著者

伊東 秀夫 藤平 隆司 原田 進 城戸 優光 加治木 章 中島 康秀 黒岩 昭夫

出版者

THE JAPANESE SOCIETY FOR TB AND NTM

雑誌

結核 (ISSN:00229776)

巻号頁・発行日

vol.59, no.4, pp.303-308, 1984-04-15 (Released:2011-05-24)

参考文献数

5

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Accelerated inactivation of corticosteroids following rifampicin therapy has beenrecognized. We observed nonresponsiveness to prednisolone treatment during rifampicinadministration in a case of systemic lupus erythematosus with diffuse alveolitis andconcomitant apical tuberculosis.A 51 year-old woman complained in September 1980, of polyarthralgia and butterflyerythema of the face. From typical clinical manifestations and positive serological tests, systemic lupus erythematosus was diagnosed and treatment with prednisolone was startedat a local hospital. To prevent exacerbation of old apical tuberculosis, isoniazid 0.2 gdaily was also administered. Good response was obtained for an initial few months butdyspnea, diffuse pulmonary infiltrates appeared following prednisolone decrement.She was transfered to our hospital in August 1981. On admission, she had a few skinulcers in bilateral hands and pigmentations over the surface of shoulder, elbow and knee.Velcro rales were audible over the lung base. No lymphadenopathy was detected.Laboratory examination revealed positive RA test, antinuclear and anti-DNA antibody. Thyroid test and microsome test were also positive, but LE test, RNP antibody, SMantibody were negative. C4, CH50 were normal but C3 was decreased. Chest X-Prevealed diffuse reticular shadows in bilateral middle and lower lung field and nodularconsolidation in right apical region. Although tubercle bacilli was negative in sputum, exacerbation of tuberculosis were suspected radiologically. Histological specimen obtained by transbronchial lung biopsy from the left lung showed mild interstitial thickening of alveoli with mononuclear cell infiltration.Prednisolone was increased from daily dose of 5mg to 80mg and 450mg of rifampicin, 1, 000mg of ethambutol were added, but no response was obtained. In December 1981, prednisolone was altered to equivalent dose of betamethasone but minimal improvementwas observed.After quitting rifampicin on January 1982, dramatic improvement in symptoms, laboratory data and chest roentgenogram was achieved. Although pharmacokineticstudies were not performed, we feel that the circumstantial evidence suggests strongly toincreased metabolism of prednisolone by rifampicin-induced microsomal enzymes.