Sertraline-Induced Rhabdomyolysis in an Elderly Patient with Dementia and Comorbidities (July/August).
Ann Pharmacother. 2009 Jun 30; Gareri P, Segura-GarcÃa C, De Fazio P, De Fazio S, De Sarro GOBJECTIVE: To describe a case of sertraline-induced rhabdomyolysis in an elderly patient with dementia and comorbidities. CASE SUMMARY: A 71-year-old woman visited a psychiatrist in September 2007 for her depressed mood. Her medical history included vascular dementia accompanied by depression, arterial hypertension, and heart failure, as well as cardiac pacemaker implantation several years earlier for severe bradyarrythmia. She had begun taking amisulpride 50 mg/day and diazepam 2 mg at bedtime 6 months prior to the psychiatrist appointment, with poor relief of her depressed mood. Her drug therapy also included nicergoline 30 mg/day, amlodipine 5 mg/day, aspirin 100 mg/day, candesartan 16 mg/day, and atenolol 25 mg/day. At this psychiatrist visit, sertraline 50 mg/day was added for her depression, and was continued after a geriatrician visit in October. Her mood improved significantly. On December 18, 2007, she was admitted to the cardiology unit to undergo a pacemaker replacement. Laboratory tests revealed creatine kinase (CK) 7952 IU/L, lactate dehydrogenase 1021 IU/L, myoglobin 2322 U/L, and aspartate aminotransferase 362 IU/L, resulting in a diagnosis of iatrogenic rhabdomyolysis. Amisulpride and sertraline were discontinued. On December 24, serum CK was 839 IU/L and myoglobin was 91 U/L and the patient was discharged. On January 22, laboratory tests showed normal values of CK, CK-MB, and myoglobin. Sertraline 50 mg/day was again prescribed for the patient's persistent depressed mood. Fifteen days later, blood tests showed CK 1327 IU/L and myoglobin 324 U/L; therefore, the drug was discontinued. CK and myoglobin levels normalized a week later. On April 2, escitalopram was started. At time of writing, there was no evidence of any increase in CK, myoglobin, or other markers of rhabdomyolysis. DISCUSSION: The Naranjo probability scale indicated a probable relationship between sertraline treatment and the onset of rhabdomyolysis. No relationship between amisulpride and rhabdomyolysis was found. Furthermore, rechallenge with sertraline caused CK and myoglobin to again increase, which was reversed following a discontinuation of sertraline. The patient's other comorbidities and medications have not been suggested as possible interactions with sertraline that can cause rhabdomyolysis. Genetic defects of sertraline demethylation and/or P-glycoprotein binding or concurrent circumstances may explain the onset of rhabdomyolysis in this particular patient. CONCLUSIONS: This patient's rhabdomyolysis was probably induced by sertraline therapy.
