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Excerpt
Mr. H. was a 49-year-old veteran with chronic posttraumatic stress disorder who had a history of alcohol dependence (in remission), depression, and type 2 diabetes mellitus. His medications on admission to our unit included slow-release bupropion 150 mg twice a day for 5 months, glipizide 10 mg twice a day for 16 months, metformin 850 mg three times a day for 4 months, a stool softener, and multivitamins. Admission laboratory test results were normal, with the exception of elevated glucose levels and mild elevations of alanine aminotransferase levels to 79 u/L (reference range, 21-72 u/L) and alkaline phosphatase levels to 200 u/L (reference range, 38-126 u/L). Hepatitis screen was consistent with past exposure to hepatitis A and was negative for exposure to hepatitis B or C.
During a routine blood test 18 days after his admission, elevations of aspartate aminotransferase level to 264 u/L (reference range, 10-47 u/L) and leukocyte dehydrogenase (LDH) level to 2,725 u/L (reference range, 313-618 u/L) were noted. Mr. H. had no complaints at that time except for "feeling cold," and his vital signs were normal. Further workup revealed a creatine kinase (CK) level of 18,394 u/L (reference range, 55-170 u/L), with 100% muscle isoenzyme fraction of CK, consistent with skeletal muscle injury, and elevation of the LDH5 fraction to 73.4% (reference range, 5-13%), consistent with hepatic or skeletal muscle injury. Urine toxicology screen was negative (for opiates, cocaine, methadone, amphetamines, barbiturates, benzodiazepines, and cannabis), and breathalyzer and blood alcohol level were 0. Mr. H. was transferred to the medical service and was treated with intravenous hydration. His vital signs remained stable. He had only minor changes in electrolytes, no elevations of blood urea nitrogen or creatinine levels, and his liver enzymes remained elevated. Despite the above findings consistent with skeletal muscle injury, no myoglobinuria was found. Abdominal ultrasound revealed parenchymal liver disease without any focal abnormality, normal spleen, and a dilated common bile duct. This dilatation was noted on a previous ultrasound performed 16 months earlier.
Bupropion was discontinued, and Mr. H. was transferred back to our unit after 2 days of intravenous hydration (CK level was 6,166 u/L). He continued to be asymptomatic, and within 8 days his CK level returned to normal. Liver enzymes remained elevated until 4 weeks after the incident. At that time, only his [small gamma, Greek]-glutamyl transferase (GGT) level was still above normal (327 u/L; reference range, 8-78 u/L). A subsequent hepatitis A, B, and C screen was unchanged, and a hepatobiliary scan was suggestive of partial biliary obstruction. A review of the patient's records revealed prior elevations of GGT and a previous diagnosis of chronic pancreatitis by abdominal ultrasound. No further workup was deemed necessary.
Because of persistently elevated glucose and hemoglobin A1 C levels, his glipizide and metformin were discontinued, and he was started on insulin treatment, with improvement in diabetes control.
The occurrence of rhabdomyolysis with hepatic dysfunction during the course of treatment with bupropion seems to be a rare event. In this particular case, the patient was also taking two oral hypoglycemic agents, which were discontinued shortly after bupropion and which cannot be excluded as possible contributors to this complication.
