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CltroaleeoslaopkOle plleaIDOBla: ftnt I'efOrt A 70-year-old diabetic (treated for 9 years with toJazamide) W&'J admittcid when erythromycin failed to cure a nonproductive coUib. elevated temperature, weakness and weight 1,* of 3-wocu' duration. Phylical and laboratory examinations were DOrmal except for a low haemoglobin ( II g percent), and elevated leucocytes ( 15,0001 mO with 996 eosinophilia. Bilateral upper lobe infiltrates were noted but bacterial and parasitic tests were negative. The patient became afebrile I day after tolazamide was withdrawn (because the diabetes could be controlled by diet alone) and was asymptomatic for the four days he was in hospital. Isoniazid and rifampicin were given because tubercuJosis was suspected, but these were witbdrawn 2 weeks later. The infiltrates were resolved J weeks after discharge, but tolazamide Was restarted because glycosuria had developed. Six weeks later the infiltrates had recurred and tolazamide was diSQOntinued be<:ause of higher eosinophilia (32 % ). Within a week the chest roentaenogram became normal and the patient became afebrile and started to gain weight. This inadvertent rechallenge with tolazamide. and subsequent improvement once the drua was withdrawn, suggests that it was the causative factor in this patient. The fact that a patient has used a drug for a long time should not preclude that drug from investigation as a possible causative agent of the chronic eosinophilic pneumonia syndrome. 8o/ldi. E. andSl8U!r. S., Chest 80, 6.S2(Nov .,'1)

0167-72"71/8210129-0007/0$00.50/0 CADIS PreIS Reactions 29 Jan 1982 7