When the bilirubin concentration in the blood is abnormally elevated, all the body tissues, including the sclerae and the skin, become yellow-tinged or greenish-yellow, a condition called jaundice. Jaundice becomes clinically evident when the serum bilirubin level exceeds 2.5 mg/dL (43 fmol/L). Increased serum bilirubin lev-els and jaundice may result from impairment of hepatic uptake, conjugation of bilirubin, or excretion of bilirubin into the biliary system. There are several types of jaundice: hemolytic, hepato-cellular, obstructive, or jaundice due to hereditary hyperbiliru-binemia. Hepatocellular and obstructive jaundice are the two types commonly associated with liver disease.
Hemolytic jaundice is the result of an increased destruction of the red blood cells, the effect of which is to flood the plasma with bilirubin so rapidly that the liver, although functioning normally, cannot excrete the bilirubin as quickly as it is formed. This type of jaundice is encountered in patients with hemolytic transfusion reactions and other hemolytic disorders. The bilirubin in the blood of these patients is predominantly of the unconjugated, or free, type. Fecal and urine urobilinogen levels are increased, but the urine is free of bilirubin. Patients with this type of jaundice, un-less their hyperbilirubinemia is extreme, do not experience symp-toms or complications as a result of the jaundice per se. Prolonged jaundice, however, even if mild, predisposes to the formation of pigment stones in the gallbladder, and extremely severe jaundice (levels of free bilirubin exceeding 20 to 25 mg/dL) poses a risk for brain stem damage.
Hepatocellular jaundice is caused by the inability of damaged liver cells to clear normal amounts of bilirubin from the blood. The cellular damage may be from infection, such as in viral hep-atitis (eg, hepatitis A, B, C, D, or E) or other viruses that affect the liver (eg, yellow fever virus, Epstein-Barr virus), from med-ication or chemical toxicity (eg, carbon tetrachloride, chloroform, phosphorus, arsenicals, certain medications), or from alcohol. Cirrhosis of the liver is a form of hepatocellular disease that may produce jaundice. It is usually associated with excessive alcohol intake, but it may also be a late result of liver cell necrosis caused by viral infection. In prolonged obstructive jaundice, cell damage eventually develops, so that both types appear together.
Patients with hepatocellular jaundice may be mildly or se-verely ill, with lack of appetite, nausea, malaise, fatigue, weakness, and possible weight loss. In some cases of hepatocellular disease, jaundice may not be obvious. The serum bilirubin concentration and urine urobilinogen level may be elevated. In addition, AST and ALT levels may be increased, indicating cellular necrosis. The patient may report headache, chills, and fever if the cause is in-fectious. Depending on the cause and extent of the liver cell damage, hepatocellular jaundice may or may not be completely reversible.
Obstructive jaundice of the extrahepatic type may be caused by occlusion of the bile duct by a gallstone, an inflammatory process, a tumor, or pressure from an enlarged organ. The obstruction may also involve the small bile ducts within the liver (ie, intrahepatic obstruction), caused, for example, by pressure on these channels from inflammatory swelling of the liver or by an inflammatory exudate within the ducts themselves. Intrahepatic obstruction re-sulting from stasis and inspissation (thickening) of bile within the canaliculi may occur after the ingestion of certain medications,which are referred to as cholestatic agents. These include phe-nothiazines, antithyroid medications, sulfonylureas, tricyclic antidepressant agents, nitrofurantoin, androgens, and estrogens.
Whether the obstruction is intrahepatic or extrahepatic, and whatever its cause may be, bile cannot flow normally into the intes-tine but is backed up into the liver substance. It is then reabsorbed into the blood and carried throughout the entire body, staining the skin, mucous membranes, and sclerae. It is excreted in the urine, which becomes deep orange and foamy. Because of the decreased amount of bile in the intestinal tract, the stools become light or clay-colored. The skin may itch intensely, requiring repeated soothing baths. Dyspepsia and intolerance to fatty foods may de-velop because of impaired fat digestion in the absence of intestinal bile. AST, ALT, and GGT levels generally rise only moderately, but bilirubin and alkaline phosphatase levels are elevated.
Increased serum bilirubin levels (hyperbilirubinemia) resulting from several inherited disorders can also produce jaundice. Gilbert’s syn-drome is a familial disorder characterized by an increased level of un-conjugated bilirubin that causes jaundice. Although serum bilirubin levels are increased, liver histology and liver function test results are normal, and there is no hemolysis. This syndrome affects 2% to 5% of the population.
Other conditions that are probably caused by inborn errors of biliary metabolism include Dubin–Johnson syndrome (chronic idiopathic jaundice, with pigment in the liver) and Rotor’s syn-drome (chronic familial conjugated hyperbilirubinemia without pigment in the liver); “benign” cholestatic jaundice of pregnancy, with retention of conjugated bilirubin, probably secondary to un-usual sensitivity to the hormones of pregnancy; and probably also benign recurrent intrahepatic cholestasis.
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