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Clinical Investigations: SLEEP AND BREATHING |

Body Fat Distribution, Serum Leptin, and Cardiovascular Risk Factors in Men With Obstructive Sleep Apnea*

Harald Schäfer, MD; Dirk Pauleit, MD; Thomas Sudhop, MD; Ioanna Gouni-Berthold, MD; Santiago Ewig, MD; Heiner K. Berthold, MD, PhD
Author and Funding Information

*From the Department of Medicine II (Drs. Schäfer and Ewig), the Department of Radiology (Dr. Pauleit), the Department of Clinical Pharmacology (Drs. Sudhop and Berthold), and the Medical Policlinic (Dr. Gouni-Berthold), University of Bonn, Bonn, Germany.

Correspondence to: Harald Schäfer, MD, Department of Pulmonary Medicine, Klinikum Saarbruecken, PO Box 102629, 66026 Saarbruecken, Germany; e-mail: h.schaefer@klinikum-saarbruecken.de



Chest. 2002;122(3):829-839. doi:10.1378/chest.122.3.829
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Study objectives: To determine whether traditional risk factors for cardiovascular disease (CVD) and regional fat distribution, especially the central obesity type and increased parapharyngeal fat pads, are associated with the degree of obstructive sleep apnea (OSA). To determine whether there are interrelationships between body fat, serum leptin levels, and the degree of OSA.

Design and setting: Prospective mono-center cross-sectional study in a university hospital in Germany.

Patients: Eighty-five consecutive male patients who were referred for evaluation of suspected OSA.

Measurements and results: The major dependent outcome variable was the apnea-hypopnea index (AHI), the average number of apneas and hypopneas per hour of sleep, determined by overnight polysomnography. Independent measures were anthropometric data, body composition analysis (bioelectrical impedance analysis [BIA]), cardiovascular risk factor evaluation (smoking, hypertension, serum lipoproteins, diabetes or impaired glucose tolerance, uric acid, fibrinogen), and leptin. Adipose tissue quantification of the abdominal and neck regions was performed by nuclear MRI (NMR). Significant linear relationships of AHI with fasting blood glucose, uric acid, fibrinogen, body weight, body mass index (BMI), sum of fat skin folds, and percentage of body fat could be established, whereas there was no correlation with age. The presence of OSA was independent of smoking, hypertension, and lipoproteins. NMR scans showed that AHI was significantly correlated with intra-abdominal fat and subcutaneous abdominal fat, whereas subcutaneous fat in the neck region and parapharyngeal fat in the airway vicinity were not correlated. Leptin concentrations correlated with AHI and with biochemical markers of the metabolic syndrome (lipoproteins, glucose) but were not dependent on AHI. Logistic regression analysis found percentage of body fat (BIA) and BMI as good predictors of AHI > 10 with a sensitivity of 95.5% but a low specificity (46.2%). Multiple regression analysis identified the sum of fat skin folds, body weight, and BMI as good predictors for the degree of OSA.

Conclusions: We conclude that OSA is independent from most traditional risk factors for CVD. Regional body fat distribution predicts the presence and degree of OSA, but fat accumulation in the neck and parapharyngeal region are of minor importance. Leptin concentrations when controlled for body fat are not related to the degree of OSA.


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