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The generation. of leukotrienes 84 (LT84) and C4 (LTC4) by leucocytes stimulated with Ca ionophore A23187 was examined in 71 patients with asthma (42 with atopic and 29 with nonatopic asthma) and 23 healthy controls. Of these patients,22 had SDIA (steroid-dependent intractable asthma). 1. The generation of LT84 and LTC4 by leucocytes was significantly more enhanced in patients with atopic, non-SOIA asthma than in healthy subjects, but not in patients with nonatopic asthma. The generation of LT84 and LTC4 in atopic asthma was significantly more decreased in patients with SOIA than in those with non-SOIA. 2. The LTC4 generation was significantly larger in attack stage than in attack-free stage of patients with atopic and nonatopic asthma when they had not SOIA. However, no significant difference was found in LT84 generation between attack and nonattack stages in these patients. 3. In patients with SOIA, no significant differences were observed in the generation of LT84 and LTC4 between attack and nonattack stages. The results suggest that IgE-mediated allergy and asthma attacks enhance and glucocorticoids inhibit the generation of LT84 and LTC4 by leucocytes., 気管支喘息71例および健康人23名を対象に､Ca ionophore A23187刺激時の末梢血白血球のロイコトリエンB4 (LTB4)およびC4(LTC4)の産生能について検討を加えた｡なお､71例中ステロイド依存性重症難治性喘息(SDIA)は22例であった。1.アトピー性､16非SDIA症例におけるLTB4､LTC4産生は､健康人と比べ有意に高い値を示したが､非アトピー性喘息では健康人との間に有意の差は見られなかった｡また､アトピー性喘息では､SDIA症例において非SDIA症例に比べ､LTB4､LTC4産生が有意に抑制されていた｡2.非SDIA症例では､アトピー性､非アトピー性を問わず､LTC4産生は､非発作時に比べ発作時に有意に亢進した状態であった｡しかし､LTB4産生には､非発作時､発作時との間に有意の差は見られなかった｡3.SDIA症例では､LTB4､LTC4産生と発作との有意の関連は見られなかった｡以上の結果より､IgE にmediateされるアレルギー反応や喘息発作はLTB4､LTC4産生に促進的に､また副腎皮質ホルモンは抑制的に作用することが示唆された｡