Department of Respiratory Medicine, Medical School of Athens University, "SOTIRIA" Hospital for Diseases of the Chest, Athens, Greece
SIR, We would like to report the case of a 23-yr-old non-smoking, immunocompetent man who developed pulmonary infiltrates with eosinophilia (PIE) after using meloxicam to alleviate shoulder-ache due to strain.
The eosinophilic lung diseases are a diverse group of pulmonary disorders characterized by an increase in circulating or tissue eosinophils [1]. A variety of drugs and chemicals have been implicated in the causation of eosinophilic lung disease [2]. To the best of our knowledge, no case of meloxicam induced eosinophilic lung disease has been reported so far. Rheumatologists should be aware of this rare complication of a common medication.
The 23-yr-old non-smoking, immunocompetent man, with a previous history of allergic rhinitis-nasal polyps, reported low grade fever (37.237.5°C) for the previous 15 days and a dry cough. The initiation of his symptoms coincided with the use of meloxicam (oral tablet 7.5 mg once per day for 4 days) to alleviate shoulder-ache due to strain. He was referred to our clinic 11 days after the discontinuation of meloxicam because the symptoms persisted and the chest radiograph had revealed peripheral infiltrates of both lungs.
He had never consumed illicit drugs, and had no history of bronchial asthma or known prior exposure to any pulmonary toxin or irritant. He had been an urban dweller all his life, had no obvious exposure to dusts or moulds and had no pets in his living environment.
On admission the patient had no respiratory distress and no abnormal findings on examination. His temperature was 37.3°C. An arterial blood gas analysis breathing room air showed an oxygen tension in arterial blood (Pa, O2) of 10.53 kPa, a carbon dioxide tension in arterial blood (Pa, CO2) of 4.66 kPa, a pH of 7.45 and an oxygen saturation of 96%. Blood analysis revealed a white blood cell count of 11.8x103 mm-3 with 25% (relative) eosinophils, 2950 (absolute) eosinophils/mm3. Erythrocyte sedimentation rate was 50 mm/h and total serum immunoglobulin (Ig)E 1040 mg/dl. There was no evidence of collagen vascular disease or vasculitis, and serological screening (autoantibodies to DNA, double stranded DNA, ANCA, rheumatoid factor) was negative. Serum precipitating antibodies against Aspergillus antigens were negative, as well as stool examinations for ova and parasites.
Computed tomography scanning disclosed patchy peripheral opacities (Fig. 1). Pulmonary function tests revealed mild restrictive and obstructive defect with an FEV1/FVC ratio 75% and a total lung capacity (TLC) 5.73 (78% predicted [3]). FEV1 was partially reversible (8%) after the use of bronchodilators. Diffusing capacity of carbon monoxide was 81% predicted and KCO 100% predicted. After spirometry inhalations of salmeterol xinafoate were started twice daily and bronchoscopy with bronchoalveolar lavage (BAL) was performed. The bronchi appeared inflamed and contained increased secretions. Gram stain and cultures of the bronchial washings did not reveal any infectious organism. Total cell count on BAL was 69x104 cells/ml with 18.5% eosinophils, 2% neutrophils, 59% macrophages and 20.5% lymphocytes. Methylprednisolone was started orally (64 mg/day) 7 days after admission and the patient was discharged followed by rapid clinical and radiological improvement. Chest X-ray returned to normal in 5 days. On tapering doses of corticosteroids the patient had normal laboratory results and a normal chest radiograph 4 weeks after discharge.
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Our patient presented with peripheral infiltrates in both lungs and eosinophilia in the setting of meloxicam usage. Numerous conditions can cause this syndrome, including simple pulmonary eosinophilia (Loeffler's syndrome), chronic eosinophilic pneumonia, acute eosinophilic pneumonia, ChurgStrauss syndrome, idiopathic hypereosinophilic syndrome, asthma, allergic bronchopulmonary aspergillosis, bronchocentric granulomatosis, certain parasitic infections and drug reactions [1]. Appropriate laboratory investigation and follow up excluded the above-mentioned possible causes. Our patient reported a history of allergic rhinitis-nasal polyps, a disease that has not been associated with eosinophilic pneumonia as far as we know from the current literature. A possible co-existence of bronchial asthma could have explained the hypereosinophilia. However, the patient did not report a history of asthma, airway obstruction was only partially reversible (8%) and pulmonary infiltrates were nonsegmental [1]. We believe the patient's clinical course to be consistent with drug reaction, which could be attributed to meloxicam use. Although the evidence presented is presumptive for a drug-induced cause-and-effect relationship, it was deemed unethical to rechallenge the patient with meloxicam because of the severity of his symptoms.
Hundreds of drugs and chemicals are involved in the causation of eosinophilic lung disease after being ingested or inhaled [4, 5]. There is evidence from individual case reports that the administration of certain non-steroidal anti-inflammatory drugs (NSAIDs) is associated with the development of PIE syndrome, fever (usually low grade), peripheral eosinophilia, pulmonary symptoms that range from none to severe dyspnoea and non-productive cough [510]. As new agents are introduced the list of these diseases is expected to grow and prompt reporting of suspected drug-related adverse effects by health professionals is necessary to facilitate characterization of patients at risk, early recognition of the disease and appropriate management. To the best of our knowledge no other case caused by meloxicam has been reported so far.
We conclude that meloxicam should be added to the list of NSAIDs capable of inducing eosinophilic lung disease.
Notes
Correspondence to: A. Karakatsani, 16A Parthenonos Street, 175 62 P. Faliro, Greece. E-mail: annakara{at}otenet.gr
References