[阿狄森氏病在干扰素治疗期间加重1例:胰岛素分泌不足]。

K Oshimoto, H Shimizu, N Sato, M Mori
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引用次数: 12

摘要

我们报告了一位患有Addison病的患者,他的临床特征在慢性活动性丙型肝炎的干扰素治疗期间变得更糟。一位47岁的男性患者在接受干扰素- α -2a治疗4周(干扰素:900 x 104U/天)期间出现嗜睡。入院时血清钠水平为113mEq/l,血浆渗透压降至238mOsm/kg。血浆ACTH水平较高,血清皮质醇、尿17-OHCS、17-KS排泄均远低于正常水平。入院时,血清催乳素、胰岛素水平和尿CPR排泄增加。通过NaCl处理使血清钠水平正常化,可减轻高胰岛素血症,并减少增加的CPR排泄。据推测,IFN可能增加Addison病患者的皮质醇消耗并加重肾上腺皮质激素低下症。此外,本病例提出了低摩尔浓度可能诱导人类高胰岛素状态的可能性。
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[A case of Addison's disease which became worse during interferon therapy: insulin secretion under hyposmolarity].

We report a patient with Addison's disease whose clinical features became worse during interferon therapy for chronically active hepatitis C. A 47-year-old male was admitted because somnolence developed during a 4 week treatment with interferon-alpha-2a (IFN: 900 x 104U/day). Serum Na level was 113mEq/l and plasma osmolarity was lowered to 238mOsm/kg on admission. Plasma ACTH level was high, while serum cortisol, urinary 17-OHCS and 17-KS excretion were far below the normal levels. On admission, serum prolactin, insulin levels and urinary CPR excretion increased. Normalization of serum Na level by NaCl administration attenuated hyperinsulinemia associated with the reduction of increased CPR excretion. It was supposed that IFN administration might increase cortisol consumption and worsen hypoadrenocortinism in a patient with Addison's disease. In addition, the present case raised the possibility that hyposmolarity may induce a hyperinsulinemic state in humans.

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