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Review
. 2010 Nov;16(6):574-82.
doi: 10.1097/MCP.0b013e32833f0d55.

Sleep-disordered breathing and pregnancy: potential mechanisms and evidence for maternal and fetal morbidity

Bilgay Izci-Balserak  1 , Grace W Pien
Affiliations
Review

Sleep-disordered breathing and pregnancy: potential mechanisms and evidence for maternal and fetal morbidity

Bilgay Izci-Balserak et al. Curr Opin Pulm Med. 2010 Nov.

Abstract

Purpose of review: This article reviews current data on pathophysiologic mechanisms by which sleep-disordered breathing during pregnancy may cause harm, and explores biological pathways for associated adverse maternal and fetal outcomes, especially pregnancy-induced hypertension and gestational diabetes.

Recent findings: Accumulating data indicate that snoring and sleep apnea during pregnancy are likely to increase the risk for gestational hypertension and preeclampsia. Several new studies have observed that sleep-disordered breathing and short sleep duration also increase the risk of gestational diabetes, similar to observations in the general population. There are varying levels of emerging evidence for potential mechanisms, including oxidative stress, increased sympathetic activity and inflammation, adipokine levels and insulin resistance, linking sleep-disordered breathing events during pregnancy to adverse outcomes.

Summary: Sleep-disordered breathing and adverse maternal-fetal outcomes such as preeclampsia and gestational diabetes share a number of mechanistic pathways, and growing data in pregnant women indicate that snoring and sleep apnea increase the risk of these and other complications for both the mother and the fetus. Nevertheless, direct evidence of the pathophysiologic mechanisms by which sleep-disordered breathing during pregnancy exerts negative effects remains sparse.

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Figures

Figure 1
Figure 1. Possible pathways for impact of sleep-disordered breathing on maternal and fetal outcomes
We propose that a number of causal pathways may link sleep during pregnancy with adverse pregnancy outcomes. 1) In the present model, short sleep duration (as a trait factor) may be a predisposing factor for adverse pregnancy outcomes. 2) Sleep loss may contribute to sleep disturbances and reduce sleep duration. 3) SDB can cause repeated arousal from sleep and intermittent hypoxemia. It should be noted that each of these phenomena (2 and 3) is probably not directly related to the various aspects of sleep disturbance, but instead has its own mediators and moderators. For the sake of simplicity, these are not contained in the schematic and include, but are not limited to, pregnancy-related physical changes affecting the respiratory system; pregnancy-related weight gain; and pregnancy-related changes in gonadotrophic hormones. 4) Short sleep duration due to sleep habits or sleep fragmentation and intermittent hypoxemia during pregnancy are associated with increased inflammatory cytokines such as tumor necrosis factor a, interleukin 6 and so on. Other predisposing factors, such as obesity and neuroendocrine changes, may also contribute to sleep disturbances and/or increased inflammation. 5) Arousals and nocturnal hypoxia due to complete or partial upper airway obstruction during sleep are linked with a reduction in both total sleep time and increased sympathetic activation. Elevated sympathetic activity is likely to be directly responsible, at least in part, for the glucose dysregulation and preeclampsia. 6) Increased oxidative stress due to the cyclical nature of hypoxia–reoxygenation has been shown to be an important mechanism for insulin resistance, the onset of diabetes and preeclampsia. 7) Intermittent hypoxia, disrupted sleep and inflammation lead to chronic HPA activation, which, in turn, causes decreased glucocorticoid sensitivity and increased inflammatory responses. 8) Adipokine levels are affected by oxidative stress, inflammation and sympathetic activation seen in SDB and may play a role in the pathogenesis of gestational diabetes mellitus and preeclampsia. These maternal metabolic and hormonal alterations associated with SDB may be implicated in the pathogenesis of adverse maternal and fetal complications. It should be noted that each of these phenomena (4, 5, 6, 7 and 8) is not likely directly related to the various adverse outcomes, but instead has its own mediators and moderators. HPA, hypothalamic–pituitary–adrenal; SDB, sleep-disordered breathing.
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References

    1. Izci B, Lee K. Sleep disturbances during pregnancy. In: Kryger M, Roth T, Dement W, editors. Principles and practice of sleep medicine. 5. Philadelphia: Saunders; 2010. (forthcoming)
    1. Maski KP, Kothare SV. Searching for marker of REM sleep behavior disorder: submentalis muscle EMG amplitude analysis during sleep in patients with narcolepsy/cataplexy. Sleep. 2009;32:137. - PMC - PubMed
    1. Arnardottir ES, Mackiewicz M, Gislason T, et al. Molecular signatures of obstructive sleep apnea in adults: a review and perspective. Sleep. 2009;32:447–470. - PMC - PubMed
    1. Izci-Balserak B. Sleep-disordered breathing in pregnancy. Int J Sleep Wakefulness. 2008;1:98–108.
    1. Pien GW, Schwab RJ. Sleep disorders during pregnancy. Sleep. 2004;27:1405–1417. - PubMed