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Rationale: Incretin hormones, namely glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide/glucose-dependent insulinotropic polypeptide (GIP), and dipeptidyl peptidase-4 (DPP-4) activity are important factors in glucose metabolism and have not been investigated in patients with obstructive sleep apnea (OSA).Objectives: The objective of this study was to investigate the association between OSA and incretin and DPP-4 activity.Methods: This study included 96 consecutive patients without diabetes who were suspected of having OSA. We investigated the fasting and post-prandial incremental area under the curve (IAUC) of GLP-1, GIP serum levels, and serum DPP-4 activity levels, as well as their association with OSA. Changes in clinical variables were evaluated in the 43 patients who continued continuous positive airway pressure therapy for 3 months.Measurements and Main Results: Apnea-hypopnea index was an independent determining factor for fasting GLP-1 (β = 0.31; P = 0.0019) and IAUC GIP (β = -0.21; P = 0.037) after adjusting for known confounding factors. In those with very severe OSA (apnea-hypopnea index ≥50), the IAUCs for GLP-1 and GIP were significantly decreased, while fasting GLP-1 and fasting GIP were significantly increased. DPP-4 activity had no relation to OSA parameters or severity, while body mass index was significantly higher in those with severe OSA. Although significant changes in incretin secretion were not seen for 3 months after onset of continuous positive airway pressure therapy, the fasting GLP-1 level in the treated patients with severe OSA decreased to the same level as in untreated patients with normal to moderately severe OSA.Conclusions: OSA is associated with elevated serum levels of the incretin hormones GLP-1 (fasting) and GIP (post-prandial) in patients without diabetes. A significant association between body mass index and DPP-4, which is said to exist in healthy persons, was not found in the patients with OSA. Fasting GLP-1 in patients without diabetes with OSA may influence fasting glucose levels. [ABSTRACT FROM AUTHOR]

Summary: Background: The level at which arterial carbon dioxide tension (PaCO2) a few months after introduction of long-term non-invasive positive pressure ventilation (NPPV) is associated with a favorable prognosis remains uncertain. Methods: Data on 184 post-tuberculosis patients with chronic restrictive ventilatory failure who were receiving long-term domiciliary NPPV were examined retrospectively. Average PaCO2 3–6 months after NPPV (3- to 6-mo PaCO2) and potential confounders were analyzed with discontinuation of long-term NPPV as the primary outcome. The effects of 3- to 6-mo PaCO2 on annual hospitalization rates due to respiratory deterioration from 1 year before to 3 years after the initiation of NPPV were examined. The effect of the difference between the PaCO2 value at the start of NPPV (0-mo PaCO2) and the PaCO2 value 3- to 6-mo later (d-PaCO2) on continuation rates for NPPV was also assessed in patients who initiated NPPV while in a chronic state. Results: Patients with relatively low 3- to 6-mo PaCO2 values maintained a relatively low PaCO2 6–36 months after NPPV (p < 0.0001) and had significantly better continuation rates (p < 0.03) and lower hospitalization rates from the 1st to 3rd year of NPPV (p = 0.008, 0.049, 0.009, respectively) than those with higher levels. The 0-mo PaCO2 (p = 0.26) or d-PaCO2 (p = 0.86) had no predictive value. Conclusion: A relatively low 3- to 6-mo PaCO2 value was predictive of long-term use of NPPV. The target values for 3- to 6-mo PaCO2 may, therefore, be less than 60 mmHg in post-tuberculosis patients, although more studies are needed. [Copyright &y& Elsevier]

Objective The effects of partial pressure of arterial oxygen (PaO 2 ) after introducing long-term noninvasive ventilation (NIV) on the prognosis of patients with restrictive thoracic disease and chronic respiratory failure are not exactly known. Methods Data from 141 patients with restrictive thoracic disease under long-term nocturnal NIV were retrospectively examined. We divided the patients into 2 groups according to the daytime PaO 2 value while breathing spontaneously with prescribed oxygen at 12 months after introducing NIV: PaO 2 ≥80 Torr group (n=76) and PaO 2 <80 Torr group (n=65). Results During the 4-year follow-up, the mortality was significantly higher in the PaO 2 <80 Torr group than in the PaO 2 ≥80 Torr group (50.8% vs. 32.9%, p=0.03). Independent factors associated with the 4-year mortality after introducing NIV determined by a multivariate logistic regression analysis were a low body mass index [odds ratio (OR) 0.87; 95% confidence interval (CI) 0.77 to 0.97; p=0.01], assisted mode with NIV (OR 4.11; 95% CI, 1.79 to 9.45; p=0.0009), hospitalization during the first year of introducing NIV (OR 1.72; 95% CI, 1.06 to 2.79; p=0.03), and daytime PaO 2 <80 Torr at 12 months after introducing NIV (OR 2.30; 95% CI, 1.03 to 5.10; p=0.04). Conclusion A low daytime PaO 2 at 12 months after introducing NIV was an independent risk factor for mortality. Keeping the daytime PaO 2 ≥80 Torr through the adjustment of the nocturnal NIV settings or increased diurnal supplemental oxygen may help improve the prognosis in patients with restrictive thoracic disease who are under NIV.

Lipocalin-type prostaglandin D synthase (L-PGDS), which is responsible for the biosynthesis of prostaglandin D2, has been reported to have a close connection with cardiovascular disease and sleep regulation. This study aimed to test the hypothesis that the L-PGDS level is a useful marker to identify patients with obstructive sleep apnoea. 64 subjects were enrolled in this prospective study. Urinary concentrations of L-PGDS were measured in the morning. Measurements were made every 4 h in 25 of the 64 patients. Endothelial function was assessed by the reactive hyperaemia peripheral arterial tone index. Circadian variations in L-PGDS concentrations had a significant time-dependent fluctuation (p = 0.0002). L-PGDS was higher in the subjects with severe obstructive sleep apnoea (median 784.7 ng per mg of creatinine, n = 23) than in control subjects (262.1 ng per mg of creatinine, n = 16; p = 0.004) and in those with moderate obstructive sleep apnoea (371.7 ng per mg of creatinine, n = 25; p = 0.0008). After 2 days of continuous positive airway pressure treatment, L-PGDS concentrations in severe obstructive sleep apnoea subjects (n = 12) decreased significantly (p = 0.02) to levels present in control subjects whereas endothelial function did not change significantly. Morning urinary L-PGDS concentrations had significant correlations with the apnoea/hypopnoea index (R2 = 13.9%) and serum high-density lipoprotein cholesterol (R2 = 6.2%), but not with sleepiness. Urinary L-PGDS might be a moderately useful marker to identify patients with severe obstructive sleep apnoea.