 |
 |
 |
 |
 |
 |
 |
|
|
|
|||||||||
|
|||||||||||
Doctoral Fellow Interdepartmental Centre for Research in Clinical Pharmacology and Experimental Therapeutics University of Pisa Via Roma 55, 56126 Pisa, Italy fax 39050562020 m.deltacca{at}ao-pisa.toscana.it
General Practitioner Italian Society of General Medicine Florence, Italy
General Practitioner Italian Society of General Medicine Florence
Professor Interdepartmental Centre for Research in Clinical Pharmacology and Experimental Therapeutics University of Pisa
Professor Interdepartmental Centre for Research in Clinical Pharmacology and Experimental Therapeutics University of Pisa
Published Online, December 27, 2005. www.theannals.com, DOI 10.1345/aph.1G382
Case Report. A 71-year-old man was admitted to the emergency department complaining of severe epigastric pain. At the time a single 30 minute intravenous infusion of omeprazole 40 mg/10 mL diluted in 100 mL of NaCl 0.9% solution was administered, the patient did not show neurovegetative or traumatic musculoskeletal symptoms. After 12 hours in the emergency department, the epigastric pain persisted and the patient was hospitalized.
Blood analysis at this time revealed an increase in creatine kinase, creatine kinase isoenzymes (MB fraction), and myoglobin levels, without concomitant symptoms of muscle injury (myalgia, weakness, cramps). Troponin I, electrolyte balance, platelet count, and thyroid-stimulating hormone levels were normal. No signs of bruising or edema were present, even at the omeprazole infusion site. An endoscopic evaluation revealed gastric hypotrophy and biliary reflux. Electrocardiogram, chest X-ray, and abdominal echography appeared normal. Electromyography and assay of creatine kinase isoenzymes (MM fraction) were not performed. Relevant laboratory evaluations are summarized in Table 1. Omeprazole-induced myopathy was suspected, the drug discontinued, and no other gastrointestinal drugs were administered.
|
At the time of event onset, the patient was receiving trazodone 75 mg daily for 3 years for depression, ramipril 5 mg daily for 4 years, and hydrochlorothiazide 25 mg daily for 2 years for hypertension, and aspirin 100 mg daily for 2 years as prophylaxis for cardiovascular events, including obesity (body mass index 30.39). The patient also presented with mild diabetes and a history of familial cardiovascular disease. In addition, he experienced sleep disturbances, described as restless leg syndrome-like symptoms, which were being treated with benzodiazepines. Renal function was normal, and there was no history of drug allergies, illicit drug use, or alcohol abuse.
During hospitalization, all drugs were discontinued with the exception of subcutaneous nadroparin sodium 11400 IU once daily to prevent possible ischemic heart complications. After one week, the patient recovered from epigastralgia with a concomitant improvement in laboratory parameters. According to the patient's family physician, these laboratory values returned to baseline a few days after hospital discharge. A causality assessment of the adverse event revealed a probable association of the myopathy with omeprazole.6
Discussion. Myopathy can be associated with many clinical conditions; an accurate differential diagnosis is needed to evaluate its possible etiology. In our patient, muscle alteration resulting from parenteral administration (such as in a crush or compartmental syndrome) seems unlikely due to the absence of pain, edema, bruising, or other external symptoms. Laboratory tests allowed the exclusion of a myocardial infarction. Literature and temporal relationship do not support an involvement of concomitant drugs.
One report of myopathy associated with a 14 day oral course of omeprazole has been described.1 Our case suggests that single parenteral administration of omeprazole might induce silent myopathy and supports the need to monitor muscle injury markers when administering PPIs with such a treatment regimen. Further investigations are required to improve our knowledge about PPI potential myotoxicity.
References
This article has been cited by other articles:
|
|
 |
|
  M. Tuccori, G. Lombardo, F. Lapi, A. Vannacci, C. Blandizzi, and M. Del Tacca Gabapentin-Induced Severe Myopathy Ann. Pharmacother., July 1, 2007; 41(7): 1301 - 1305. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
 |
 |
 |
 |
 |
 |
