Obstructive sleep apnea can be linked to the development of non-alcoholic fatty liver disease.
David Hui, BBS
A team, led by David Hui, BBS, Medicine & Therapeutics, Chinese University of Hong Kong, examined whether intrahepatic triglyceride content measured by proton-magnetic resonance spectroscopy (MRS) could be the new gold standard for liver fat quantification.
While obstructive sleep apnea is linked to the development of NAFLD, proton-magnetic resonance spectroscopy estimating proton density fat fraction is a novel biomarker that is more sensitive than liver biopsies to determine steatosis grade in assessing changes in the liver fat content.
In the trial, the investigators examined 60 patients at the NAFLD clinic at the Prince of Wales Hospital where each individual was invited to undergo home sleep tests with a validated level-3 Emblett device.
There were no differences in demographics between the patient population, with an average age of 4.5 (10.4) years, body mass index (BMI) of 28.6 (4.5) kg/m2, endometrial stromal sarcomas of 9.2(5.6), REI of 30.4(22.4)/hour, minimum SaO2 of 77.0(9.6)%, ODI4 of 31.5(12.3)/hr, IHTG of 13.5(9.0)%, liver stiffness of 6.5(2.5)kPa, controlled attenuation parameter (CAP) of 319(46) db/m, serum cytokeratin 18 segment of 244(241), and liver function test parameters.
Patients with a respiratory events index (REI) ≥ 5/hr were randomized into either an autoCPAP in auto-adjusting mode with pressure range 4-20 cmH20 group or a Subtherapeutic CPAP with the autoCPAP fixed at 4cmH20 by a balanced block design group.
The investigators sought primary endpoints of the difference of changes in IHTG measured by proton-MRS after 6 months. They also sought secondary endpoints of the changes in FibroScan vibration-controlled transient elastography CAP and liver stiffness measurements in assessing steatosis and fibrosis, serum cytokeratin-18 fragment, and objective CPAP usage.
The investigators did find some correlations between CAP and REI (r = 0.206; P = 0.025), min SaO2 (r = -0.173; P = 0.060), %TST with SaO2<90% (r = 0.220; P = 0.019), and ODI4 (r = 0.187; P = 0.048).
After 6 months of autoCPAP compared to subtherapeutic treatment, objective CPAP usage was 4.37(2.14) and 3.84(2.29) hours, respectively (P = 0.191).
However, there were no significant differences of changes in primary and secondary endpoints between either treatment group.
CPAP withdrawal can also lead to a number of negative outcomes for patients, including worsening the severity of the obstructive sleep apnea and increasing morning arterial stiffness.
A team of researchers from Johns Hopkins University examined whether CPAP withdrawal will worsen the augmentation index (AIx) and if the extent of AIx change is influenced by various factors, including obstructive sleep apnea severity, age, body mass index (BMI), sex, and diabetes.
In the single-center randomized crossover study also planned for presentation ATS, the investigators examined 69 patients with moderate to severe obstructive sleep apnea acclimated to CPAP.
The researchers found CPAP withdrawal yielded severe obstructive sleep apnea. The AHI 3% on CPAP and off CPAP was 5.8 ± 0.9 and 57.3 ± 3.6 events/hr, respectively, while arterial stiffness also worsened with CPAP withdrawal. The augmentation index on CPAP and off CPAP was 6.8 ± 2.06 and 2.8 ± 1.9% (mean ± SE) respectively (P = 0.0001) and the Δ AIx following CPAP withdrawal was not correlated with Δ AHI 3%, age, or BMI.
For the Hong Kong-based study, investigators found other ways to mark the severity of OSA for patients with non-alcoholic fatty liver disease.
“Where there were some correlations between CAP and markers of severity of OSA, there were no significant differences between therapeutic and subtherapeutic CPAP effects on non-invasive markers of liver fat, steatosis and fibrosis,” the authors wrote.
The study, “Obstructive Sleep Apnea and CPAP Treatment Response in Patients with Non Alcoholic Fatty Liver Disease,” was published online by the ATS International Conference.