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糖皮质激素无反应性发热的可能机制。脂皮质素1缺陷?

Possible mechanisms of glucocorticoid--unresponsive pyrexia. Defect in lipocortin 1?

作者信息

Akama H, Tanaka H, Kawai S

机构信息

Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.

出版信息

Mater Med Pol. 1995 Apr-Jun;27(2):75-8.

PMID:8935195
Abstract

Glucocorticoids have a strong anti-inflammatory action, and are indispensable in the treatment of inflammatory diseases. We had a patient with the Weber-Christian disease having an intractable high fever that did not respond to even a high-dose glucocorticoid therapy, but was responsive to a nonsteroidal antiinflammatory drug. To elucidate possible mechanisms of the glucocorticoid-unresponsive fever, we have investigated the in vitro production of two eicosanoids, prostaglandin (PG)E2 and leukotriene (LT)B4, from the peripheral blood polymorphonuclear leukocytes after stimulation by ionophore A23187. The patient's leukocytes produced much larger amount of PGE2, but the same amount of LTB4, as did those of two control groups. More interestingly, the production of eicosanoids was inhibited by dexamethasone less in the patients than in the controls. Indomethacin suppressed the production of PGE2 both in the patients and in the controls. These results might be relevant in the glucocorticoid-unresponsive pyrexia.

摘要

糖皮质激素具有强大的抗炎作用,在炎症性疾病的治疗中不可或缺。我们有一位患韦氏-克里斯蒂安病的患者,患有顽固性高热,即使大剂量糖皮质激素治疗也无效,但对非甾体抗炎药有反应。为阐明糖皮质激素无反应性发热的可能机制,我们研究了离子载体A23187刺激后外周血多形核白细胞中两种类花生酸——前列腺素(PG)E2和白三烯(LT)B4的体外产生情况。该患者的白细胞产生的PGE2量比两个对照组的多得多,但LTB4量相同。更有趣的是,与对照组相比,地塞米松对患者类花生酸产生的抑制作用较小。吲哚美辛在患者和对照组中均抑制了PGE2的产生。这些结果可能与糖皮质激素无反应性发热有关。

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Possible mechanisms of glucocorticoid--unresponsive pyrexia. Defect in lipocortin 1?糖皮质激素无反应性发热的可能机制。脂皮质素1缺陷?
Mater Med Pol. 1995 Apr-Jun;27(2):75-8.
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Glucocorticoid-unresponsive fever in a patient with Weber-Christian disease.一位患有韦格纳-克里斯蒂安病的患者出现糖皮质激素无反应性发热。
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Macrophage-specific eicosanoid synthesis inhibition and lipocortin-1 induction by glucocorticoids.糖皮质激素对巨噬细胞特异性类花生酸合成的抑制作用及脂皮质素-1的诱导作用。
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