Drug points: Acute eosinophilic pneumonia associated with tenidapBMJ 1997; 314 doi: http://dx.doi.org/10.1136/bmj.314.7077.349 (Published 01 February 1997) Cite this as: BMJ 1997;314:349
- a Department of Internal Medicine, Hospital de la Santa Creu I Sant Pau, Universitat Autonoma de Barcelona, Barcelona, Spain
Acute eosinophilic pneumonia may be an adverse effect of non-steroidal anti-inflammatory drugs, particularly naproxen, although sulindac, fenoprofen, ibuprofen, and diclofenac have been described in a few cases.1 2 We report the first case associated with tenidap, a new drug of this class.
A 60 year old man with chronic osteoarthrosis, complained of two weeks' progressive dyspnoea and non-productive cough. He had no history of asthma or other atopic illness, nor had he been knowingly exposed to respiratory infections or to toxic oil syndrome. After informed consent he had started treatment with tenidap 40 mg/day one month before admission; he had not been taking other drugs. His temperature was 37.8°C, blood pressure 130/80 mm Hg, heart rate 84 beats/min, and respiratory rate 28 breaths/min. He was in mild respiratory distress, and auscultation showed only faint basal rales bilaterally without wheezes or ronchi. Peripheral white blood cell count was 6.5x109/l (56% neutrophils, 22% lymphocytes, 6% monocytes, and 16% eosinophils); haemoglobin concentration was 136 g/l, and platelet count was 170x109/l. Erythrocyte sedimentation rate was 60 mm in the first hour. Routine serum and urine tests gave normal results. Room air arterial blood showed partial pressures of 6.7 kPa (51 mm Hg) of oxygen and 5.06 kPa (38 mm Hg) of carbon dioxide; saturation was 85%. Radiography and computed tomography of the thorax showed peripheral interstitial infiltrates over the bilateral middle and lower lung fields. Gram and acid fast stains of the sputum gave negative results. IgE concentration was 332 kU/l (normal<110), and antinuclear antibodies were 1/80. Total haemolytic complement (CH50), C3, and C4; B, T, CD4, and CD8 lymphocyte subsets; and IgG, IgM, and IgA concentrations were normal. He was negative for rheumatoid factor and the following antibodies: DNA native, smooth muscle, gastric mucosa, mitochondrial, and thyroid. Differential cell count in bronchoalveolar lavage showed macrophages 43%, neutrophils 15%, lymphocytes 10% (T, 92%; B, 0.9%; CD4, 23%; and CD8, 67%), and eosinophils 32%. Aspergillus precipitin was not found. Gram, acid fast, and methenamine silver stains showed no organisms. Bacterial, mycobacterial, fungal, and viral cultures of lavage fluid gave negative results. Pulmonary function tests showed moderate restrictive ventilatory defect and moderate reduction of the diffusing capacity for carbon monoxide.
With no evidence of infection, acute eosinophilic pneumonia was diagnosed by exclusion.3 4 Tenidap was withdrawn, and further treatment with prednisone 1 mg/kg/day for one week rapidly resolved clinical and radiological abnormalities. During three years of follow up he did not show relapse of respiratory symptoms despite treatment with diclofenac and piroxicam, and chest radiographs showed nothing abnormal.