Liver Disorders
Nizar N. Zein
POINTS TO REMEMBER:
Serum-Based Liver Tests
Basic approach to the interpretation of serum-based liver tests: The first pattern distinction is to determine whether the abnormalities are more suggestive of cholestatic or liver cell injury.
Cholestatic liver disease refers to impairment of hepatic excretion into the biliary system. This type of “blockage” of excretion may occur at any level (intrahepatic or extrahepatic). The alkaline phosphatase and γ-glutamyl transpeptidase (GGTP) are elevated to a much greater degree than that of the transaminases. The bilirubin level may or may not be elevated.
When liver disease primarily affects hepatocytes, as in viral hepatitis, alcoholic hepatitis, and many drug-induced problems, a pattern of liver cell injury is seen. The transaminases are elevated predominantly.
Fatty Liver
Fatty liver or steatohepatitis (termed nonalcoholic steatohepatitis) in patients who do not drink alcohol should be suspected in patients with mild-to-moderate transaminase elevations and whose serologic studies for viral hepatitis, iron overload, and autoimmune disorders are negative.
Neither blood tests nor scans are able to distinguish benign fatty liver from steatohepatitis before cirrhotic changes become apparent and therefore a liver biopsy is often necessary.
Weight loss in obese patients with steatohepatitis has shown to be associated with normalization of liver enzymes and improved hepatic histology.
Alcoholic Liver Disease
In the United States, alcohol is the most common cause of liver cirrhosis.
The so-called Maddrey discriminant function (MDF) identifies a group of patients at substantial risk for dying from alcoholic hepatitis.
MDF = 4.6 [pro time – control (in seconds)] + [serum bilirubin (mg/dL)]
When severely ill patients (severe alcoholic hepatitis) with a discriminant function score of ≥32 (with or without encephalopathy) are given 40 mg of prednisone daily for 28 days, survival is nearly twice as likely and should always be considered in the absence of a contraindication for the use of corticosteroids.
Viral Hepatitis A, B, C
Hepatitis A vaccination is recommended for all susceptible persons with chronic liver disease.
Hepatitis B antigen and antibodies: examples of select clinical situations.
Acute hepatitis B: Serologically identified by the presence of hepatitis B surface antigen (HBsAg) and the presence of IgM class anti-hepatitis B core (IgM anti-HBc).
Remote resolved infection: These patients have a serological profile consistent of anti-hepatitis B surface (anti-HBs) and IgG anti-hepatitis B core (anti-HBc) in the serum. In some cases and over time, patients may lose anti-HBs and maintain an isolated anti-HBc as the only serological evidence of old exposure to HBV.
Chronic hepatitis B: The key serological feature is the presence of hepatitis Bs antigen (HBsAg). In cases of chronic inactive infection (previously termed healthy carrier), patients will have normal liver enzymes, low hepatitis B DNA (HBV DNA) titer and minimal histological changes on liver biopsy. In contrast, those with chronic active infection may have elevated liver
enzymes, high HBV DNA and necroinflammation on liver biopsy.
Successful immunization status: The patient has anti-HBs as the only serological finding.
Hepatitis C is much more likely than hepatitis B to become chronic (70% to 85%) with more than three-fourths of patients developing chronic liver disease. Daily alcohol consumption increases the risk of developing symptomatic cirrhosis.
Hepatitis C increasingly is recognized as a risk factor for liver cancer and currently is believed to be the most common cause of hepatocellular carcinoma in the United States.
Several extrahepatic manifestations of hepatitis C may overshadow hepatic involvement.
Cryoglobulinemia with its associated vasculitis and skin rash is perhaps the most established extrahepatic feature of hepatitis C and responds well to viral eradication with therapy.
Renal injury particularly membranoproliferative glomerulonephritis has been well established and may also improve if the hepatitis C is treated successfully using interferon.
Porphyria cutanea tarda (PCT), as a result of reduced activity of the enzyme uroporphyrinogen decarboxylase, may be either inherited as an autosomal dominant trait or acquired. Hepatic dysfunction is nearly always seen in PCT, and anti-HCV antibodies are present in 80% patients with acquired PCT but not in patients with familial PCT.Related posts:
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