Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2003
Metformin-induced cholestatic hepatitis.
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Nammour Fadel E, Fayad Nabil F, Peikin Steven R
Аннотация
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.
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.