Correlation of Epworth Sleepiness Scale with multiple sleep latency test and its diagnostic accuracy in assessing excessive daytime sleepiness in patients with obstructive sleep apnea hypopnea syndrome / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Excessive daytime sleepiness (EDS) is often associated with obstructive sleep apnea hypopnea syndrome (OSAHS) and contributes to a number of comorbidities in these patients. Therefore, early detection of EDS is critical in disease management. We examined the association between Epworth Sleepiness Scale (ESS) and multiple sleep latency test (MSLT) and diagnostic accuracy of ESS in assessing EDS in OSAHS patients.</p><p><b>METHODS</b>The ESS, MSLT and overnight polysomnography were administered to 107 Chinese patients to assess EDS and its correlations with polysomnographic parameters. The diagnostic accuracy of ESS in classifying EDS (mean sleep latency (MSL) ≤ 10 minutes) was evaluated by calculating the area under ROC curve.</p><p><b>RESULTS</b>As the severity of OSAHS increased, MSL decreased with increase in ESS score. Conversely, patients with worsening EDS (shorter MSL) were characterized by advanced nocturnal hypoxaemia and sleep disruption compared to those with normal MSL, suggesting EDS is associated with more severe OSAHS. There was a negative correlation between ESS score and MSL and both moderately correlated with some polysomnographic nocturnal hypoxaemic parameters. The area under ROC curve of ESS for identifying EDS was 0.80 (95% CI: 0.71 to 0.88) and ESS score ≥ 12 provided the best predictive value with a sensitivity of 80% and specificity of 69%.</p><p><b>CONCLUSION</b>The ESS score moderately correlates with MSL and our ROC study supports ESS as a screening strategy for assessing EDS in OSAHS.</p>

Changes in genioglossus and their association with serum adiponectin levels in rats subjected to chronic intermittent hypoxia / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The genioglossus (GG) is involved in the maintenance of an open airway for effective breathing. Although the pathogenesis of obstructive sleep apnea hypopnea syndrome (OSAHS) was closely associated with GG dysfunction, its causes and possible treatment have not been elucidated. The aim of the study was to investigate the effects of chronic intermittent hypoxia (CIH) on serum adiponectin levels, electromyograph (EMG) activity and ultrastructure of GG, as well as the effect of an adiponectin supplement in anesthetized rats.</p><p><b>METHODS</b>Forty-two healthy male Wistar rats were randomly divided into normal control (A), CIH (B) and adiponectin treatment (C) groups, 14 rats in each group. CIH was performed eight hours per day for five weeks in both groups B and C. Group C received transvenous injection of adiponectin at the dosage of 10 microg per injection, twice a week for five weeks. At the end of the 5th week the GG EMG voltage was measured and compared among the three groups. Transmission electron microscope was used to observe the ultrastructure of the GG.</p><p><b>RESULTS</b>CIH caused significant hypoadiponectinemia, weakened activity of GG EMG at both baseline and hypoxia stimulation, and induced ultrastructural pathological changes, such as, myofibril discontinuities, lysis of myofilament, edema of mitochondria and disruption of cristae, vacuolus and lysis of some mitochondria. Venous supplement of adiponectin improved the above pathological changes resulting from CIH.</p><p><b>CONCLUSION</b>CIH resulted in pathological changes in GG's EMG and ultrastructure, which could be improved by supplement of adiponectin and be associated with hypoadiponectinemia caused by CIH.</p>

Effect of chronic intermittent hypoxia on genioglossus and its intervention by adiponectin / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To investigate the effects of chronic intermittent hypoxia (CIH) on electromyograph (EMG) and ultrastructure of genioglossus (GG) and the interventive effects with adiponectin supplement.</p><p><b>METHODS</b>Forty-two healthy male Wistar rats were randomly divided into normal control (A), CIH (B) and adiponectin treatment (C) groups with 14 rats in each. CIH was performed 8 hours per day for 5 weeks in both group B and C. In group C, transvenous injection of adiponectin of 10 microg dosage each time, twice a week for 5 weeks. While in group A and B, transvenous injection of saline was performed twice a week for 5 weeks. At the beginning of 6th week the GG EMG voltages were measured before, during and following hypoxia stimulation by inserted bipolar needle electrodes and compared among three groups. Transmission electron microscope was used for observation of ultrastructure of GG.</p><p><b>RESULTS</b>The serum adiponectin level in group B (1226.0 +/- 112.0) ng/ml (x(-) +/- s) was significantly lower than that in group A (2491.8 +/- 117.9) ng/ml, q = 38.2, P < 0.01), and adiponectin level in group C (1988.3 +/- 114.7) ng/ml was significantly higher than that in group B (q = 23.0, P < 0.01). Comparison of GG EMG activity showed that the baseline amplitude of GG EMG before hypoxia stimulation was significantly lower in group B than that in both group A and group C (all P < 0.01). At the 5th min of hypoxia stimulation the GG EMG activities were significantly enhanced among three groups (all P < 0.01). Such an enhancement was the most evident in group A but the least remarkable in group B, with a significant difference among three groups (q(ab) = 17.5; q(ac) = 8.9; q(bc) = 8.6, all P < 0.01). 15 min, 30 min and 45 min after hypoxia stimulation the amplitude of GG EMG remained at relative higher levels in group A and C, significantly higher than that in group B (all P < 0.01). CIH could cause significant ultrastructural pathological changes such as myofibril discontinuities, lysis of myofilament, edema of mitochondria and disruption of cristae, vacuoles and lysis of some mitochondria in group B. Venous supplement of adiponectin could improve pathological changes resulting from CIH.</p><p><b>CONCLUSIONS</b>CIH could resulted in pathological changes in EMG and ultrastructure of GG, which might be associated with hypoadiponectinemia caused by CIH.</p>