慢性阻塞性肺疾病和骨质疏松症合并的现代资料

V. Pavlenko, Y. Schegortsova, А. А. Bakina
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摘要

介绍。慢性阻塞性肺疾病(COPD)的一个重要特征是,在病理生理机制的作用下,发生累及多个器官和组织的全身性炎症。骨质疏松症是慢性阻塞性肺病系统性影响的最严重和最具社会意义的表现之一。骨质疏松症限制了患者及其家庭成员的社会活动,导致高材料成本和高水平的残疾和死亡率。的目标。目的:研究国外和俄罗斯COPD患者骨质疏松的患病率、发病机制及临床意义。材料和方法。这篇综述主要包括过去五年在PubMed和library发表的文献数据。如有必要,将较早的出版物纳入审查。结果。根据不同作者的研究,60-86.7%的COPD患者发生骨质减少。骨骼矿物质密度损失的程度与COPD的严重程度成正比。COPD患者脊柱压缩性骨折、股骨颈骨折的发生率高于非COPD患者。细胞因子在COPD骨质疏松形成的发病机制中起着至关重要的作用。同时,研究仅限于早期反应细胞因子(白介素1和6,肿瘤坏死因子α)的意义。关于脂肪因子在COPD患者骨重塑中的作用,目前仅有单一的研究。结论。为了更深入地了解细胞因子和其他免疫因子在COPD中调节骨代谢的机制,还需要进一步的研究。
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Modern data on a combination of chronic obstructive pulmonary disease and osteoporosis
Introduction. The development of systemic inflammation involving a number of organs and tissues with the implementation of pathophysiological mechanisms is an important characteristic of chronic obstructive pulmonary disease (COPD). Osteoporosis is one of the most serious and socially significant manifestation of the systemic effects of COPD. Osteoporosis limits the social activity of the patient and his family members, leads to high material costs and a high level of disability and mortality. Aim. To study the data of foreign and Russian studies on the prevalence of osteopenia, pathogenic mechanisms of development and the clinical meaning of osteoporosis in COPD. Materials and methods. The review includes literature data published mainly over the past five years in PubMed and eLibrary. Earlier publications were included in the review if necessary. Results. According to different authors, osteopenia occurs in 60-86.7% of patients with COPD. The degree of loss of mineral density of bones is proportional to the severity of COPD. Compression fractures of the spine and fractures and femoral neck are found in patients with COPD more often than in patients without COPD. Cytokines have a crucial role in the pathogenesis of the formation of osteoporosis in COPD. At the same time, studies are limited only by the significance of early response cytokines (interleukins 1 and 6, tumor necrosis factor-alpha). There are only single studies on the role of adipokines in bone remodeling with COPD. Conclusion. Further studies must be carried out for a deeper understanding of the mechanisms of regulating bone metabolism by cytokines and other immune factors in COPD. 
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