Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (198 page)

   Drugs (e.g., estrogens, anabolic steroids)—most common cause (Table
5-13
)

   Normal pregnancy

   Alcoholic hepatitis

   Infections (e.g., acute viral hepatitis, gram-negative sepsis, toxic shock syndrome, AIDS, parasitic, fungal)

   Sickle cell crisis

   Postoperative state following long procedure and multiple transfusions

   Benign recurrent familial intrahepatic cholestasis—rare condition

   Autosomal recessive condition; attacks begin after age 8, last weeks to months, complete resolution between episodes, may recur after months or years; exacerbated by estrogens

TABLE 5–13. Comparison of Various Types of Cholestatic Disease

CBD, common bile duct; N, normal; sl D, slightly decreased.
*Serum value, times normal.

   Laboratory Findings

   
Core laboratory
: Increased serum ALP, but GGT is usually normal. Serum direct bilirubin may be normal or ≤10 mg/dL. Transaminase usually <100 U.

   
Histology
: Liver biopsy shows centrolobular cholestasis without inflammation, bile pigment in hepatocytes and canaliculi; little or no fibrosis.

CIRRHOSIS, PRIMARY BILIARY (CHOLANGIOLITIC CIRRHOSIS, HANOT HYPERTROPHIC CIRRHOSIS, CHRONIC NONSUPPURATIVE DESTRUCTIVE CHOLANGITIS, ETC.)

   Slow progressive multisystem autoimmune disease; chronic nonsuppurative inflammation and asymmetric destruction of small intrahepatic bile ducts producing chronic cholestasis, cirrhosis, and ultimately liver failure