Diclofenac- and Pantoprazole-Induced Rhabdomyolysis: A Potential Drug Interaction

Abstract

Background: Drugs represent one of the etiologic causes of acute rhabdomyolysis (AR) with drug-induced rhabdomyolysis most commonly associated with HMG-CoA reductase inhibitors. AR etiology can also result from the use of diclofenac, a non-steroidal anti-inflammatory drug, and omeprazole, a proton pump inhibitor. Cases of AR triggered by pantoprazole have never before been reported, although it has been observed that its inclusion in multiple drug therapies can result in muscle events.

Case presentation: A 45-year-old man presenting with complaints of fatigue and extensive body pain was diagnosed with acute rhabdomyolysis. His symptoms started on the fourth day of the concomitant use of diclofenac and pantoprazole. The patient was using diclofenac 50-mg tablets once daily for 1 month and pantoprazole 40-mg tablets once daily during the previous week for headaches and pyrosis, resulting in an increase in his creatinine kinase levels to 3114 IU/L (reference range 24-190 IU/L) on the fifth day of concomitant use. His creatinine kinase levels returned to normal and his complaints disappeared after the seventh day of discontinuation of both treatments.

Discussion: A third case of diclofenac-induced rhabdomyolysis was defined in which, different from previous cases, AR was detected during the concomitant use of diclofenac and pantoprazole. The timing of the symptom development and the limited number of AR cases induced by diclofenac and pantoprazole suggested a drug interaction.

Conclusion: The close relationship between diclofenac and pantoprazole, and the cytochrome P450 and P-glycoprotein systems offers a strong indication that a drug interaction may be occurring. While evaluating the side effects of drugs in patients undergoing monotherapy, clinicians should also consider the mechanisms that play a part in drug absorption and distribution.

Fig. 1

Etiology of acute rhabdomyolysis and its complications