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The role of system inflammation in bronchial asthma and obesity

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The prevalence of bronchial asthma and obesity has grown in the recent decades worldwide. The urgency of this problem due to its medical and social significance for the society in connection with a reduction of patients ‘ quality of life and considerable economic damage to the health system. The relationship of these diseases, there are gender-related, age-related characteristics no doubt. Growing clinical-epidemiological evidence indicates that obesity might be an independent risk factor for bronchial asthma. On the other hand, the clinical data of bronchial asthma is a consequence of obesity remain indicative. The presence of concomitant obesity, bronchial asthma is considered as a state, significantly worsens its course. Etiology the causal relationship between obesity and asthma, despite the proposed mechanical, immunological, genetic and hormonal concepts still remains unclear. The underlying mechanism for this association is still unclear although several theories have been postulated in an attempt to describe it. Many studies demonstrate that bronchial asthma and obesity have some common mechanisms, including chronic systemic inflammation. In the review, we outline the current understanding of the role of systemic inflammation linked to obesity in the pathophysiology of bronchial asthma. An important role in the pathophysiology of systemic inflammation is given to changing levels of key adipose tissue hormones - leptin and adiponectin, respectively, having proinflammatory and anti-inflammatory activity. '/'his review article will focus on the leptin and adiponectin. Understanding the mechanisms of correlation between the metabolic activity of adipose tissue and the functional status of the respiratory tract with the development of systemic inflammation with comorbid asthma and obesity will review a number of existing provisions for the diagnosis and treatment of associated course of these diseases, to expand understanding the phenotypes of asthma and to develop new treatment strategies.
Title: The role of system inflammation in bronchial asthma and obesity
Description:
The prevalence of bronchial asthma and obesity has grown in the recent decades worldwide.
The urgency of this problem due to its medical and social significance for the society in connection with a reduction of patients ‘ quality of life and considerable economic damage to the health system.
The relationship of these diseases, there are gender-related, age-related characteristics no doubt.
Growing clinical-epidemiological evidence indicates that obesity might be an independent risk factor for bronchial asthma.
On the other hand, the clinical data of bronchial asthma is a consequence of obesity remain indicative.
The presence of concomitant obesity, bronchial asthma is considered as a state, significantly worsens its course.
Etiology the causal relationship between obesity and asthma, despite the proposed mechanical, immunological, genetic and hormonal concepts still remains unclear.
The underlying mechanism for this association is still unclear although several theories have been postulated in an attempt to describe it.
Many studies demonstrate that bronchial asthma and obesity have some common mechanisms, including chronic systemic inflammation.
In the review, we outline the current understanding of the role of systemic inflammation linked to obesity in the pathophysiology of bronchial asthma.
An important role in the pathophysiology of systemic inflammation is given to changing levels of key adipose tissue hormones - leptin and adiponectin, respectively, having proinflammatory and anti-inflammatory activity.
'/'his review article will focus on the leptin and adiponectin.
Understanding the mechanisms of correlation between the metabolic activity of adipose tissue and the functional status of the respiratory tract with the development of systemic inflammation with comorbid asthma and obesity will review a number of existing provisions for the diagnosis and treatment of associated course of these diseases, to expand understanding the phenotypes of asthma and to develop new treatment strategies.

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