No abstract

Nasal continuous positive airway pressure (nasal CPAP) and polysomnography were used to analyze the time course of the effect of bedtime ethanol on resistance of upper airways and on the number of respiratory pauses during sleep. On one night, six asymptomatic nonalcoholic male snorers drank 2 ml/kg of 100 proof vodka mixed in orange juice (ethanol dose, 0.79 gm/kg, giving a peak blood alcohol level of 71.8 +/- 33.3 mg/dl). On a second night they received a placebo (1-2 drops of vodka floated on top of the orange juice). We measured (a) the minimum nasal (CPAP) required to eliminate snoring, (b) the number of hypopneas and apneas during each hour of sleep and (c) the arterial oxygen saturation (SaO2) by ear oximetry. On the alcohol night there was a significant increase in the CPAP pressure required to eliminate snoring (placebo 4.8 +/- 1.7 cm H2O, alcohol 6.2 +/- 1.5 cm H2O). The number of respiratory events per hour of sleep (apnea index) was 7.5 +/- 2.1 for ethanol nights versus 3.8 +/- 2.7 for placebo nights (p less than 0.0125). An apnea index of greater than 5 is generally considered abnormal. There was no significant difference in the number of desaturation events (declines of 4% or more in the SaO2) or in the mean SaO2, but the minimum SaO2 was significantly lower on the ethanol night (placebo 89.8% +/- 1.6, alcohol 86.8% +/- 2.7, p less than 0.05). The effect of this dose of alcohol on airway resistance was most pronounced during the first 2 hr after ingestion.

SciEnTific invESTigATiOnSBackground: Type 2 diabetes and obstructive sleep apnea (OSA) are frequently comorbid conditions. OSA is associated with increased insulin resistance, but studies of continuous positive airway pressure (CPAP) have shown inconsistent effects on glycemic control. However, endpoints such as hemoglobin A1c and insulin sensitivity might not reflect short-term changes in glycemic control during sleep. Methods: We used a continuous glucose-monitoring system to measure interstitial glucose every 5 minutes during polysomnography in 20 patients with type 2 diabetes and newly diagnosed OSA. The measurements were repeated after an average of 41 days of CPAP (range 26-96 days). All patients were on a stable diet and medications. Each 30-second epoch of the polysomnogram was matched with a continu-second epoch of the polysomnogram was matched with a continu-epoch of the polysomnogram was matched with a continuous glucose-monitoring system reading, and the sleeping glucose level was calculated as the average for all epochs scored as sleeping. Results: The mean sleeping glucose decreased from untreated (122.0 ± 61.7 mg/dL) to treated (102.9 ± 39.4 mg/dL; p = 0.03 by Wilcoxon paired rank test). The sleeping glucose was more stable after treatment, with the median SD decreasing from 20.0 to 13.0 mg/dL (p = 0.005) and the mean difference between maximum and minimum values decreasing from 88 to 57 mg/dL (p = 0.003). The change in the mean hemoglobin A1c from 7.1% to 7.2% was not significant. conclusions: Our study is limited by the lack of a control group, but the results suggest that sleeping glucose levels decrease and are more stable after patients with type 2 diabetes and OSA are treated with CPAP.

Recent meta-analyses raising concern about risks of hypnotics suggest a need for more clarification of these risks. Methods: Because of preliminary suggestions that eszopiclone causes infections, we studied US Food and Drug Administration files on the 4 most-recently approved hypnotics, combined with published studies, to compile the risk ratios of infections for groups randomly assigned to receive hypnotics versus those assigned to receive placebos in controlled trials. Parallel controlled clinical trials of eszopiclone, ramelteon, zaleplon, and zolpidem were included when data on subjects, duration of exposure, and adverse effects were available. Results of trials were combined by meta-analyses. Results: Of 8828 participants assigned to the 4 hypnotics and 4383 participants who randomly received placebos, 606 in the hypnotics groups and 200 in the placebo groups were reported to develop some kind of infection (risk ratio = 1.44, 95% confidence interval 1.25-1.64, p < 0.00001). Most infections were apparently mild and did not lead to dropouts. Subanalyses for individual drugs indicated that eszopiclone and zolpidem individually were associated with reported infections. There were insufficient data concerning individual studies of zaleplon and ramelteon for valid secondary meta-analyses of zaleplon or ramelteon by themselves. Conclusions: Research is needed to objectively determine whether the use of hypnotics increases the risk of infections. Immune compromise or esophageal reflux and aspiration should be studied as possible mechanisms.