Nowadays, corticosteroids are indispensable for treatment of various disorders, especially for allergic and immunologic ones. Immunological suppression resulted from corticosteroid administration can improve such disorders, but, on the other hand, this suppressive state may induce opportunistic infections.
In this stud y, five cases, i. e. two cases of systemic lupus erythematosus (SLE) and three cases of bronchial asthma, having been treated with corticosteroids, were examined on the correlation between corticosteroid administration and immunologic alterations, as well as on their relationship to the incidence of infections, especially of tuberculosis which was found in three of the cases.
Case 1. M. K.,21 y. o., F., SLE. She had been administered with corticosteroids for her original disease. During this therapy, she suffered once from herpes zoster, and about one year thereafter died of complicating systemic tuberculous infection which had grown worse rapidly, in spite of potent anti-tuberculous chemotherapy. In this case, the term of corticosteroid therapy was about 30 months, the total dosage being 12g, and the daily dosage was equivalent to 5mg prednisolone (PSL) when the tuberculous infection was found. In this case, suppression of cellmediated immunity (CMI) was suggested on the basis of false positive of tuberculin reaction and decreased peripheral lymphocyte count (820/cmm)
Case 2. M. O.,33 y. o., F., SLE. During corticosteroid therapy, she suffered from cholecystitis, ostitis of mandible and pulmonary tuberculosis. All of these infectious complications were completely cured by conventional anti-microbial chemotherapy. In this case, corticosteroids had been administered for about 24 months,16.5g in total, and its daily dosage was 17.5 mg PSL when the, tuberculosis was found. No findings suggesting CMI suppression were obtained.
Case 3. Y. N.,57 y. o., M., bronchial asthma and diabetes mellitus. His b ronchial asthma had become steroid-dependent and his diabetes mellitus had grown worse due to the steroid therapy. The seral IgG level was 1,564mg/d1 under PSL 5mg/day administration, which went down to 749mg/d1 under 10mg/day of it. On the other hand, seral IgA level rose from 445mg/dl to 836mg/d1 coincidently. The peripheral lymphocyte count was low (680-1,000/cmm). About one year later, his old pulmonary tuberculosis relapsed, which well responded to conventional anti-tuberculous chemotherapy.
Case 4. M. T.,66 y. o., M., bronchial asthma. His bronchial asthma, too, had been steroiddependent. Seral IgE level rose as PSL dosage was reduced: Namely, the IgE level was 81.2--143 u/m1 under PSL 10 mg/day,851 u/ml under intermittent administration of 10-7.5 mg/day and 1473.5 u/ml under 5 mg/day administration. Throughout the corticosteroid therapy, his peripheral lymphocyte count remained within normal limit, but in regard to its subsets examin ed using monoclonal antibody of OK-series, the percentage of helper T cell tended to be high, while that of suppressor T cell tended to be low.
Case 5. H. T.,20 y. o., F., bronc h ial asthma. Her bronchial asthma had been steroiddependent for a long time, being treated with PSL 25mg/day combined with ACTH 20u/week. Later, she died of anaphylactic shock caused by intramuscular injection of ACTH. In this case, seral IgE level tended to increase (65→641u/ml) in concomitance with the decrement of PSL dosage down to 5mg/day.
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