Abstract

Obstructive sleep apnea–hypopnea syndrome (OSAHS) is frequently present in patients with severe obesity, but its prevalence especially in women is not well defined. OSAHS and non-alcoholic fatty liver disease are common conditions, frequently associated in patients with central obesity and metabolic syndrome and are both the result of the accumulation of ectopic fat mass. Identifying predictors of risk of OSAHS may be useful to select the subjects requiring instrumental sleep evaluation. In this cross-sectional study, we have investigated the potential role of hepatic left lobe volume (HLLV) in predicting the presence of OSAHS. OSAHS was quantified by the apnea/hypopnea index (AHI) and oxygen desaturation index in a cardiorespiratory inpatient sleep study of 97 obese women [age: 47 ± 11 years body mass index (BMI): 50 ± 8 kg/m2]. OSAHS was diagnosed when AHI was ≥5. HLLV, subcutaneous and intra-abdominal fat were measured by ultrasound. After adjustment for age and BMI, both HLLV and neck circumference (NC) were independent predictors of AHI. OSAHS was found in 72% of patients; HLLV ≥ 370 cm3 was a predictor of OSAHS with a sensitivity of 66%, a specificity of 70%, a positive and negative predictive values of 85 and 44%, respectively (AUC = 0.67, p < 0.005). A multivariate logistic model was used including age, BMI, NC, and HLLV (the only independent predictors of AHI in a multiple linear regression analyses), and a cut off value for the predicted probability of OSAHS equal to 0.7 provided the best diagnostic results (AUC = 0.79, p < 0.005) in terms of sensitivity (76%), specificity (89%), negative and positive predictive values (59 and 95%, respectively). All patients with severe OSAHS were identified by this prediction model. In conclusion, HLLV, an established index of visceral adiposity, represents an anthropometric parameter closely associated with OSAHS in severely obese women.

Highlights

  • Obstructive sleep apnea–hypopnea syndrome (OSAHS), an emerging public health issue, is characterized by recurrent episodes of upper airway occlusion during sleep, which results in reduction or cessation of the airflow, and lead to chronic intermittent hypoxia and sleep fragmentation [1]

  • Patients with OSAHS were 8-year older (p < 0.005) and had greater intra-abdominal fat (IAF) and hepatic left lobe volume (HLLV) compared to patients without OSAHS despite similar body weight, body mass index (BMI), and subcutaneous fat (SCF)

  • Higher levels of γ-GT were observed in patients with OSAHS (p < 0.05), and there was a positive association between apnea/hypopnea index (AHI) and γ-GT (Rho = 0.21; p < 0.05)

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Summary

Introduction

Obstructive sleep apnea–hypopnea syndrome (OSAHS), an emerging public health issue, is characterized by recurrent episodes of upper airway occlusion during sleep, which results in reduction or cessation of the airflow, and lead to chronic intermittent hypoxia and sleep fragmentation [1]. The main cause seems to be an anatomical upper airway narrowing, where the increased negative intrathoracic pressure during inspiration exceeds the counteracting forces of the dilating muscles [2,3,4]. The mechanisms linking obesity to OSAHS include pharyngeal narrowing due to fatty tissue in the lateral airway walls, muscle functional impairment due to fatty deposits, enlargement of the abdomen resulting in reduced lung volumes, decreased longitudinal tracheal traction forces and increased tendency of pharyngeal collapse during inspiration, the low-grade systemic inflammation associated with obesity [3, 9]

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