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Laboratory findings include mildly abnormal liver tests (AST, alkaline phosphatase), an elevated plasma iron with greater than 50% transferrin saturation in men and 45% in women (after an overnight fast), and an elevated serum ferritin (although a normal iron saturation and a normal ferritin do not exclude the diagnosis) Affected men are more likely than affected women to have an elevated ferritin level
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MRI and CT may show changes consistent with iron overload of the liver, and MRI can quantitate hepatic iron stores; however, these techniques are not sensitive enough for screening Testing for HFE mutations is indicated in any patient with evidence of iron overload and in siblings of patients with confirmed hemochromatosis
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In patients who are homozygous for C282Y, liver biopsy is often indicated to determine whether cirrhosis is present Biopsy can be deferred, however, in patients in whom the serum ferritin level is < 1000 mcg/L, serum AST level is normal, and hepatomegaly is absent; the likelihood of cirrhosis is low in these persons Liver biopsy is also indicated when iron overload is suspected even though the patient is not homozygous for C282Y In patients with hemochromatosis, the liver biopsy characteristically shows extensive iron deposition in hepatocytes and in bile ducts and the hepatic iron index hepatic iron content per gram of liver converted to micromoles and divided by the patient s age is generally greater than 19 Only 5% of patients with hereditary hemochromatosis identified by screening in a primary care setting have cirrhosis
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Genetic testing is recommended for all first-degree family members of the proband; children of an affected person (C282Y homozygote) need to be screened only if the patient s spouse carries the C282Y or H63D mutation Screening all white men over age 30 years or all adults over age 20 years by
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WILSON S DISEASE
ESSENTIALS OF DIAGNOSIS
Excessive deposition of copper in the liver and brain Rare autosomal recessive disorder that usually occurs in persons under age 40 Serum ceruloplasmin, the plasma copper-carrying protein, is low Urinary excretion of copper and hepatic copper concentration are high
is usually most marked at the superior and inferior poles of the cornea It is sometimes seen with the naked eye and is readily detected by slit-lamp examination It may be absent in patients with hepatic manifestations only but is usually present in those with neuropsychiatric disease Renal calculi, the Fanconi defect, renal tubular acidosis, hypoparathyroidism, and hemolytic anemia may occur in patients with Wilson s disease
Diagnosis
The diagnosis can be challenging and is generally based on demonstration of increased urinary copper excretion (> 100 mcg/24 h) or low serum ceruloplasmin levels (< 20 mcg/dL), and elevated hepatic copper concentration (> 250 mcg/g of dry liver) However, increased urinary copper and low serum ceruloplasmin levels are neither completely sensitive nor specific for Wilson s disease In equivocal cases (when the serum ceruloplasmin level is normal), the diagnosis may require demonstration of low radiolabeled copper incorporation into ceruloplasmin or urinary copper determination after a penicillamine challenge Liver biopsy may show acute or chronic hepatitis or cirrhosis MRI of the brain may show increased basal ganglia copper even early in the course of the disease
General Considerations
Wilson s disease (hepatolenticular degeneration) is a rare autosomal recessive disorder that usually occurs in persons under age 40 The worldwide prevalence is about 30 per million population The condition is characterized by excessive deposition of copper in the liver and brain The genetic defect, localized to chromosome 13, has been shown to affect a copper-transporting adenosine triphosphatase (ATP7B) in the liver and leads to copper accumulation in the liver and oxidative damage of hepatic mitochondria Most patients are compound heterozygotes (ie, carry two different mutations) Over 200 different mutations in the Wilson disease gene have been identified, making genetic diagnosis impractical except within families in which the mutation has been identified in the index case The H1069Q mutation accounts for 40% of disease alleles in populations of Northern European descent The major physiologic aberration in Wilson s disease is excessive absorption of copper from the small intestine and decreased excretion of copper by the liver, resulting in increased tissue deposition, especially in the liver, brain, cornea, and kidney
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