2022
DOI: 10.1016/j.arbres.2021.05.005
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Impact of Obstructive Sleep Apnea on Gestational Diabetes Mellitus

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Cited by 14 publications
(10 citation statements)
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“…Our study aim was to compare inflammatory/sympathetic biomarkers in women with GDM with and without OSA, and the sample size of the present study may be not sufficiently powered to find differences in the sleep symptoms. As other studies, we did not find differences in subjective self-reported OSA symptoms among OSA and control subjects (Table 2 ) [ 15 , 19 ].…”
Section: Discussionsupporting
confidence: 70%
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“…Our study aim was to compare inflammatory/sympathetic biomarkers in women with GDM with and without OSA, and the sample size of the present study may be not sufficiently powered to find differences in the sleep symptoms. As other studies, we did not find differences in subjective self-reported OSA symptoms among OSA and control subjects (Table 2 ) [ 15 , 19 ].…”
Section: Discussionsupporting
confidence: 70%
“…Previous studies did not find differences in subjective sleep time or daytime sleepiness when comparing OSA and non-OSA pregnant women with GDM [ 15 , 19 ]. Also, ESS shows low predictive value of OSA during pregnancy [ 20 ].…”
Section: Discussionmentioning
confidence: 97%
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“…repeated exposure to stressful situations caused by poor sleep quality increases the amount of cortisol secretion, leading to decreased pancreatic function and increased risk of diabetes. [10][11][12] Also, repeated stoppage of the respiratory system reduces air circulation, which can increase the incidence of respiratory diseases such as pneumonia. 13,14 It is necessary to be fully aware of the risks of OSA, which can cause these chronic diseases, and to actively treat them.…”
Section: Resultsmentioning
confidence: 99%
“…The main consequence of OSA is nocturnal intermittent hypoxaemia, which, in turn, sets in motion a series of mechanisms capable of intensifying cardiovascular risk factors such as arteriosclerosis and arterial hypertension, as well as cardiovascular events, metabolic dysfunction and neuropsychiatric diseases, and making them more difficult to control [6]. Among the pathophysiological mechanisms mediated by intermittent hypoxemia to produce these phenomena are: sympathetic hyperactivity, increased plasma volume, RAS hyperactivity, increased peripheral insulin resistance, hypercoagulability, endothelial dysfunction, nocturnal fluid redistribution, sleep inefficiency, oxidative stress and inflammation [7][8][9][10][11][12][13]. Therefore, even in an initial approximation, it is already clear that some of the mechanisms capable of generating the aforementioned phenotypes of nocturnal arterial hypertension are similar to those that produce the respiratory events during sleep that define OSA.…”
Section: T He Latest European Society Of Hypertension (Esh)mentioning
confidence: 99%