HEPATIC PANEL

Overview
 AST (SGOT)
 ALT (SGPT)
 Alkaline Phosphatase
 LDH
 Bilirubin
 GGT
AST/ALT
 Normal levels do not = normal liver
 Both found in many organs
o Largest amounts in liver, kidney, heart
 Rise in the presence of hepatocellular injury
 Evaluation of levels based on degree of elevation
o Mild
o marked
 Important to look at ratio of AST to ALT
 Mild elevations
o AST:ALT Ratio > 1
 Alcoholic liver disease (levels usually <400)
 Cirrhosis
 Statins
 Tylenol
o ALT:AST Ratio > 1
 Liver disease (viral hepatitis)
 Glitazones (Avandia, Actos)
 Toxins
 Marked elevations >1000units/L
o Acute viral hepatitis
o Drugs/toxins
o Ischemic hepatitis
o Autoimmune hepatitis
o Acute biliary obstruction
Alkaline Phosphatase
 Found in many organs but most often elevations associated with Liver and Bone disease
 Factors that can cause elevations
o BMI
o Eating (should check fasting)
o Pregnancy
o Race (African Americans)
o Smoking
 Decreased levels
o OCs
 Causes of elevation
o Cholestasis
 o Liver disease
o Infiltrative
 Tumors
 Parenchymal
o Bone disorders
 Fractures
 Bone growth
 Paget’s
 Tumors
Bilirubin
 Produced via breakdown of old RBCs & other hemoproteins
 Most bilirubin becomes conjugated
o Most excreted in feces (becomes urobilinogen), some resorbed
o Reabsorbed either gets excreted in urine or into bile
 Increased levels of unconjugated bilirubin not always associated with liver/biliary disease
 Conjugated 4% of total
o Direct-
 Hepatocellular disease
 Hepatitis
o Viral, ETOH, Auto-immune
 Gilbert’s Syndrome
o 4-13% of US population
 Unconjugated
o Indirect – insoluble – travels through blood to liver to be metabolized into
soluble conjugated bilirubin (direct)
 Usually hemolysis
 NB jaundice
 Large hematomas
 Chronic hepatitis
 Over production of RBCs
 Causes of abnormal bilirubin levels
o Problem between production and clearance
o Elevation of levels due to one or combination of the following:
 Overproduction of bilirubin
 Impaired uptake, conjugation, or excretion of bilirubin
 Backwards leakage from damaged hepatocytes or bile ducts
HEPATITIS OVERVIEW
CATEGORIES
Viral
 Hep A
 Hep B
 Hep C
 Hep D
 Hep E
Toxins/Substances
 ETOH
 Medications
 Chemical toxins
Metabolic
 Fatty Liver Disease (FLD)
 NASH
Autoimmune
 Reactionary – Mononucleosis associated hepatitis
 Autoimmune destruction
HEPATITIS OVERVIEW
HEPATITIS A

DEFINITION
 Liver inflammation due to hepatitis A
EPIDEMIOLOGY
 NA
ETIOLOGY
Transmission Routes
 Ingestion of fecal matter, even in microscopic amounts
Persons at Risk
 Close person-to-person contact
 Sexual contact with infected person
 MSM
 Illicit drug use-non injection and injection
 Persons with clotting disorders (transfusions)
 Ingestion of contaminated food or drinks
 Travel to high risk countries
o Endemic areas (asia, Africa)
PATHOPHYSIOLOGY
Incubation Period
 15 to 50 days (average 28 days)
Duration
 Mild to severe illness lasting 1-2 weeks
 Can last up to 9 months – disabling
o >50, liver disease
CLINICAL FEATURES
Acute Symptoms
 Loss of appetite
 Nausea
 Vomit
 Abdominal pain
 Gray-colored bowel movement
 Joint pain
 jaundice
Chronic Symptoms
 NA
DIAGNOSTIC TESTS
 Anti-HAV
o IgM during acute phase
 Present 2 weeks prior to and up to 6 months after onset of symptoms
o IgG during convalescence and for life (life long)
 LFT
o Markedly elevated
 o ALT>AST
 Immunity
o Positive total anti-HAV
o Negative IgM anti-HAV
DIAGNOSIS
 NA
DIFFERENTIAL DIAGNOSES
 NA
PLAN
Prevention
Vaccination: Immunization or immune globulin (IG)
 Immunization
o All children 12-23 months old
o All persons identified as at risk
 Travelers to high risk areas
 MSM
 Persons with clotting disorders
 Persons who work with HAV-infected primates
 Persons with chronic liver disease, including HBV and HCV-infected
people with chronic liver disease
o 2 dose series – separated by 6-18 months
o 95% of persons receiving 1st dose demonstrate immunity by 1 month
o No need to start series again if longer than 18 months

 Immune Globulin
o If traveling to endemic areas within <2 weeks of 1st dose
 < 12 months or > 40 years old
 Immunocompromised
 Allergic to component of HAV IZ
o Protection lasts about 3 months
 Note:
 o Preexposure: If person over 40 with other comorbidities you want vaccine plus
immunoglobulin for prevention. If under 40 just given vaccine.
o Post exposure prophylaxis given within two weeks of exposure
o If given within two weeks of travel, they get vaccination and immune globulin
Other
 Food and water regulations and maintaining standards
 Most recover and immune for life. %5 progress to fulminant hepatitis
Acute Treatment
 Supportive
 Monitor LFTs for persistent inflammation
 For those at risk for poor outcomes
o Monitor liver function periodically and consider impact of medications and
treatments in future
 Consider providing protection from Hep B infection if not immune with Hep B IZ
Chronic Treatment
 NA
WHEN TO ADMIT TO HOSPITAL
 NA
COMPLICATIONS
 NA
PROGNOSIS
 NA
HEPATITIS B

DEFINITION
 Liver inflammation due to Hepatitis B
EPIDEMIOLOGY
 NA
ETIOLOGY
Transmission Routes
 Contact with infectious blood, semen, and other body fluids, primarily through
o Sex with infected partner
o Injection drug use – sharing needles, syringes, drug paraphernalia
o Sharing razors, toothbrushes with infected person
o Vertical transmission from mom to fetus
o Contact with blood or open sores of infected person
o Needle sticks, sharp instruments
Persons at Risk
 Infants of infected mothers
 Sex partners of infected persons
 Persons in non-monogamous relationships
 MSM
 Injection drug users
 Household contacts of persons with chronic HepB
 Healthcare and public safety workers – exposed to blood or body fluids
 Hemodialysis patients
 Residents and staff at facilities for developmentally disabled
 Travelers to high and intermediate prevalent countries (Sub-Saharan Africa, Western S
America, Asia)
PATHOPHYSIOLOGY
Incubation Period
 45 to 160 days (average 120 days)
Duration
 Risk of chronicity
o 90% of infants, 20-25% kids 1-5
o 5% of adults
CLINICAL FEATURES
Acute Symptoms
 Loss of appetite
 Nausea
 Vomit
 Abdominal pain
 Gray-colored bowel movement
 Joint pain
 jaundice
Chronic Symptoms
 May be asymptomatic
  May be found in screening labs
o Mild elevation in LFTs
o If AST > ALT consider cirrhosis
 25%of kids and 15% of adults who became chronically infected will die prematurely due
to cirrhosis or liver cancer
 Majority remain asymptomatic until onset of cirrhosis or end stage liver disease
DIAGNOSTIC TESTS
Labs

Lab Interpretation
DIAGNOSIS
 NA
DIFFERENTIAL DIAGNOSES
 NA
PLAN
Prevention
Vaccination:
 Immunization
o 3 dose series
 0, 1-2, 6 months
o All children birth through adolescence
o All individuals identified at risk
o All persons with age < 60 with DM as soon as diagnosed
 > 60 consider risk of HBV infection
o Do not need to restart series if exceed suggested intervals
 Immune Globulin HBIG
o Infants born to moms +HBsAG within 12hours of birth
o If Mom’s status unknown
 infant < 2000gm – give HBV IZ and HBIG
 Infant >2000gm – give HBV IZ and check mom’s status ASAP – give
HBIG if mom’s +HBsAG
 Note:
o Post exposure prophylaxis 1 vaccine within 24 hours if not previously vaccinated
 o If they have documented vaccination of first/second dose, you can just give
second/third dose without repeating series
o If patient does not respond to vaccine (develop antibodies after series/booster),
they are either a nonresponder or have Chronic Hepatitis B
Other
 NA
Acute Treatment
 No medication available
 Best addressed through supportive care
Chronic Treatment
 Regular monitoring for signs of liver disease progression.
 Some patients are treated with antiviral therapy.
 Determine if immune active or immune tolerant CHB infection
 Treatment of CHB based on this determination
WHEN TO ADMIT TO HOSPITAL
 NA
COMPLICATIONS
 NA
PROGNOSIS
 NA
HEPATITIS C

DEFINITION
 Liver inflammation due to hepatitis C
EPIDEMIOLOGY
 NA
ETIOLOGY
Transmission Routes
 Blood and body fluids
o Percutaneous
 Injection drug use
o Most common cause in US
 Receipt of blood products, transplanted organs – rare since changes in US screening of
products in 1992
 Needle sticks
 Infant born to HCV infected mother
 Less frequently
o Sex with infected person
o Sharing personal items (razors, toothbrushes)
o Health care procedures involving invasive procedures - injections
o Standard precautions significantly reduces risk
Persons at Risk
 Current or former injection drug users
 Even if only tried once
 Transfusions and organ transplants < July 1992
 Receiving clotting factor concentrates < 1987
 Hemodialysis patients
 Known HCV exposures
 Needle sticks
 HIV positive
 Children born to HCV=positive mothers
 Population risk – those born between 1945-1965 are at higher risk so should be
screened
PATHOPHYSIOLOGY
Incubation Period
 14 to 180 days (average 45 days)
Duration
 NA
CLINICAL FEATURES
Acute Symptoms
 Loss of appetite
 Nausea
 Vomit
 Abdominal pain
 Gray-colored bowel movement
  Joint pain
 jaundice
Chronic Symptoms
 Often diagnosed in screening
 Often LFTs are normal
 75-85% of HCV becomes chronic
o Factors and reasons for clearing disease is unclear and difficult to predict
 If cirrhosis present – AST may > ALT
DIAGNOSTIC TESTS
DIAGNOSIS
 NA
DIFFERENTIAL DIAGNOSES
 NA
PLAN
Prevention
Vaccination: Immunization or immune globulin (IG)
 None available
Screening
 Persons born between 1945-1965
 Person with ANY history of injection drug use
 Recipients of clotting factors < 1987, transfusion, solid organ transplant < July 1992
 Hemodialysis patients
 Known exposure to HCV
 ALL persons with HIV
 All persons with signs/symptoms of liver disease – elevated LFTs
 Children born to mothers who are HCV positive
o Not before 18 months – may detect maternal antibody before 18 months
Other
 NA
Acute Treatment
 Similar to chronic HCV
Chronic Treatment
 Early referral to GI, ID, or HCV specialist for genotype testing and initiation of
appropriate treatment
 Treatment dependent on viral genotype, presence of cirrhosis and other factors
WHEN TO ADMIT TO HOSPITAL
 NA
COMPLICATIONS
 Of those diagnosed with HCV
 75-85% will develop chronic infection
 60-70% will develop chronic liver disease
 5-20% will develop cirrhosis over 20-30 years
 1-5% will die from the consequences of chronic HCV infection
PROGNOSIS
 NA
HEPATITIS D
 Transmission: mucosal or percutaneous contact with infeced blood
 Risks: Hepatitis B, because it only occurs with Hepatitis B
 Vaccine: No, but immunize for Hepatitis B
 Chronic State: Yes
FATTY LIVER DISEASE
 Fatty deposits in liver cells
o Causes
 Impaired ability of liver to remove fatty acids
 Increased production of fatty acids for the liver to remove & store
 Hyperinsulinemia
 Alcoholism
 Increased iron stores (hemochromatosis)
 Fatty Liver Syndrome
o Fat deposits in > 30% of liver cells
o Obesity
o High insulin levels
 NASH – non-alcoholic steatohepatitis
o Fat deposits in > 50% of liver cells
o Acute & chronic inflammation
o Increased fibrosis
o Associated with hyperinsulinemia & oxidative stress
 Laboratory studies
o Elevated LFT’s – ALT>AST
o Lipids almost always abnormal
 Total – 60% elevated
 HDL – 45% decreased
 LDL – 58% elevated
 Tgs – 50 – 80% elevated
o Abdominal US
 Hepatomegaly with fat deposits
o CT scan
 Good visualization of structures, fat deposits
 Treatment
o Weight loss
o Good, tight control of blood glucose, lipids
o Monitoring for hemochromatosis
o Check LFT’s q2-4 months
o US or CT scan every year to monitor
o Liver failure/cirrhosis usually only in NASH
o Cirrhosis in 25% after 20-30 years
o Liver failure after cirrhosis in 1-5%
HEPATITIS E
 Transmission fecal – oral
o Genotype 1 & 2 – fecal contaminated drinking water
o Genotype 3 & 4 – water and food borne transmission
 Presentation
o Similar to Hep A, B, C
 More often than not asymptomatic
 When symptomatic
o ages 15-44
o pregnant women
o More likely to be severe – fulminant hepatitis and death
 Infectious period not well documented but virus has been noted in stool from 1 week
before onset up to 30 days after onset of jaundice
 Most often self limiting – low morbidity about 1%
o More serious poor outcomes
 pregnant women – morbidity 10-30%
 Those with pre-existing liver disease
 Organ transplant recipients, Immunocompromised
o Genotypes 1, 2, 4 - no progression to chronic state
o Genotype 3 – can progress but exclusively those on immunosuppressive therapy
for organ transplantation
 No current treatment - supportive
 Serum markers
o Testing for antiHEV antibody or HEV RNA
o No test currently approved by FDA for HEV RNA– only those for research
o Clinically diagnosed
 Viral hepatitis symptoms
 Travel to HEV endemic area
 Negative for Hepatitis A, B, C or other hepatotoxic viruses
 IgM HEV and IgG HEV checked when other viruses ruled out
o Prevention
 No immunization in US - one approved in China
 Immune globulin not effective
 Sanitation and use of clean drinking water