[Parasternal curvature in a sports rifleman].
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Biomedical subjects
Publications and source records attributed to Joachim H Ficker.
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The obstructive sleep apnea syndrome is typically associated with conditions known to increase insulin resistance as hypertension, obesity, and diabetes. We investigated whether obstructive sleep apnea itself is an independent risk factor for increased insulin resistance and whether continuous positive airway pressure (CPAP) treatment improves insulin sensitivity. Forty patients (apnea-hypopnea index > 20) were treated with CPAP. Before, 2 days after, and after 3 months of effective CPAP treatment, hyperinsulinemic euglycemic clamp studies were performed. Insulin sensitivity significantly increased after 2 days (5.75 +/- 4.20 baseline versus 6.79 +/- 4.91 micromol/kg.min; p = 0.003) and remained stable after 3 months of treatment. The improvement in insulin sensitivity after 2 days was much greater in patients with a body mass index less than 30 kg/m2 than in more obese patients. The improved insulin sensitivity after 2 nights of treatment may reflect a decreasing sympathetic activity, indicating that sleep apnea is an independent risk factor for increased insulin resistance. The effect of CPAP on insulin sensitivity is smaller in obese patients than in nonobese patients, suggesting that in obese individuals insulin sensitivity is mainly determined by obesity and, to a smaller extent, by sleep apnea.
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STUDY OBJECTIVES: To investigate the frequency of microarousals (MA) associated with pressure changes during auto-CPAP therapy (APAP) for obstructive sleep apnea (OSA). DESIGN: Patients with OSA were studied by polysomnography during APAP therapy (Somnosmart). The MA were classified on the basis of concomitant changes in APAP pressure. SETTING: Sleep laboratory of a university hospital PARTICIPANTS: 30 patients with moderate to severe OSA. MEASUREMENTS AND RESULTS: The mean AHI during APAP was 4.7+/-4.7, the mean arousal index was 14.5+/-6.6 per hour. During epochs with a pressure variation greater than 0.5 mbar, significantly more MA occurred (0.30+/-0.17 MA per epoch) than in epochs with constant treatment pressure (0.10+/-0.054 MA per epoch; p<0.001). There were more MA during pressure-increase epochs than during pressure-decrease epochs (0.42+/-0.24 vs. 0.16+/-0.12 MA per epoch; p<0.001). 82.5 percent of the MA were not preceded by a significant change in pressure (at least 0.5 mbar within 30 sec.), 10.6% were associated with a significant prior increase and 6.9% with a significant prior decrease in pressure. The percentage of MA preceded by a significant pressure variation varied between 2.3% and 61%, with a mean of 18.9%. CONCLUSIONS: The overall frequency of MA was low, and in most individuals the relative amount of "pressure-associated MA" was not significant. However in some individuals it cannot be excluded that some additional MA may have been induced by pressure variations. Should it prove possible to prevent such "pressure-associated MA" by optimizing the regulation of APAP pressure, the overall clinical effect of APAP treatment may be improved.
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OBJECTIVE: Launois-Bensaude Syndrome (LBS) is a very rare cause of obesity, characterized by a symmetrical accumulation of a very large number of lipomata in different regions of the body, excluding the face, the forearms, and the shanks. Obesity is known to be closely associated with insulin resistance, hyperleptinemia, and obstructive sleep apnea (OSA). We were interested in studying whether these conditions are also present in patients with obesity due to LBS with a similar frequency as in patients with "simple" truncal obesity. RESEARCH METHODS AND PROCEDURES: We performed polysomnography and hyperinsulinemic euglycemic clamp studies and measured serum leptin in three patients with LBS and in six patients with "simple" truncal obesity, matched for sex and body mass index (LBS group, 36.39 kg/m(2); controls, 35.82 kg/m(2)). RESULTS: Polysomnography revealed severe OSA in one LBS patient with marked "horsecollar lipomata." In the other LBS patients, no OSA could be demonstrated. The leptin levels of the two groups were comparable (LBS group, 36.39 microg/liter; controls, 37.18 microg/liter) and the insulin responsiveness index was also comparable in the two groups (LBS group, 3.47 micromol/kg. minute; controls, 3.79 micromol/kg. minute). DISCUSSION: Patients with LBS demonstrated similar metabolic features in terms of insulin sensitivity and hyperleptinemia as patients with "simple" truncal obesity. LBS is not strictly associated with OSA.