Acarbose, a competitive inhibitor of -glucosidases, delays absorption of carbohydrates in the gut, thereby decreasing postprandial glucose levels [1]. A recent clinical trial published in Annals supports the efficacy of acarbose in improving long-term glycemic control in patients with non-insulin-dependent diabetes mellitus [2]. We describe a patient who developed hepatic injury caused by acarbose treatment.

A 65-year-old woman had received a diagnosis of non-insulin-dependent diabetes mellitus 7 years before presentation, for which glibenclamide was indicated. By mid-1993, acarbose (100 mg three times daily) was added to the treatment. Two months later, the patient presented with malaise and anorexia. She had no toxic habits, and she denied taking any other medications. Results of physical examination were unremarkable except for the presence of jaundice. Her aspartate aminotransferase level was 638 U/L, her alanine aminotransferase level was 690 U/L, her total bilirubin level was 9.9 mg/dL (with a direct bilirubin level of 7.84 mg/dL), her -glutamyltransferase level was 156 U/L, and her alkaline phosphatase level was 221 U/L. Serologic examination ruled out viral hepatitis. No antinuclear or antismooth-muscle antibodies were present. Ultrasonography showed a normal liver and no expanded bile ducts. The patient refused hospitalization and was managed on an outpatient basis. Acarbose was stopped, and 4 weeks later her serum total bilirubin level had decreased to 1.8 mg/dL, her aspartate aminotransferase level had decreased to 159 U/L, and her alanine aminotransferase level had decreased to 155 U/L. Laboratory results were normal within 9 months.

The mechanism of acarbose-induced liver injury is unknown. The drug is minimally absorbed in unchanged form after oral administration [1]. The absence of hypersensitivity symptoms in our patient did not suggest an immunoallergic reaction but could have been compatible with metabolic idiosyncrasy. The latter hypothesis is also supported by the relatively long latency period between drug intake and symptom onset. Although no liver biopsy was done, the liver damage can be classified as "hepatocellular," according to international consensus criteria [3]. Indeed, liver biopsy is usually not diagnostic for drug-induced liver disease and is primarily used for prognostic purposes [4]. Our report indicates that acarbose can cause substantial hepatotoxicity. Clinicians should be aware of this possibility when prescribing the drug.