The aim of the study was to analyze the professional literature concerning general principles of medicamental correction for endothelial dysfunction and their peculiarities in patients with chronic obstructive pulmonary disease.  The development of chronic obstructive pulmonary disease (COPD) is based on certain trigger factors and pathogenetic processes (chronic inflammation of low intensity, oxidative stress, endothelial dysfunction). These factors are common for a number of other pathological processes, promoting the development of systemic extrapulmonary effects and comorbid conditions. Endothelial dysfunction is of particular interest because it causes, first of all, cardiovascular system pathology. Therefore, modern treatment of COPD, in addition to the drugs approved by clinical protocols, must be supplemented by methods of endothelial dysfunction correction in the long-term management for patients beyond the exacerbation period, which at the same time have no negative effect on the disease course.   At present, medicines of various pharmacological groups with a positive effect on the endothelial function are known. Among them are those ones that replenish the deficiency of endothelial relaxing factors or have a direct effect on endothelial receptors; stimulate endothelial nitric oxide synthase activation; prevent endothelial dysfunction caused by mediator influences; regulate the blood coagulation system; provide protection from endothelial cell membrane damage or affect various pathogenetic links of the disease (inflammatory process, immune disorders, dysbiosis, etc.), that indirectly reduces endothelial dysfunction.   Conclusions. The key role of endothelial dysfunction in the formation of comorbid pathology in COPD, first of all lesions of cardiovascular system, determines the necessity for complex treatment of these patient groups with additional correction of endothelial dysfunction, especially in long-term management programs beyond the exacerbation period. Given the multifactorial mechanisms of endothelial dysfunction development, the treatment choice for its correction should be personalized taking into account all the disease peculiarities and the comorbid pathology spectrum.

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Today, chronic obstructive pulmonary disease is considered as a multifactorial disease with systemic extrapulmonary manifestations and a high level of comorbidity. Differentiation of the polymorbidity and comorbidity concepts for patients with this pathology is very important. The common trigger factors and/or pathogenetic mechanisms lay in the basis of comorbid conditions, and their progression is comparable in time with the underlying disease. This determines the necessity for appropriate integrated management of such patients. The presence of other diseases that are not related to the main pathological process through common causative factors and/or pathogenetic mechanisms should be regarded as concomitant and lying in the basis for polymorbidity. The domestic and foreign scientific literature data on the mechanisms of potential comorbid pathology in this group of patients have been summarized. Information concerning the leading role of oxidative stress and systemic inflammatory process of low intensity in the development of comorbidity in chronic obstructive pulmonary disease is presented. The mechanisms of their influence, relationship, discussion questions and actual data on genetic and molecular mechanisms of development of these pathological processes are highlighted. Special attention is paid to the metabolic processes that develop as a result of oxidative stress and systemic inflammation. In particular, it has been shown that systemic inflammation leads to the development of insulin resistance, diabetes and other metabolic disorders. Data is outlined, supporting rationale for stratification of the metabolic profiles or phenotypes, as well as the pathogenetic significance of endotoxemia. Endothelial dysfunction and associated diseases of the cardiovascular system are also the consequences of oxidative stress and systemic inflammation. The analysis has been performed for the peculiarities of the manifestations of some of them in this group of patients.

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The second part of the review examines in detail the questions of diagnostics and peculiarities of the metabolic syndrome manifestations, which presents the link between most comorbid conditions at patients with chronic obstructive pulmonary disease. The metabolic syndrome is based on the insulin resistance and compensatory hyperinsulinemia, caused by both chronic low‑intensity inflammation and increased adipose tissue, often against the background of aggravated heredity at diabetes mellitus. The authors elucidate aspects of the effects of obesity, cachexia and some endocrine disorders on the disease course. The deficiency of researches on endocrine status, especially thyroid function and related metabolic disorders was emphasized. Possible pathogenetic mechanisms of osteoporosis development in this contingent of patients are considered. The need for further research of the pathogenetic role of vitamin D is discussed. Data on the role of the functional state of kidneys in the development of metabolic disorders in an organism have been presented, though kidney pathology in patients with chronic obstructive pulmonary disease is not currently considered as a comorbid condition. The contradictory literature data on the development of anemia in these patients were analysed. The authors presented data on the development of oncological processes as a systemic manifestation at COPD and performed analysis of common and mutually aggravating mechanisms of the development of these pathological conditions. Attention has been paid to the relationship between gastroesophageal reflux disease, bronchiectasis and obstructive sleep apnea with chronic obstructive pulmonary disease. The prospects of modern genetic research in chronic obstructive pulmonary disease and comorbid conditions have been determined.