Abstract
PurposeObstructive sleep apnea (OSA) is suggested as a potential risk factor of nonalcoholic fatty liver disease (NAFLD). However, the underlying mechanism is still far from clear. The aim of this observational study was to investigate the influence of OSA-related hypoxia on severity of liver injury in patients with NAFLD.MethodsConsecutive patients with ultrasound-diagnosed NAFLD who underwent standard polysomnography were enrolled. Fasting blood samples were obtained from all patients for biological profile measurements, and demographic data were collected. Subjects were divided into control, moderate, and severe groups.ResultsA total of 85 subjects with 73 males and 12 females were included (mean age, 44.67 ± 1.28 years; mean body mass index, 27.28 ± 0.33 kg/m2). Alanine aminotransferase (ALT), aspartate aminotransferase (AST), ALT/AST, gamma glutamyltransferase, total cholesterol, low density lipoprotein-cholesterol, fasting glucose, and high-sensitivity C-reactive protein significantly increased with the aggravation of OSA. In multivariate analysis, oxygen desaturation index was the major contributing factor for elevated ALT (β = 0.435, p = 0.000), average O2 saturation was the major independent predictor of elevated AST (β = −0.269, p = 0.020).ConclusionsOSA-related hypoxia was independently associated with the biochemical evidence of liver injury in the presence of NAFLD.
Highlights
Obstructive sleep apnea (OSA) is characterized by repetitive episodes of partial or complete obstruction of the upper airway during sleep, resulting in sleep fragmentation and hypoxemia
Polysomnographical parameters including LaSO2, average SpO2 decreased significantly with an increase in OSA severity, whereas Body mass index (BMI), neck circumference, waist circumference, apnea-hypopnea index (AHI), ODI, and T90 % increased with OSA severity
Nocturnal hypoxia was associated with the elevation of liver enzymes, independent of a variety of relevant factors such as age, gender, obesity, inflammation, blood pressure, serum glucose, and lipid profile, which suggested that nocturnal hypoxia might be a risk factor in the progression of nonalcoholic fatty liver disease (NAFLD)
Summary
Obstructive sleep apnea (OSA) is characterized by repetitive episodes of partial or complete obstruction of the upper airway during sleep, resulting in sleep fragmentation and hypoxemia. There is accumulating evidence supporting the relationship of OSA with all manifestations of the metabolic syndrome, including visceral obesity, hypertension, dyslipidemia, and insulin resistance [3, 4]. Recent data suggest that OSA is associated with another manifestation of metabolic dysfunction, nonalcoholic fatty liver disease (NAFLD) [7,8,9]. NAFLD represents a wide spectrum of liver disorders from isolated steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. NAFLD is a common cause of chronic liver disease, affecting 30 % of the general adult population and up to 60 to 70 % of diabetic and obese patients [10]. The “first hit” consists of excess hepatic triglyceride accumulation due to dysregulation of fatty acids and insulin resistance, in the absence of significant alcohol consumption or other liver disease. Whereas oxidative stress and cytokine expression constitute a “second hit”, leading to the shift from steatosis to NASH [11, 13]
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