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溴隐亭诱发胸膜炎的提示性证据。

Suggestive evidence for bromocriptine-induced pleurisy.

作者信息

Klaassen R J, Troost R J, Verhoeven G T, Krepel H P, van der Lely A J

机构信息

Department of Internal Medicine I, University Hospital Dijkzigt, Netherlands.

出版信息

Neth J Med. 1996 Jun;48(6):232-6. doi: 10.1016/0300-2977(95)00069-0.

DOI:10.1016/0300-2977(95)00069-0
PMID:8710045
Abstract

Pleurisy of initially unknown origin was found in a patient who was treated with bromocriptine for Parkinson's disease for 6 years. At presentation, bilateral pleural thickening existed that caused severe restriction of pulmonary function. There were an elevated erythrocyte sedimentation rate, polyclonal hypergammaglobulinaemia, increased levels of acute phase proteins and anaemia. After withdrawal of the bromocriptine the patient's complaints as well as the laboratory parameters markedly improved. Further loss of pulmonary function did not occur. However, the pleural thickening did not resolve, not even upon subsequent corticosteroid treatment, probably due to fibrosis. Together, these findings strongly suggest a causative role of bromocriptine. The results of the laboratory studies suggested an immunopathogenetic mechanism, but in vitro lymphocyte-proliferation studies and skin patch tests with bromocriptine were negative. Bromocriptine should be considered as a cause of pleurisy. The drug must be stopped immediately upon the occurrence of pleural thickening in order to prevent impairment of pulmonary function. In addition, periodic laboratory and X-ray studies in patients on long-term bromocriptine treatment should be considered.

摘要

一名因帕金森病接受溴隐亭治疗6年的患者被发现患有起初病因不明的胸膜炎。就诊时,存在双侧胸膜增厚,导致肺功能严重受限。红细胞沉降率升高、多克隆高球蛋白血症、急性期蛋白水平升高以及贫血。停用溴隐亭后,患者的症状以及实验室指标明显改善。未再出现肺功能进一步丧失的情况。然而,胸膜增厚并未消退,即使随后接受皮质类固醇治疗也未消退,可能是由于纤维化所致。这些发现共同强烈提示溴隐亭具有致病作用。实验室研究结果提示存在免疫发病机制,但溴隐亭的体外淋巴细胞增殖研究和皮肤斑贴试验均为阴性。应考虑溴隐亭为胸膜炎的病因。一旦出现胸膜增厚,必须立即停用该药物,以防止肺功能受损。此外,对于长期接受溴隐亭治疗的患者,应考虑定期进行实验室检查和X线检查。

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