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Early treatment to remove excess copper is essential before it can produce hepatic or neurologic damage Early in the treatment phase, restriction of dietary copper (shellfish, organ foods, and legumes) may be of value Oral penicillamine (075 2 g/d in divided doses) is the drug of choice and enhances urinary excretion of chelated copper Oral pyridoxine, 50 mg per week, is added, since penicillamine is an antimetabolite of this vitamin If penicillamine treatment cannot be tolerated because of gastrointestinal, hypersensitivity, or autoimmune reactions, consider the use of trientine, 250 500 mg three times a day Oral zinc acetate, 50 mg three times a day, interferes with intestinal absorption of copper, promotes fecal copper excretion, and may be used as maintenance therapy after decoppering with a chelating agent or as first-line therapy in presymptomatic or pregnant patients Ammonium tetrathiomolybdate, which complexes copper in the intestinal tract, has shown promise as initial therapy for neurologic Wilson s disease Treatment should continue indefinitely Supplemental vitamin E, an antioxidant, has been recommended but not rigorously studied Once the serum nonceruloplasmin copper level is within the normal range, the dose of chelating agent can be reduced to the minimum necessary for maintaining that level The prognosis is good in patients who are effectively treated before liver or brain damage has occurred Liver transplantation is indicated for fulminant hepatitis (often after plasma exchange as a stabilizing measure), endstage cirrhosis, and, in selected cases, intractable neurologic disease, although survival is lower when liver transplantation is undertaken for neurologic disease than for liver disease Family members, especially siblings, require screening with serum ceruloplasmin, liver biochemical tests, and
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Wilson s disease tends to present as liver disease in adolescents and neuropsychiatric disease in young adults, but there is great variability The diagnosis should always be considered in any child or young adult with hepatitis, splenomegaly with hypersplenism, Coombs-negative hemolytic anemia, portal hypertension, and neurologic or psychiatric abnormalities Wilson s disease should also be considered in persons under 40 years of age with chronic or fulminant hepatitis Hepatic involvement may range from elevated liver tests (although the alkaline phosphatase may be low) to cirrhosis and portal hypertension The neurologic manifestations are related to basal ganglia dysfunction and include a resting, postural, or kinetic tremor and dystonia of the bulbar musculature with resulting dysarthria and dysphagia Psychiatric features include behavioral and personality changes and emotional lability The pathognomonic sign of the condition is the brownish or gray-green KayserFleischer ring, which represents fine pigmented granular deposits in Descemet s membrane in the cornea The ring
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thrombosis, and the clinical presentation is mild but the course is frequently complicated by hepatocellular carcinoma
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slit-lamp examination or, if the causative mutation is known, with mutation analysis
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Ferenci P Wilson s disease Clin Gastroenterol Hepatol 2005 Aug;3(8):726 33 [PMID: 16233999] Medici V et al Diagnosis and management of Wilson s disease: results of a single center experience J Clin Gastroenterol 2006 Nov Dec;40(10):936 41 [PMID: 17063115] Merle U et al Clinical presentation, diagnosis and long-term outcome of Wilson s disease: a cohort study Gut 2007 Jan; 56(1):115 20 [PMID: 16709660]
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A Symptoms and Signs
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The presentation may be fulminant, acute, subacute, or chronic An insidious (subacute) onset is most common Clinical manifestations generally include tender, painful hepatic enlargement, jaundice, splenomegaly, and ascites With chronic disease, bleeding varices and hepatic coma may be evident; hepatopulmonary syndrome may occur
HEPATIC VEIN OBSTRUCTION (BUDD CHIARI SYNDROME)
B Imaging
Hepatic imaging studies may show a prominent caudate lobe, since its venous drainage may not be occluded The screening test of choice is contrast-enhanced, color, or pulsed-Doppler ultrasonography, which has a sensitivity of 85% for detecting evidence of hepatic venous or inferior vena caval thrombosis MRI with spin-echo and gradient-echo sequences and intravenous gadolinium injection allows visualization of the obstructed veins and collateral vessels Direct venography can delineate caval webs and occluded hepatic veins ( spiderweb pattern) most precisely
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