JAUNDICE
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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