Dataset Information

Mechanism of Gastroesophageal Reflux in Obstructive Sleep Apnea: Airway Obstruction or Obesity?

ABSTRACT:

Study objectives

This is the first study to compare reflux events during wake and sleep in obese and non-obese individuals with obstructive sleep apnea (OSA) and obese individuals without OSA. The primary aim of the study was to investigate any additive effect of OSA on gastroesophageal reflux (GER) above that of obesity.

Methods

Twenty obese individuals (body mass index, BMI > 30 kg/m(2)), 9 non-obese individuals (BMI < 30 kg/m(2)) with moderate-to-severe OSA, and 17 obese control subjects (BMI > 30 kg/m(2)) underwent high-resolution esophageal manometry, 24-h esophageal pH-impedance monitoring, and in-laboratory polysomnography.

Results

Mean body mass index was 40 ± 6 and 27 ± 4 kg/m(2) for the obese and non-obese OSA groups, respectively, and 34 ± 5 kg/m(2) for the obese control group. Apnea-hypopnea index (AHI) was 50 ± 30 and 30 ± 25 per hour for the obese and non-obese OSA groups (p > 0.05), significantly higher than that of the obese control group (3 ± 3 per hour, p < 0.05). The two obese groups did not show any significant differences in the total number of acidic reflux events (41 ± 20 vs 28 ± 16); however, the obese OSA group had a greater number of acidic reflux events compared to the non-obese OSA group (22 ± 12 events, p < 0.05). In multivariate analysis, BMI significantly predicted number of acidic reflux events (r(2) = 0.16, p = 0.01) during the 24-h period; however, AHI showed no significant association with any measure of GER severity.

Conclusions

This study confirms an important role for obesity, rather than OSA per se in the relationship between OSA and GER.

SUBMITTER: Shepherd K

PROVIDER: S-EPMC4702204 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature

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Publications

Mechanism of Gastroesophageal Reflux in Obstructive Sleep Apnea: Airway Obstruction or Obesity?

Shepherd Kelly K Orr William W

Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine 20160101 1

<h4>Study objectives</h4>This is the first study to compare reflux events during wake and sleep in obese and non-obese individuals with obstructive sleep apnea (OSA) and obese individuals without OSA. The primary aim of the study was to investigate any additive effect of OSA on gastroesophageal reflux (GER) above that of obesity.<h4>Methods</h4>Twenty obese individuals (body mass index, BMI > 30 kg/m(2)), 9 non-obese individuals (BMI < 30 kg/m(2)) with moderate-to-severe OSA, and 17 obese contro ...[more]

PMID: 26446244

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Project description:BackgroundThe interactions and associations between obstructive sleep apnea (OSA), sleep-related phenotypes (SRPs), and gastroesophageal reflux disease (GERD) are complex, thus it is hard to explore the effect and direction of causalities.Study objectivesA bidirectional Mendelian randomization (MR) study was performed to explore causal associations of GERD with OSA and SRPs (including insomnia, morningness, sleep duration, ease of getting up, daytime napping, daytime dozing, and snoring).MethodsFirst, we gathered summary statistics from publicly available databases. Subsequently, we identified single-nucleotide polymorphisms without strong linkage (r2 ≤ 0.001) by referencing relevant genome-wide association studies that met genome-wide significance criteria. Our primary analysis relied on inverse variance weighted to estimate the causal relationship. To ensure the validity of our findings, we also conducted several sensitivity analyses. These included MR Pleiotropy RESidual Sum and Outlier to detect and correct for potential pleiotropic effects, MR-Egger to assess directional pleiotropy, and weighted median analysis to further evaluate heterogeneity and pleiotropy. For the initial MR analysis, when causality was indicated by the results, instrumental variables that were significantly linked to the aforementioned confounding factors were removed. We will re-analyze the data after excluding outcome-related single nucleotide polymorphisms to confirm that the results are still consistent with the previous results.ResultsGERD was found to increase the risk of OSA (OR = 1.53, 95% CI = 1.37-1.70, p = 5.3 × 10-15), insomnia (OR = 1.14, 95% CI = 1.10-1.19, p = 1.3 × 10-10), snoring (OR = 1.09, 95% CI = 1.04-1.13, p = 6.3 × 10-5) and less sleep duration (OR = 0.94, 95% CI = 0.91-0.97, p = 3.7 × 10-4). According to the reverse-direction analysis, there is an elevated risk of GERD associated with OSA (OR = 1.07, 95% CI = 1.02-1.12, p = 0.005), insomnia (OR = 1.95, 95% CI = 1.60-2.37, p = 1.92 × 10-11) and snoring (OR = 1.74, 95% CI = 1.37-2.21, p = 4.4 × 10-6).ConclusionGenetic susceptibility to GERD can elevate the likelihood of experiencing insomnia, snoring, and OSA, in addition to diminishing sleep duration. Conversely, a reverse MR analysis indicates that ameliorating any one of insomnia, snoring, or OSA can mitigate the risk of developing GERD.

Project description:Study objectivesDrug-induced sleep endoscopy (DISE) using propofol is commonly used to identify the pharyngeal structure involved in collapse among patients with obstructive sleep apnea. DISE has never been compared with zolpidem-induced sleep endoscopy. We hypothesized that propofol at recommended sedation levels does not influence upper airway collapsibility nor the frequency of multilevel pharyngeal collapse as compared with zolpidem-induced sleep.MethodsTwenty-one patients with obstructive sleep apnea underwent polysomnography and sleep endoscopy during zolpidem-induced sleep and during DISE with propofol. A propofol target-controlled infusion was titrated to achieve a bispectral index between 50 and 70. Airway collapsibility was estimated and compared in both conditions by peak inspiratory flow and the magnitude of negative effort dependence. Respiratory drive was estimated by the difference between end-expiratory and peak-negative inspiratory pharyngeal pressure (driving pressure). Site and configuration of pharyngeal collapse during zolpidem-induced sleep and DISE with propofol were compared.ResultsThe frequency of multilevel collapse during zolpidem-induced sleep was similar to that observed during DISE with propofol (72% vs 86%, respectively; difference: 14%; 95% confidence interval: -12% to 40%; P = .453). The endoscopic classification of pharyngeal collapse during both conditions were similar. Peak inspiratory flow, respiratory drive (effect size: 0.05 and 0.03, respectively), and negative effort dependence (difference: -6%; 95% confidence interval: -16% to 4%) were also similar in both procedures.ConclusionsIn this pilot study, recommended propofol doses did not significantly increase multilevel pharyngeal collapse or affect upper airway collapsibility and respiratory drive as compared with zolpidem-induced sleep.Clinical trial registrationRegistry: clinicaltrials.gov; Name: Natural and Drug Sleep Endoscopy; URL: https://clinicaltrials.gov/ct2/show/study/NCT03004014; Identifier: NCT03004014.

Dataset Information

Mechanism of Gastroesophageal Reflux in Obstructive Sleep Apnea: Airway Obstruction or Obesity?

Study objectives

Methods

Results

Conclusions

Publications

Mechanism of Gastroesophageal Reflux in Obstructive Sleep Apnea: Airway Obstruction or Obesity?

Similar Datasets

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