Can Obstructive Sleep Apnoea Lead to Fatty Liver Disease?

Obstructive sleep apnoea is becoming more of a common medical condition nowadays. This problem is characterized by repeated upper airway collapse during sleep resulting in sleep fragementation and decreased oxygen levels in the blood. Obstructive sleep apnoea can increase both morbidity and mortality due to its complications such as heart problems, stroke, and diabetes. It can also lead to ther problems such as visceral obesity, hypertension, dyslipidemia, and insulin resistance.

Recent studies have pointed out that obstructive sleep apnoea can increase insulin levels which are independent of obesity. Insulin resistance can bring about abnormal blood cholesterol levels, which can further bring about non-alcoholic fatty liver disease. It is in this regard that an article by Mirrakhimov in 2012 has aimed to discuss whether obstructive sleep apnoea is linked to liver disease.

For us to further understand this matter, let us first review what non-alcoholic fatty liver disease is all about. Non-alcoholic fatty liver disease is a disease characterized by steatosis without inflammation to non-alcoholic steatohepatitis (NASH) and liver cirrhosis. It is a progressively fibrotic disease and can soon lead to death in some cases. Non-alcoholic fatty liver disease can lead to liver cirrhosis which can further lead to liver failure, multi-organ failure and death.

According to experts, non-alcoholic fatty liver disease is caused by the accumulation of triglyceride in liver cells, which may be a result of insulin resistance and obesity. Once there is fatty infiltration of liver cells, inflammatory cells also infiltrate, leading to inflammation and liver cell death. The researchers of the above study examined several studies examining levels of lover enzymes in the serum of patients with obstructive sleep apnoea. In one study, abnormally elevated morning AST levels were found in 14 out of 40 studied OSA patients (35%). In another study, it was found out that in patients with obstructive sleep apnoea, ALT and AST levels directly correlated with the severity of low oxygen levels at night, but not with the apnoea-hypopnoea index (AHI) or BMI. Still, other investigators have found out that increased ALT, AST, and AP was observed in adult patients with moderate and severe obstructive sleep apnoea.

As to liver imaging studies, in one study, obstructive sleep apnoea was associated with increased visceral adiposity, but not with the degree of hepatic steatosis. Liver CT findings revealed that obstructive sleep apnoea was associated with hepatic steatosis. The effect of CPAP treatment for 3 years was examined in 11 patients. CPAP therapy was associated with a decrease in hepatic steatosis in six compliant patients, despite unchanged BMI, but not in five non-compliant patients.

In terms of liver biopsy, it was found out that subjects with severe OSA defined as the AHI > 50/h (n = 9), exhibited more severe liver steatosis, necrosis, and fibrosis than subjects with the AHI ≤ 50/h (n = 9). There was a trend toward a higher prevalence of obstructive sleep apnoea in patients with inflammation and fibrosis compared with those with inflammation alone.

Experts believe that obstructive sleep apnoea promotes the development and progression of non-alcoholic fatty liver disease such to its physiological mechanisms such as negative intra-thoracic pressure swings, sleep fragmentation, hypercapnoea, and intermittent hypoxia. Indeed these processes stimulate the sympathetic nervous system and further lead to insulin resistance.

To conclude, obstructive sleep apnoea may indeed lead to the development of non-alcoholic fatty liver disease. Still more studies are needed to prove this point.

Reference:

Mirrakhimov AE, Polotsky VY.Obstructive sleep apnoea and non-alcoholic Fatty liver disease: is the liver another target? Front Neurol. 2012 Oct 17;3:149.

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