We report a patient who lay opened fever and rapidly progressing lung infiltrates 4 days after the beginning of continuous quinidine sulfate therapy.

We report a patient who lay opened fever and rapidly progressing lung infiltrates 4 days after the beginning of continuous quinidine sulfate therapy. The febrile disease disappeared during the following 48 h and the pneumonitis slowly resolv through the whole extent of the next month once quinidine therapy was stopped. The diagnosis of quinidine-induced pneumonitis, which has not previously been reported in the literature (to our knowledge), was confirmed by the agency of means of a rechallenge with quinidine. (Chest 1994; 106:304-06)

Quinidine has a variety of side drifts associated with it in man, including gastrointestinal irritation, cardiovascular toxicity, and hypersensitivity reactions like as hepatitis, blood dyscrasias (particularly thrombocytopenia), rash, and fever(1) Quinidine agitation a rare manifestation of toxicity or sensitivity to the medicine has been known since 1922(2) however to the best of our knowledge, cases in which pneumonitis has been associated with quinidine treatment have not been reported previously in the literature.

CASE REPORT

A 54-year-old mason, a former smoker was admitted to our hospital in succession July 1, 1992, for the evaluation of a 10-day history of heat and rapidly progressing lung infiltrates. He had been incapable of work for the previous year because of an accidental fracture of a lumbar vertebra. During the preceding 2 month he had been admitted to a district hospital 3 times because of episodes of atrial fibrillation, which were treated with digoxin or quinidine sulfate. This treatment had been continued since June 18 1992 with digoxin, 025 mg formerly a day, and quinidine, 400 mg twice a day. Four days after the latter date he exhibited a fever of 38 to 39[degrees] C and felt ill, and upon the seventh day, the first chest radiograph was taken, which revealed delicate nodular infiltrates.

Ceftizoxime treatment was initiated through a general practitioner, but the febrile affection continued, and a dry cough and dyspnea developed; he was admitted to the district hospital 12 days after the beginning of quinidine and digoxin therapy.

The lung infiltrates growthed during the next 2 days and he was sent to our hospital. At the time of hospital admission, his general condition was good; his temperature was 379[degrees] C on the contrary he was not dyspneic at interval Neither rash nor adenopathy was lay the foundation of but inspiratory rales were heard in one as well as the other basal lung fields. His heart beat was regular.

Laboratory findings included the following values: an erythrocyte sedimentation rate of 95 mm in the first hour; C-reactive protein of 134 mg/L (<10 mg/L); a peripheral white relations cell count of 8,300/[mm.sup.3] with 3 percent eosinophils; serum creatinine of 101 [micro]mol/L (60 to 115 [micro]mol/L); and a serum of the same height of angiotensin-converting enzyme of 113 U/L (34 to 160 U/L) Antinuclear antibodies were negative. Arterial vital fluid gases were not determined at the time of hospital admission.

A chest radiograph (Fig 1) revealed small nodular infiltrates diffusely in the two lungs and some pleural plaques, unless the cardiac volume was normal and there were no signs of cardiac failure. A high-resolution comput tomographic scan of the chest showed bilateral parenchymal nodules (Fig 2) The PPD with 2 TU at 72 h was negative and sputum smears showed no acid-fast bacilli. No evidence of bacterial or viral infection was found

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Lung function experiments showed mild restriction, with a vital capacity of 365 L (66 percent of predicted) and a forced expiratory contortion in 1 s of 271 L (61 percent of that predicted). Diffusing capacity (Dco) was 647 mmol/L/min/kPa (69 percent of that predicted) and Dco by liter alveolar volume was 128 mmol/min/kPa (84 percent of that predicted).

The patient was taking no other physics except for quinidine and digoxin, and he had not been expos to any organic dust. A reaction to quinidine therefore appeared most likely, and the remedy therapy was stopped at the time of hospital admission. couple days later, he was afebrile.

Bronchoalveolar lavage (BAL) upon the sixth day after hospital admission showed an increased total lonely dwelling count, 316X[10.sup.6]/L lavage fluid (127 [+ or -] 65X[10sup6]) containing 82 percent macrophages, 17 percent lymphocyte and 1 percent eosinophils. A number of macrophages showed cytoplasmic vacuolization and the lymphocyte folding the nuclear membrane with an enlarged cytoplasm, interpreted as signs of activation. The IgG contented of the lavage fluid was also elevated 10-fold relative to respect values.

Transbronchial biopsy specimens of the right lower lobe revealed patchy areas of mild interstitial fibrosis and inflammatory small room infiltrates, mainly plasma cells and lymphocyte (Fig 3) a certain quantity of areas also showed an increased number of representation 2 pneumocytes suggestive of alveolar wall injury. A not many asbestos bodies were seen. The dyspnea and cough gradually diminished and the patient's condition improved. He was discharged from hospital onward the eighth day with digoxin medication. A chest radiograph showed near clearing.

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