Moxonidine-induced cholestatic hepatitis

1997 
1822 Vol 350 • December 20/27, 1997 showed parakeratosis. Treatment was supportive including vitamin K, albumin, and diuretics for a few days. Within 4 weeks, he was discharged from hospital. 8 weeks after the end of treatment with moxonidine, laboratory indices were normal (table). 1 year after discontinuation he is in good health and liver indices remain normal. His arterial hypertension is controlled with an ACE inhibitor and diuretics. Cholestatic hepatitis is a frequent complication of drugs, and hepatitis is a known side-effect of centrally acting antihypertensive drugs such as clonidine. To our knowledge no case of cholestatic hepatitis during treatment with moxonidine has been reported. Moxonidine is increasingly used for the treatment of hypertension. Frequent side-effects include dryness of the mouth, headache, tiredness, disturbance of sleep, and gastric symptoms. In a postmarketing surveillance programme by the manufacturer none of more than 20 000 patients observed has developed cholestatic hepatitis. There is convincing evidence of a causative role of moxonidine in this case. No other drug was given to this previously healthy patient and he denied taking any non-prescription drugs; a liver biopsy specimen showed features compatible with drug-induced inflammatory intrahepatic cholestasis; other diseases of the liver and bile ducts were excluded; and the patient recovered after stopping the drug. Rechallenge with moxonidine was considered unethical— given the fact that considerable liver damage had occurred and that effective therapeutic alternatives are available.
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