전 세계적으로 알벤다졸에 의한 독성간염은 극히 드물게 보고되고 있으며 모두 포낭충증에 대해 알벤다졸을 400 mg 하루 두 번 장기간 복용한 경우였다. 이에 저자들은 만성 알코올 섭취로 싸이토카인P450산화효소의 기능이 저하되었을 것으로 추정되는 환자에서 알벤다졸 400 mg 1회 복용으로 급성 간독성이 유발된 1예를 경험하고, 이를 보고한다.
전 세계적으로 알벤다졸에 의한 독성간염은 극히 드물게 보고되고 있으며 모두 포낭충증에 대해 알벤다졸을 400 mg 하루 두 번 장기간 복용한 경우였다. 이에 저자들은 만성 알코올 섭취로 싸이토카인 P450 산화효소의 기능이 저하되었을 것으로 추정되는 환자에서 알벤다졸 400 mg 1회 복용으로 급성 간독성이 유발된 1예를 경험하고, 이를 보고한다.
Drug-induced hepatotoxicity is injury to the liver as a result of drug exposure. Due to their unpredictable nature, drug-induced liver injuries pose a serious problem for clinicians, health agencies, and pharmaceutical firms. Albendazole is a benzimidazole with wide spectrum coverage as an antiparas...
Drug-induced hepatotoxicity is injury to the liver as a result of drug exposure. Due to their unpredictable nature, drug-induced liver injuries pose a serious problem for clinicians, health agencies, and pharmaceutical firms. Albendazole is a benzimidazole with wide spectrum coverage as an antiparasitic drug. Very few cases of high-dose albendazoleinduced hepatotoxicity have been reported so far, and no case in response to a single dose. A 25-year-old man presented to our hospital with dark urine. Twenty days prior to presentation, he took a tablet of albendazole (400 mg) as a prophylactic treatment for lumbricosis. Upon laboratory analysis, aspartate aminotransferase (AST) was 748 IU/L, alanine transaminase (ALT) was 939 IU/L, and total/direct bilirubin was 9.3/7.3 mg/dL. The patient was negative for viral markers (HAV, HBV, and HCV) and autoantibodies. Abdominal ultrasonography revealed no evidence of chronic liver damage. The pathology was compatible with drug-induced hepatotoxicity. The patient improved with conservative management only.
Drug-induced hepatotoxicity is injury to the liver as a result of drug exposure. Due to their unpredictable nature, drug-induced liver injuries pose a serious problem for clinicians, health agencies, and pharmaceutical firms. Albendazole is a benzimidazole with wide spectrum coverage as an antiparasitic drug. Very few cases of high-dose albendazoleinduced hepatotoxicity have been reported so far, and no case in response to a single dose. A 25-year-old man presented to our hospital with dark urine. Twenty days prior to presentation, he took a tablet of albendazole (400 mg) as a prophylactic treatment for lumbricosis. Upon laboratory analysis, aspartate aminotransferase (AST) was 748 IU/L, alanine transaminase (ALT) was 939 IU/L, and total/direct bilirubin was 9.3/7.3 mg/dL. The patient was negative for viral markers (HAV, HBV, and HCV) and autoantibodies. Abdominal ultrasonography revealed no evidence of chronic liver damage. The pathology was compatible with drug-induced hepatotoxicity. The patient improved with conservative management only.
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