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      The Ventilatory and Diffusion Dysfunctions in Obese Patients with and without Obstructive Sleep Apnea-Hypopnea Syndrome

      research-article
      1 , 2 , , 1 , 2 , 1 , 1 , 2
      Journal of Obesity
      Hindawi

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          Abstract

          Objective

          To analyze the ventilatory and alveolar-capillary diffusion dysfunctions in case of obesity with or without an OSAS.

          Methods

          It is a cross-sectional study of 48 obese adults (23 OSAS and 25 controls). Anthropometric data (height, weight, and body mass index (BMI)) were collected. All adults responded to a medical questionnaire and underwent polysomnography or sleep polygraphy for apnea-hypopnea index (AHI) and percentage of desaturation measurements. The following lung function data were collected: pulmonary flows and volumes, lung transfer factor for carbon monoxide (DLCO), and fraction of exhaled nitric oxide (F eNO).

          Results

          Obesity was confirmed for the two groups with a total sample mean value of BMI = 35.06 ± 4.68 kg/m 2. A significant decrease in lung function was noted in patients with OSAS compared with controls. Indeed, when compared with the control group, the OSAS one had a severe restrictive ventilatory defect (total lung capacity: 93 ± 14 vs. 79 ± 12%), an abnormal DLCO (112 ± 20 vs. 93 ± 22%), and higher bronchial inflammation (18.40 ± 9.20 vs. 31.30 ± 13.60 ppb) ( p < 0.05).

          Conclusion

          Obesity when associated with OSAS increases the severity of pulmonary function and alveolar-capillary diffusion alteration. This can be explained in part by the alveolar inflammation.

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          Most cited references41

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          Estimation of the clinically diagnosed proportion of sleep apnea syndrome in middle-aged men and women.

          The proportion of sleep apnea syndrome (SAS) in the general adult population that goes undiagnosed was estimated from a sample of 4,925 employed adults. Questionnaire data on doctor-diagnosed sleep apnea were followed up to ascertain the prevalence of diagnosed sleep apnea. In-laboratory polysomnography on a subset of 1,090 participants was used to estimate screen-detected sleep apnea. In this population, without obvious barriers to health care for sleep disorders, we estimate that 93% of women and 82% of men with moderate to severe SAS have not been clinically diagnosed. These findings provide a baseline for assessing health care resource needs for sleep apnea.
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            Obstructive sleep apnea-hypopnea and related clinical features in a population-based sample of subjects aged 30 to 70 yr.

            The prevalence and related clinical features of obstructive sleep apnea-hypopnea (OSAH) in the general population were estimated in a two-phase cross-sectional study. The first phase, completed by 2,148 subjects (76.9%), included a home survey, blood pressure, and a portable respiratory recording, whereas in the second, subjects with suspected OSAH (n = 442) and a subgroup of those with normal results (n = 305) were invited to undergo polysomnography (555 accepted). Habitual snoring was found in 35% of the population and breathing pauses in 6%. Both features occurred more frequently in men, showed a trend to increase with age, and were significantly associated with OSAH. Daytime hypersomnolence occurred in 18% of the subjects and was not associated with OSAH. An apnea-hypopnea index (AHI) > or = 10 was found in 19% of men and 15% of women. The prevalence of OSAH (AHI > or = 5) increased with age in both sexes, with an odds ratio (OR) of 2.2 for each 10-yr increase. AHI was associated with hypertension after adjusting for age, sex, body mass index, neck circumference, alcohol use, and smoking habit. This study adds evidence for a link between OSAH and hypertension.
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              Obstructive sleep apnea: a cardiometabolic risk in obesity and the metabolic syndrome.

              Obstructive sleep apnea (OSA) is an underdiagnosed condition characterized by recurrent episodes of obstruction of the upper airway leading to sleep fragmentation and intermittent hypoxia during sleep. Obesity predisposes to OSA, and the prevalence of OSA is increasing worldwide because of the ongoing epidemic of obesity. Recent evidence has shown that surrogate markers of cardiovascular risk, including sympathetic activation, systemic inflammation, and endothelial dysfunction, are significantly increased in obese patients with OSA versus those without OSA, suggesting that OSA is not simply an epiphenomenon of obesity. Moreover, findings from animal models and patients with OSA show that intermittent hypoxia exacerbates the metabolic dysfunction of obesity, augmenting insulin resistance and nonalcoholic fatty liver disease. In patients with the metabolic syndrome, the prevalence of moderate to severe OSA is very high (∼60%). In this population, OSA is independently associated with increased glucose and triglyceride levels as well as markers of inflammation, arterial stiffness, and atherosclerosis. A recent randomized, controlled, crossover study showed that effective treatment of OSA with continuous positive airway pressure for 3 months significantly reduced several components of the metabolic syndrome, including blood pressure, triglyceride levels, and visceral fat. Finally, several cohort studies have consistently shown that OSA is associated with increased cardiovascular mortality, independent of obesity. Taken together, these results support the concept that OSA exacerbates the cardiometabolic risk attributed to obesity and the metabolic syndrome. Recognition and treatment of OSA may decrease the cardiovascular risk in obese patients. Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Journal
                J Obes
                J Obes
                JOBE
                Journal of Obesity
                Hindawi
                2090-0708
                2090-0716
                2020
                10 February 2020
                : 2020
                : 8075482
                Affiliations
                1Laboratory of Physiology and Explorations, Faculty of Medicine Sousse, University of Sousse, Sousse, Tunisia
                2Heart Failure (LR12SP09) Research Laboratory, Farhat Hached Hospital, Sousse, Tunisia
                Author notes

                Academic Editor: Mario Musella

                Author information
                https://orcid.org/0000-0003-1347-0100
                https://orcid.org/0000-0002-7477-2965
                Article
                10.1155/2020/8075482
                7035560
                32104601
                6d6e3909-631d-4f29-98a5-dd5c3b50cb36
                Copyright © 2020 Sonia Rouatbi et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 2 July 2019
                : 11 January 2020
                : 14 January 2020
                Categories
                Research Article

                Nutrition & Dietetics
                Nutrition & Dietetics

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