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慢性阻塞性肺疾病不是过敏。慢性阻塞性肺疾病不是过敏。

COPD is not COPD is not allergy.

作者信息

Suskovic Stanislav

出版信息

Wien Klin Wochenschr. 2009;121(9-10):289-92. doi: 10.1007/s00508-009-1189-4.

Abstract

Chronic obstructive pulmonary disease (COPD) is still a poorly understood disease. Its pathogenesis is excitingly complex and has systemic consequences caused not only by increased production of certain cytokines but also by neurohumoral activation, chronic bacterial infection, muscle wasting and cachexia. Asthma and COPD have many overlapping clinical features so it should not be surprising that in the pathogenesis of COPD mediators such as leukotrienes, complement activation, atopic or even autoimmune processes are possibly involved. The pathogenesis of cardiovascular system involvement in COPD is also multifaceted and includes chronic heart hypoxia, damage by smoking and pulmonary hypertension; it must also be viewed as a consequence of systemic inflammation and neurohormonal activation. COPD is among the leading causes of morbidity and mortality worldwide and therefore it should be studied intensively beyond the lung itself. Treatments directed at neurohumoral activation in COPD have not been fully addressed; this aspect of COPD should be better understood, as it may direct novel therapeutic approaches.

摘要

慢性阻塞性肺疾病(COPD)仍然是一种了解甚少的疾病。其发病机制极其复杂,不仅会因某些细胞因子产生增加,还会因神经体液激活、慢性细菌感染、肌肉萎缩和恶病质而产生全身性后果。哮喘和慢性阻塞性肺疾病有许多重叠的临床特征,因此在慢性阻塞性肺疾病的发病机制中,白三烯、补体激活、特应性甚至自身免疫过程等介质可能参与其中,这并不奇怪。慢性阻塞性肺疾病中心血管系统受累的发病机制也是多方面的,包括慢性心脏缺氧、吸烟损伤和肺动脉高压;它也必须被视为全身炎症和神经激素激活的结果。慢性阻塞性肺疾病是全球发病和死亡的主要原因之一,因此,应该在肺本身之外进行深入研究。针对慢性阻塞性肺疾病中神经体液激活的治疗尚未得到充分解决;慢性阻塞性肺疾病的这一方面应该得到更好的理解,因为它可能指导新的治疗方法。

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