Association Between the Severity of Nocturnal Hypoxia in Obstructive Sleep Apnea and Non-Alcoholic Fatty Liver Damage

Abstract

Background:Obstructive sleep apnea (OSA) is a major disease that can cause significant mortality and morbidity. Chronic intermittent hypoxia is a potential causal factor in the progression from fatty liver to nonalcoholic steatohepatitis.Objectives:This study evaluated the association between the degree of liver steatosis and severity of nocturnal hypoxia.Patients and Methods:In this study, between December 2011 and December 2013, patients with ultrasound-diagnosed NAFLD evaluated by standart polysomnography were subsequentally recorded. Patients with alcohol use, viral hepatitis and other chronic liver diseases were excluded. We analyzed polysomnographic parameters, steatosis level and severity of obstructive sleep apnea (OSA) in consideration of body mass index (BMI), biochemical tests and ultrasonographic liver data of 137 subjects. Patients with sleep apnea and AHI scores of < 5, 5 - 14, 15 - 29 and ≥30 are categorized as control, mild, moderate and severe, respectively.Results:One hundred and thirty-seven patients (76 women, 61 men) with a mean age of 55.75 ± 10.13 years who underwent polysomnography were included in the study. Of 118 patients diagnosed with OSA, 19 (16.1%) had mild OSA, 39 (33.1%) moderate OSA and 60 (50.8%) severe OSA. Nineteen cases formed the control group. Apnea/hypopnea index and oxygen desaturation index (ODI) values were significantly higher in moderate and severe non-alcoholic fatty liver disease (NAFLD) compared to the non-NAFLD group. Mean nocturnal SpO2 values were significantly lower in mild NAFLD and severe NAFLD compared to the non-NAFLD group. Lowest O2 saturation (LaSO2) was found low in mild, moderate and severe NAFLD compared to the non-NAFLD group in a statistically significant manner.Conclusions:We assessed polysomnographic parameters of AHI, ODI, LaSO2 and mean nocturnal SpO2 levels, which are especially important in the association between NAFLD and OSAS. We think that it is necessary to be attentive regarding NAFLD development and progression in patients with OSA whose nocturnal hypoxia is severe.

Oxidative Stress and Inflammation after Continuous Positive Airway Pressure Therapy in Patients with Severe Obstructive Sleep Apnea

“…We observed a significantly positive correlation between apnea severity and ALT. This observation is in lines with previous studies that showed the association between liver enzyme levels and sleep apnea parameters (Aron- Wisnewsky et al, 2016;Cakmak et al, 2015). However, other studies found no correlations between sleep apnea severity with liver function (Daltro et al, 2010;Kallwitz et al, 2007).…”

“…This disagreement is probably due to severity of OSA patients recruited to each study. The positive correlation between liver enzyme levels and indices of sleep apnea severity observed in OSA patients indicates that as the severity of sleep apnea increases, there is a concomitant increase in ischemia reperfusion inducing oxidative stress and inflammation in hepatocytes cells (Cakmak et al, 2015).…”

“…OSA causes accumulation of fatty acids in the liver and inflammation as a result of recurrent nocturnal hypoxia, insulin resistance, oxidative stress and dysregulation of adipokines. Previous studies show that apnea hypopnea index (AHI) and apnea index are positively correlated with alanine aminotransferase (ALT ) and aspartate aminotransferase (AST) where as lowest oxygen saturation (SpO 2 ), a consequence of nocturnal hypoxia, shows a negative correlation with ALT and AST (Aron-Wisnewsky, Clement, & Pépin, 2016;Cakmak et al, 2015). The authors concluded that OSA patients progressively develop nonalcoholic liver fatty liver disease (NAFLD).…”

Tauroursodeoxycholic acid attenuates endoplasmic reticulum stress and protects the liver from chronic intermittent hypoxia induced injury

“…It is widely recognized that OSA and its associated CIH is implicated in the pathogenesis of various liver diseases ( 31 – 33 ). Different studies have proved over the previous decades that TUDCA could recovery liver function from variety of liver diseases ( 34 – 37 ); however, whether TUDCA has protective effects against CIH-induced liver injury remains unknown.…”

Intermittent hypoxia in obese Zucker rats: cardiometabolic and inflammatory effects

“…; Cakmak et al . ; see Muraja‐Murro et al . for a comprehensive analysis of the value of nadir over AHI for the detection of OSA patients at risk).…”