Fadel E Nammour1, Nabil F Fayad, Steven R Peikin. 1. Department of Medicine, Division of Gastroenterology, Cooper Hospital, University Medical Center, and Robert Wood Johnson Medical School, Camden, New Jersey 08103, USA.
Abstract
OBJECTIVE: To report a case of metformin-induced cholestatic hepatitis. METHODS: We present a detailed case report, including laboratory and biopsy findings. In addition, similar cases from the literature are reviewed. RESULTS: In a 68-year-old man with newly diagnosed diabetes mellitus, metformin therapy was begun. The dosage initially was 500 mg twice daily and later was increased to 850 mg twice a day. Four weeks after met-formin treatment was initiated, jaundice, pruritus, and liver enzyme abnormalities were noted. The patient underwent an extensive work-up, including a hepatitis screen, ultrasonography, magnetic resonance imaging, and endoscopic retrograde cholangiopancreatography, all of which showed normal findings. A liver biopsy revealed severe cholestasis and mild portal inflammation. Treatment with metformin was discontinued, and the liver enzymes normalized except for a persistently increased level of alkaline phosphatase, most likely related to a prolonged cholestatic effect of metformin. CONCLUSION: Although rare, metformin can be responsible for inducing liver damage, and patients and physicians should be aware of this side effect.
OBJECTIVE: To report a case of metformin-induced cholestatic hepatitis. METHODS: We present a detailed case report, including laboratory and biopsy findings. In addition, similar cases from the literature are reviewed. RESULTS: In a 68-year-old man with newly diagnosed diabetes mellitus, metformin therapy was begun. The dosage initially was 500 mg twice daily and later was increased to 850 mg twice a day. Four weeks after met-formin treatment was initiated, jaundice, pruritus, and liver enzyme abnormalities were noted. The patient underwent an extensive work-up, including a hepatitis screen, ultrasonography, magnetic resonance imaging, and endoscopic retrograde cholangiopancreatography, all of which showed normal findings. A liver biopsy revealed severe cholestasis and mild portal inflammation. Treatment with metformin was discontinued, and the liver enzymes normalized except for a persistently increased level of alkaline phosphatase, most likely related to a prolonged cholestatic effect of metformin. CONCLUSION: Although rare, metformin can be responsible for inducing liver damage, and patients and physicians should be aware of this side effect.
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