",
" Paget disease of the breast (PDB) is clinically defined as a persistent
scaling, eczematous, or ulcerated lesion involving the",
" <span class=\"nowrap\">",
" nipple/areolar",
" </span>",
" complex. The pathologic hallmark is the presence of malignant,
intraepithelial adenocarcinoma cells (Paget cells) within the epidermis of the
nipple. (See",
" <a class=\"local\" href=\"#H1\">",
" 'Introduction'",
" </a>",
" above.)",
" </li>",
" <li>",
" PDB is associated with an underlying breast cancer (in situ",
" <span class=\"nowrap\">",
" and/or",
" </span>",
" invasive) in 85 to 88 percent of cases, often without an associated breast
mass or mammographic abnormality. (See",
" <a class=\"local\" href=\"#H3\">",
" 'Clinical presentation'",
" </a>",
" above.)",
" </li>",
" <li>",
" The diagnosis of PDB can usually be established by punch or full-thickness
wedge biopsy of the nipple. Biopsy of any underlying mass or mammographic
abnormality is needed to assist in decisions about local treatment of the breast
and the need for evaluation of the axilla. (See",
" <a class=\"local\" href=\"#H4\">",
" 'Diagnostic work up'",
" </a>",
" above.)",
" </li>",
" <li>",
" The diagnostic workup of all patients with PDB should include careful
physical examination of both breasts and mammography. Breast magnetic resonance
imaging (MRI) could be considered in a patient with a negative physical examination
and mammogram. All mammographically occult lesions that are identified by MRI do
not represent cancer, and confirmatory biopsy is needed. Thus, MRI should only be
obtained at institutions with the capability of performing MRI-guided biopsy.
(See",
" <a class=\"local\" href=\"#H4\">",
" 'Diagnostic work up'",
" </a>",
" above.)",
" </li>",
" <li>",
" Women who have a palpable mass in association with PDB are more likely to
harbor invasive breast cancer than are those with no palpable mass, and they are
also more likely to have involved axillary lymph nodes. (See",
" <a class=\"local\" href=\"#H16\">",
" 'PDB with a palpable mass or abnormal imaging'",
" </a>",
" above.)",
" </li>",
" <li>",
" Women with PDB and no palpable underlying mass or radiographic abnormality
have a low likelihood of harboring invasive breast cancer; the majority have
underlying ductal carcinoma in situ (DCIS). (See",
" <a class=\"local\" href=\"#H17\">",
" 'PDB with no palpable mass or imaging abnormality'",
" </a>",
" above.)",
" </li>",
" <li>",
" If an invasive breast cancer is found, it should be treated like any other
invasive breast cancer, with consideration of adjuvant systemic therapy. (See",
" <a class=\"local\" href=\"#H15\">",
" 'Treatment'",
" </a>",
" above.)",
" </li>",
" <li>",
" Evaluation and treatment of the axilla in PDB are the same as for any breast
cancer and depends on the underlying cancer. (See",
" <a class=\"local\" href=\"#H18\">",
" 'Management of the axilla'",
" </a>",
" above.)",
" </li>",
" <li>",
" Both mastectomy and breast-conserving surgery followed by whole breast
radiotherapy (RT) are acceptable treatment options. Breast-conserving surgery and
RT should only be performed when a nipple-areolar resection and wide local excision
of the underlying cancer can be performed with an acceptable cosmetic result and
negative margins. (See",
" <a class=\"local\" href=\"#H15\">",
" 'Treatment'",
" </a>",
" above.)",
" </li>",
" <li>",
" We suggest not performing excision alone without RT or RT alone after a
diagnostic biopsy (",
" <a class=\"grade\" href=\"._grade_6?title=Grade 2C\">",
" Grade 2C",
" </a>",
" ). (See",
" <a class=\"local\" href=\"#H19\">",
" 'Alternative approaches'",
" </a>",
" above.)",
" </li>",
" <li>",
" Recommendations regarding the use of",
" <a class=\"drug drug_general\" href=\"UTD.htm?32/27/33208?
source=see_link\">",
" tamoxifen",
" </a>",
" as well as other forms of adjuvant systemic therapy in patients with PDB
should be based upon the characteristics of the underlying carcinoma. There are no
data to support the use of tamoxifen in women with PDB without an associated ductal
cancer or DCIS. (See",
" <a class=\"local\" href=\"#H20\">",
" 'Use of tamoxifen'",
" </a>",
" above.)",
" </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",
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" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/14/abstract/51\">",
" Bulens P, Vanuytsel L, Rijnders A, van der Schueren E. Breast conserving
treatment of Paget's disease. Radiother Oncol 1990; 17:305.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/14/abstract/52\">",
" Stockdale AD, Brierley JD, White WF, et al. Radiotherapy for Paget's disease
of the nipple: a conservative alternative. Lancet 1989; 2:664.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/14/abstract/53\">",
" Rissanen PM, Holsti P. Paget's disease of the breast: the influence of the
presence or absence of an underlying palpable tumor on the prognosis and on the
choice of treatment. Oncology 1969; 23:209.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/14/abstract/54\">",
" Solin LJ, Kurtz J, Fourquet A, et al. Fifteen-year results of breast-
conserving surgery and definitive breast irradiation for the treatment of ductal
carcinoma in situ of the breast. J Clin Oncol 1996; 14:754.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/14/abstract/55\">",
" Eusebio, RB, Deckers, PJ. Paget's disease of the nipple-areola complex: A
plea for conservatism. Contemp Surg 1992; 40:13.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/14/abstract/56\">",
" Laronga C, Hasson D, Hoover S, et al. Paget's disease in the era of sentinel
lymph node biopsy. Am J Surg 2006; 192:481.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/14/abstract/57\">",
" Lagios MD, Westdahl PR, Rose MR, Concannon S. Paget's disease of the nipple.
Alternative management in cases without or with minimal extent of underlying breast
carcinoma. Cancer 1984; 54:545.",
" </a>",
" </li>",
" <li>",
" <a class=\"nounderline abstract\" href=\"UTD.htm?0/0/14/abstract/58\">",
" Polg&aacute;r C, Orosz Z, Kov&aacute;cs T, Fodor J. Breast-conserving
therapy for Paget disease of the nipple: a prospective European Organization for
Research and Treatment of Cancer study of 61 patients. Cancer 2002; 94:1904.",
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negative breast cancer",
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" <a class=\"medical medical_review\" href=\"UTD.htm?19/40/20106?
source=related_link\">",
" Adjuvant endocrine therapy for hormone receptor-positive breast cancer",
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" </a>",
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>",
" </div>",
" <div class=\"lgnd\">",
" Tubal intraepithelial carcinoma.",
" <br/>",
" (A, B) Hematoxylin and eosin stained section depicting disorganized epithelial
growth in a tubal plica.",
" <br/>",
" (C) Intense nuclear staining for p53, characteristic of an inactivating
mutation.",
" <br/>",
" (D) Staining for KI67, a cell cycle marker, discloses increased proliferative
activity.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" <p>",
" &nbsp;",
" </p>",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
var script_f0_0_15=[""].join("\n");
var outline_f0_0_15=null;
var title_f0_0_2="Clinical dementia rating";
var content_f0_0_2=[" <div id=\"graphicsToolbar\">",
" <div id=\"graphicsCopy\">",
" &copy;2013 UpToDate",
" <sup>",
" &reg;",
" </sup>",
" </div>",
" <div id=\"graphicsLinks\">",
" <a href=\"?imageKey=NEURO
%2F53706&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\">",
" <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
title=\"Print this page\"/>",
" </a>",
" <a class=\"icontxt textLink\" href=\"?imageKey=NEURO
%2F53706&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" 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\">",
" <div class=\"ttl\">",
" Clinical dementia rating (CDR): 0, 0.5, 1, 2, 3",
" </div>",
" <div class=\"cntnt\">",
" <table cellspacing=\"0\">",
" <tr>",
" <td class=\"subtitle1\">",
" Impairment",
" </td>",
" <td class=\"subtitle1\">",
" None (0)",
" </td>",
" <td class=\"subtitle1\">",
" Questionable (0.5)",
" </td>",
" <td class=\"subtitle1\">",
" Mild (1)",
" </td>",
" <td class=\"subtitle1\">",
" Moderate (2)",
" </td>",
" <td class=\"subtitle1\">",
" Severe (3)",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Memory",
" </td>",
" <td>",
" No memory loss or slight inconstant forgetfulness",
" </td>",
" <td>",
" Consistent slight forgetfulness; partial recollection of events",
" </td>",
" <td>",
" Moderate memory loss; more marked for recent events; defect interferes with
everyday activities",
" </td>",
" <td>",
" Severe memory loss; only highly learned material retained; new material
rapidly lost",
" </td>",
" <td>",
" Severe memory loss; only fragments remain",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Orientation",
" </td>",
" <td>",
" Fully oriented",
" </td>",
" <td>",
" Fully oriented or slight difficulty with time relationships",
" </td>",
" <td>",
" Moderate difficulty with time relationships; oriented for place at
examination; may have geographic disorientation elsewhere",
" </td>",
" <td>",
" Severe difficulty with time relationships; usually disoriented in time,
often to place",
" </td>",
" <td>",
" Oriented to person only",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Judgment and problem",
" </td>",
" <td>",
" Solves everyday problems and handles business and financial affairs well;
judgment good in relation to past performance",
" </td>",
" <td>",
" Slight impairment to solving problems, similarities, differences",
" </td>",
" <td>",
" Moderate difficulty in handling problems, similarities, differences; social
judgment usually maintained",
" </td>",
" <td>",
" Severely impaired in handling problems, similarities, differences; social
judgment usually impaired",
" </td>",
" <td>",
" Unable to make judgments or solve problems",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Community affairs",
" </td>",
" <td>",
" Independent function at usual level in job, shopping, volunteer and social
groups",
" </td>",
" <td>",
" Slight impairment in these activities",
" </td>",
" <td>",
" Unable to function independently at these activities though may still be
engaged in some; appears normal to casual inspection",
" </td>",
" <td>",
" No pretense of independent function outside of home; appears well enough to
be taken to functions outside of family home",
" </td>",
" <td>",
" No pretense of independent function outside of home; appears too ill to be
taken to functions outside a family home",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Home and hobbies",
" </td>",
" <td>",
" Life at home, hobbies, intellectual interests well maintained",
" </td>",
" <td>",
" Life at home, hobbies, intellectual interests slightly impaired",
" </td>",
" <td>",
" Mild but definite impairment of function at home; more difficult chores
abandoned; more complicated hobbies and interests abandoned",
" </td>",
" <td>",
" Only simple chores preserved; very restricted interests, poorly
maintained",
" </td>",
" <td>",
" No significant function in home",
" </td>",
" </tr>",
" <tr>",
" <td>",
" Personal care",
" </td>",
" <td>",
" Fully capable of self care",
" </td>",
" <td>",
" Fully capable of self care",
" </td>",
" <td>",
" Needs prompting",
" </td>",
" <td>",
" Requires assistance in dressing, hygiene keeping of personal effects",
" </td>",
" <td>",
" Requires much help with personal care; frequent incontinence",
" </td>",
" </tr>",
" </table>",
" </div>",
" <div class=\"lgnd\">",
" <div class=\"footnotes\">",
" Score only as decline from previous usual level due to cognitive loss, not
impaired due to other factors.",
" </div>",
" <div class=\"reference\">",
" Reproduced with permission from: Morris JC. The clinical dementia rating
(CDR): Current version and scoring rules. Neurology 1993; 43:2412. Copyright &copy;
1993 Lippincott Williams &amp; Wilkins.",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
var script_f0_0_2=[""].join("\n");
var outline_f0_0_2=null;
var title_f0_0_3="Pretreatment eval AML";
var content_f0_0_3=[" <div id=\"graphicsToolbar\">",
" <div id=\"graphicsCopy\">",
" &copy;2013 UpToDate",
" <sup>",
" &reg;",
" </sup>",
" </div>",
" <div id=\"graphicsLinks\">",
" <a href=\"?imageKey=HEME
%2F56955&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=5\" onclick=\"\">",
" <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
title=\"Print this page\"/>",
" </a>",
" <a class=\"icontxt textLink\" href=\"?imageKey=HEME
%2F56955&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=5\" 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\">",
" <div class=\"ttl\">",
" Test/procedures in the initial work-up of a patient with acute myeloid
leukemia (AML)",
" </div>",
" <div class=\"cntnt\">",
" <table cellspacing=\"0\">",
" <colgroup width=\"70%\">",
" </colgroup>",
" <tbody>",
" <tr>",
" <td class=\"subtitle1\">",
" Test/procedure",
" </td>",
" <td class=\"subtitle1\">",
" General practice",
" </td>",
" <td class=\"subtitle1\">",
" Clinical trial",
" </td>",
" </tr>",
" <tr>",
" <td class=\"subtitle2_left\" colspan=\"3\">",
" Tests to establish the diagnosis",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Complete blood counts and differential count",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Bone marrow aspirate",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Bone marrow trephine biopsy",
" </td>",
" <td>",
" Optional*",
" </td>",
" <td>",
" Optional*",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Immunophenotyping",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Cytogenetics",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" RUNX1-RUNX1T1, CBFB-MYH11, PML-RARA, or other gene fusion screening",
" </td>",
" <td>",
" Optional",
" <sup>",
" &bull;",
" </sup>",
" </td>",
" <td>",
" Optional",
" <sup>",
" &bull;",
" </sup>",
" </td>",
" </tr>",
" <tr>",
" <td class=\"subtitle2_left\" colspan=\"3\">",
" Additional tests/procedures at diagnosis",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Demographics and medical history",
" <sup>",
" &Delta;",
" </sup>",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Performance status (ECOG/WHO score)",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Analysis of comorbidities",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Biochemistry, coagulation tests, urine analysis",
" <sup>",
" &loz;",
" </sup>",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Serum pregnancy test",
" <sup>",
" &sect;",
" </sup>",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Information on oocyte and sperm cryopreservation",
" </td>",
" <td>",
" Optional",
" <sup>",
" &yen;",
" </sup>",
" </td>",
" <td>",
" Optional",
" <sup>",
" &yen;",
" </sup>",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Eligibility assessment for allogeneic HSCT",
" </td>",
" <td>",
" Yes",
" <sup>",
" ������",
" </sup>",
" </td>",
" <td>",
" Yes",
" <sup>",
" ������",
" </sup>",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Hepatitis A, B, C; HIV-1 testing",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Chest x-ray, 12-lead ECG; echocardiography (on indication)",
" </td>",
" <td>",
" Yes",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Lumbar puncture",
" <sup>",
" ������",
" </sup>",
" </td>",
" <td>",
" No",
" </td>",
" <td>",
" No",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Biobanking**",
" </td>",
" <td>",
" Optional",
" <sup>",
" &bull;&bull;",
" </sup>",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"subtitle2_left\" colspan=\"3\">",
" Prognostic/predictive marker assessment",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" NPM1, CEBPA, FLT3 gene mutation",
" </td>",
" <td>",
" Optional",
" <sup>",
" &Delta;&Delta;",
" </sup>",
" </td>",
" <td>",
" Yes",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" WT1, RUNX1, MLL, KIT, RAS, TP53, TET2, IDH1 gene mutation",
" </td>",
" <td>",
" No",
" </td>",
" <td>",
" Investigational",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" ERG, MN1, EVI1, BAALC gene expression",
" </td>",
" <td>",
" No",
" </td>",
" <td>",
" Investigational",
" </td>",
" </tr>",
" <tr>",
" <td class=\"indent1\">",
" Detection of minimal residual disease",
" </td>",
" <td>",
" No",
" </td>",
" <td>",
" Investigational",
" </td>",
" </tr>",
" </tbody>",
" </table>",
" </div>",
" <div class=\"lgnd\">",
" <div class=\"footnotes\">",
" * Mandatory in patients with a dry tap",
" <em>",
" (punctio sicca)",
" </em>",
" and strongly recommended for all others.",
" <br/>",
" <span class=\"bullet\">",
" &bull;",
" </span>",
" Should be performed if chromosome morphology is of poor quality, or if there
is typical morphology but the suspected cytogenetic abnormality is not present.",
" <br/>",
" &Delta; Including race or ethnicity, family history, prior exposure to toxic
agents, prior malignancy, therapy for prior malignancy, information on smoking.",
" <br/>",
" <span class=\"lozenge\">",
" &loz;",
" </span>",
" <em>",
" Biochemistry",
" </em>",
" : glucose, sodium, potassium, calcium, creatinine, aspartate amino
transferase (AST), alanine amino transferase (ALT), alkaline phosphatase, lactate
dehydrogenase, bilirubin, urea, total protein, uric acid, total cholesterol, total
triglycerides, creatinine phosphokinase (CPK).",
" <em>",
" Coagulation tests",
" </em>",
" : prothrombin time (PTT), international normalized ratio (INR) where
indicated, activated partial thromboplastin time (aPTT).",
" <em>",
" Urine analysis",
" </em>",
" : pH, glucose, erythrocytes, leukocytes, protein, nitrite.",
" <br/>",
" &sect; In women with childbearing potential.",
" <br/>",
" &yen; Cryopreservation to be done in accordance with the wish of the
patient.",
" <br/>",
" &Dagger; HLA typing and CMV testing should be performed in those patients
eligible for allogeneic stem cell transplantation.",
" <br/>",
" &dagger; Required in patients with clinical symptoms suspicious of central
nervous system involvement; patient should be evaluated by imaging study for
intracranial bleeding, leptomeningeal disease, and mass lesion; lumbar puncture
considered optional in other settings (eg, high WBC).",
" <br/>",
" ** Pretreatment leukemic bone marrow and blood sample.",
" <br/>",
" <span class=\"double_bullet\">",
" &bull;&bull;",
" </span>",
" Biobanking should also be performed in general practice if at all possible.",
" <br/>",
" &Delta;&Delta; Strongly encouraged for all patients.",
" </div>",
" <div class=\"reference\">",
" Modified from research originally published in Blood. Dohner H, Estey EH,
Amadori S, et al. Diagnosis and management of acute myeloid leukemia in adults:
recommendations from an international expert panel on behalf of the European
LeukemiaNet. Blood 2009. Copyright &copy; American Society of Hematology.",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
var script_f0_0_3=[""].join("\n");
var outline_f0_0_3=null;
var title_f0_0_4="Radiograph of gibbus deformity";
var content_f0_0_4=[" <div id=\"graphicsToolbar\">",
" <div id=\"graphicsCopy\">",
" &copy;2013 UpToDate",
" <sup>",
" &reg;",
" </sup>",
" </div>",
" <div id=\"graphicsLinks\">",
" <a href=\"?imageKey=ALLRG
%2F78628&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\">",
" <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
title=\"Print this page\"/>",
" </a>",
" <a class=\"icontxt textLink\" href=\"?imageKey=ALLRG
%2F78628&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" 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: 470px\">",
" <div class=\"ttl\">",
" Lateral spine radiograph of acutely angled kyphosis (gibbus deformity) in a
patient with type 3 Gaucher disease",
" </div>",
" <div class=\"cntnt\" style=\"width: 325px; height: 432px; background-image:
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" </div>",
" <div class=\"lgnd\">",
" Sagittal T1-weighted section through the lung mass shows extension through the
apical fat pad into the base of the neck (white arrow). The mass partially
surrounds a patent left subclavian artery (black arrow) and obliterates the tissue
plane containing the brachial plexus. The left brachiocephalic vein is occluded and
cannot be seen. A corresponding section from the right side of the neck (next
figure) is included for comparison.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Courtesy of Paul Stark, MD.",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
var script_f0_0_5=[""].join("\n");
var outline_f0_0_5=null;
var title_f0_0_6="Chest x-ray intraperitoneal free air";
var content_f0_0_6=[" <div id=\"graphicsToolbar\">",
" <div id=\"graphicsCopy\">",
" &copy;2013 UpToDate",
" <sup>",
" &reg;",
" </sup>",
" </div>",
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" <a href=\"?imageKey=RADIOL
%2F83050&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\">",
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title=\"Print this page\"/>",
" </a>",
" <a class=\"icontxt textLink\" href=\"?imageKey=RADIOL
%2F83050&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" 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: 470px\">",
" <div class=\"ttl\">",
" Chest radiograph of intraperitoneal free air",
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" </div>",
" <div class=\"lgnd\">",
" This plain AP x-ray of the chest&nbsp;taken with the
patient&nbsp;upright&nbsp;reveals a small amount of free air under the right
hemidiaphragm confirming the diagnosis of a perforated abdominal viscus. The
lucent, crescent shaped free air is noted between the arrows. The dome of the liver
(black arrow) and the soft tissue shadow of the right hemidiaphragm (white arrow)
border the free air.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" </div>",
" </div>",
" </div>",
" </div>",
"</div>"].join("\n");
var script_f0_0_6=[""].join("\n");
var outline_f0_0_6=null;
var title_f0_0_7="Gangrene due to RV";
var content_f0_0_7=[" <div id=\"graphicsToolbar\">",
" <div id=\"graphicsCopy\">",
" &copy;2013 UpToDate",
" <sup>",
" &reg;",
" </sup>",
" </div>",
" <div id=\"graphicsLinks\">",
" <a href=\"?imageKey=RHEUM
%2F74320&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\">",
" <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
title=\"Print this page\"/>",
" </a>",
" <a class=\"icontxt textLink\" href=\"?imageKey=RHEUM
%2F74320&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" 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: 524px\">",
" <div class=\"ttl\">",
" Gangrene of the foot and toes resulting from rheumatoid vasculitis",
" </div>",
" <div class=\"cntnt\" style=\"width: 504px; height: 334px; background-image:
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" </div>",
" <div class=\"lgnd\">",
" Gangrene due to rheumatoid vasculitis.",
" <div class=\"footnotes\">",
" </div>",
" <div class=\"reference\">",
" Courtesy of John Stone, MD, MPH.",
" </div>",
" </div>",
" </div>",
" </div>",
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" </div>",
" <div class=\"lgnd\">",
" <span style=\"color: #ff0000;\">",
" Red:",
" </span>",
" life-threatening conditions.",
" <div class=\"footnotes\">",
" * More likely in older children and adolescents.",
" <br>",
" <span class=\"bullet\">",
" &bull;",
" </span>",
" More likely in infants and young children.",
" </br>",
" </div>",
" <div class=\"reference\">",
" </div>",
" </div>",
" </div>",
" </div>",
" <div class=\"graphic\">",
" <div class=\"figure\" style=\"width: 628px\">",
" <div class=\"ttl\">",
" Diarrhea: Acute in a child",
" </div>",
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" </div>",
" <div class=\"lgnd\">",
" <span style=\"color: #ff0000;\">",
" Red:",
" </span>",
" life-threatening cause.",
" <br/>",
" <span style=\"color: #008000;\">",
" Green:",
" </span>",
" common cause.",
" <div class=\"footnotes\">",
" * More likely in infants and young children.",
" <br>",
" <span class=\"bullet\">",
" &bull;",
" </span>",
" More likely in older children and adolescents.",
" <br>",
" &Delta; Only in infants.",
" </br>",
" </br>",
" </div>",
" <div class=\"reference\">",
" </div>",
" </div>",
" </div>",
" </div>",
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var title_f0_0_9="Tracheobronchopathia osteochondroplastica 2";
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" &copy;2013 UpToDate",
" <sup>",
" &reg;",
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" <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
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" </div>",
" <div class=\"graphic\">",
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