[胸膜肺纤维化与溴隐亭]。

J Vergeret, M Barat, A Taytard, P Bellvert, P Domblides, J J Douvier, P Fréour
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引用次数: 0

摘要

从个案和文献回顾,它是忆及溴隐亭可能诱发胸膜肺纤维化。描述了这种情况的各种表现形式。指标患者为56岁男性,帕金森病,呼吸系统疾病阴性病史,大剂量服用溴隐亭(60mg /d)。在这种治疗下,患者表现出体重减轻和炎症综合征,并发间质性肺病伴继发性胸膜肺纤维化,在停止治疗后部分缓解。溴隐亭是一种具有多巴胺能特性的麦角生物碱,自1965年以来一直用于治疗。它的适应症最初仅限于内分泌学,1972年扩展到帕金森病,从1979年起剂量显著增加。1981年,Rinne根据5例患者的资料怀疑其在胸膜肺纤维化中的作用。截至目前,共报告8例。所有帕金森患者均在不同的时间间隔(15天至3年)后出现胸膜肺疾病的统一症状,运动时呼吸困难迅速加重,总体健康状况恶化。这些特征反映了胸膜和肺组织的炎症和纤维化,从而导致不同程度的慢性限制性呼吸衰竭。病程同样一致,在皮质类固醇治疗下部分缓解,在停止治疗时或多或少显著残留纤维化。似乎与免疫过敏机制有关,而不是毒性或血管舒缩机制。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Pleuropulmonary fibrosis and bromocriptine].

From a personal case and a review of the literature, it is recalled that bromocriptine may induce pleuropulmonary fibrosis. The various presentations of this condition are described. The index patient is a 56-year-old man, with Parkinson disease and a negative history for respiratory disease, who was taking bromocriptine in a high dose (60 mg/d). Under this treatment, he exhibited weight loss and an inflammatory syndrome and developed interstitial pneumopathy with secondary pleuropulmonary fibrosis, which resolved in part once therapy was discontinued. Bromocriptine, which is an ergot alcaloid with dopaminergic properties, has been used since 1965 in therapy. Its indications, which at the outset were restricted to endocrinology, were extended in 1972 to Parkinson disease, with a significant increase in dosages from 1979. Its responsibility in pleuropulmonary fibroses was suspected in 1981 by Rinne on data from 5 patients. As of now, 8 cases have been reported. All are Parkinson patients who, after a variable time interval (15 days to 3 years), developed a uniform picture of pleuropulmonary disease with rapidly increasing dyspnea upon exertion and deterioration of general health. These features mirror inflammation then fibrosis of the pleura and lung tissue, which results in a variable degree of chronic restrictive respiratory failure. The course is equally uniform, with partial resolution under corticosteroid therapy and more or less significant residual fibrosis at discontinuation of treatment. Immunoallergic rather than toxic or vasomotor mechanisms seem involved.(ABSTRACT TRUNCATED AT 250 WORDS)

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