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Consultant Physician Department of Medicine Arta General Hospital 47100 Arta Greece fax 30-210-6630113 dipapaio{at}otenet.gr
Senior Resident Department of Medicine Arta General Hospital
Consultant Physician Department of Medicine Arta General Hospital
Published Online, November 25, 2003. www.theannals.com, DOI 10.1345/aph.1D238
Case Report. A 65-year-old woman began taking celecoxib 200 mg/d for the treatment of osteoarthritis. Five days after she began treatment, she developed fever up to 38.6 °C, headache, nausea, photophobia, confusion, and neck discomfort. On admission to the emergency department, she showed marked nuchal rigidity, positive Brudzinski and Kerning sign, mental status changes, and unremarkable cranial nerve functioning. She had no known history of drug allergies or autoimmune rheumatic disorders. Empiric ceftriaxone sodium and acyclovir therapy was administered, and celecoxib was discontinued. A chest X-ray was normal and a computed tomography scan of the head revealed no intracranial abnormalities. A complete blood cell count was within normal limits and serum biochemistry investigations showed normal results. The results of a Gram stain, tuberculosis smear, and India ink procedure were negative. There was no evidence of bacterial, acid-fast bacillary, or fungal growth. Serologic tests for herpes viruses, antinuclear antibody, and rheumatoid factor were negative. The patient was diagnosed as having aseptic meningitis. Following celecoxib withdrawal, the patient's clinical condition improved. On hospital day 6, all symptoms had subsided and she was discharged from the hospital.
Discussion. In our patient, there was a temporal association between the prescription of celecoxib and the development of aseptic meningitis. Furthermore, other possible causes of meningitis were carefully excluded. Use of the Naranjo probability scale indicated a possible relationship between the aseptic meningitis and celecoxib therapy in this patient.4
The clinical features of aseptic meningitis in our patient are similar to those described with the use of rofecoxib and other NSAIDs. Symptoms appear during the first 2–3 weeks of treatment and mononuclear cells usually predominate in the cerebrospinal fluid. All meningeal and systemic signs resolve in a few days following withdrawal of the offending NSAID.
The mechanism of NSAID-induced aseptic meningitis is unclear. Our patient did not have eosinophilia, urticaria, pruritus, or other clinical features to suggest a hypersensitivity reaction involving the meninges. Also, the lack of a history of NSAID allergies in our patient does not support prostaglandin synthetase inhibition as a mechanism. The mechanism of aseptic meningitis may be described as an idiosyncratic central nervous system (CNS) reaction to celecoxib therapy. Celecoxib has been shown to penetrate the CNS in experimental animals, demonstrating a potent direct central action on COX-2 in CNS.5 As with other NSAIDs, celecoxib should be considered as a possible cause of aseptic meningitis in patients with or without rheumatologic disease.
References
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