ABSTRACT
BACKGROUND: Rosiglitazone maleate (Avandia, SmithKline Beecham, Philadelphia, Pennsylvania) is a new oral hypoglycemic agent approved for the treatment of type 2 diabetes. It acts primarily by increasing insulin sensitivity. In controlled trials, there has been no evidence of rosiglitazone-induced hepatocellular injury. OBJECTIVE: To report a case of hepatocellular injury in a patient receiving rosiglitazone. DESIGN: Case report. SETTING: Community teaching hospital. PATIENT: 61-year-old man receiving rosiglitazone, 4 mg/d for 2 weeks. INTERVENTION: Discontinuation of rosiglitazone therapy. MEASUREMENTS: Clinical evaluation and assessment of liver function test results were done daily during hospitalization and periodically after discharge. The outpatient record was also reviewed. RESULTS: After receiving rosiglitazone for 2 weeks, the patient presented with anorexia, vomiting, and abdominal pain. Liver function tests revealed severe hepatocellular injury. Discontinuation of rosiglitazone therapy led to rapid improvement of liver function and resolution of symptoms. CONCLUSION: Rosiglitazone may be associated with hepatocellular injury. We believe that patients receiving rosiglitazone should have liver enzyme levels monitored earlier and more frequently than initially recommended.
Subject(s)
Chemical and Drug Induced Liver Injury/etiology , Hypoglycemic Agents/adverse effects , Thiazoles/adverse effects , Thiazolidinediones , Chemical and Drug Induced Liver Injury/diagnosis , Diabetes Mellitus, Type 2/drug therapy , Humans , Liver/enzymology , Liver Function Tests , Male , Middle Aged , Monitoring, Physiologic , RosiglitazoneABSTRACT
Historically, diabetic ketoacidosis has been attributed exclusively to the accumulation of ketoacids resulting in wide anion gap metabolic acidosis. An unusual patient with non-insulin-dependent diabetes mellitus who presented with mild hyperglycemia, ketonemia, and acidosis with a normal anion gap is described. No other known causes of hyperchloremic metabolic acidosis were present, and resolution of acidosis followed administration of intravenous insulin. This case illustrates that the finding of a normal anion gap, per se, may not exclude the presence of diabetic ketoacidosis.
