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Severe sleep apnea may be a risk factor for liver damage
May 25, 2005A study examines the connection between obstructive sleep apnea and liver disease
Many patients with obstructive sleep apnea (OSA) are obese and therefore at risk of having fatty liver, a condition in which fat accumulates in the liver cells. But the link between OSA and liver injury independent of weight has yet to be examined.
In the first study to examine liver injury in patients with OSA, researchers led by Lawrence Serfaty, M.D. at the Hepatology Department at Saint-Antoine Hospital in Paris, France tested liver function in patients being evaluated for OSA in order to determine if sleep apnea by itself was a risk factor for liver disease and if so, the mechanism involved.
The results of the study appear in the June 2005 issue of Hepatology, the official journal of the American Association for the Study of Liver Diseases (AASLD), published by John Wiley & Sons, Inc. Hepatology is available online via Wiley InterScience at http://www.interscience.wiley.com/journal/hepatology.
The study included 163 patients who were referred to the Sleep Unit of Saint-Antoine Hospital between September 2000 and May 2001 to undergo evaluation for OSA. Blood levels of liver enzymes were measured in the morning after sleeping at the clinic, and patients with elevated levels underwent liver biopsies, also in the morning. Patients were categorized into groups according to the level of severity of OSA: severe (44 patients), moderate (84 patients), or non-existent (35 patients). This last group, who did not have OSA, was used as the control group. Elevated liver enzymes were found in 32 patients, 29 of whom were in the severe or moderate group. Liver biopsies were performed in 18 of these patients: 9 with severe OSA, 6 with moderate OSA and 3 with no OSA. Patients with severe OSA had a significantly higher percentage of steatosis (fatty liver disease), lobular necrosis and fibrosis (two signs of liver damage) than patients in the other two groups, regardless of body mass index (BMI), which itself is a known risk factor for fatty liver disease. They also had significantly higher levels of insulin and were more insulin resistant than the other patients.
Although the authors note that the results should be considered with caution due to the limited number of patients who underwent liver biopsy, they conclude that severe OSA, independent of being overweight, is a risk factor for liver disease. In addition, they postulate that OSA may contribute to insulin resistance and fatty liver disease, since insulin responsiveness improves after treating OSA. They suggest that the striking relationship between the severity of sleep apnea and liver damage indicates that OSA may play a role in how fatty liver disease develops.
"In conclusion," the authors state, "OSA is a risk factor for abnormal liver enzymes independently from BMI, and should be investigated in patients without other cause of liver disease." They conclude: "Further studies are needed to assess the prevalence of OSA in patients with NASH [nonalcoholic steatohepatitis, or fatty liver disease with inflammation] and to evaluate whether treatment of OSA may improve liver injury."
John Wiley & Sons, Inc.
The study included 163 patients who were referred to the Sleep Unit of Saint-Antoine Hospital between September 2000 and May 2001 to undergo evaluation for OSA. Blood levels of liver enzymes were measured in the morning after sleeping at the clinic, and patients with elevated levels underwent liver biopsies, also in the morning. Patients were categorized into groups according to the level of severity of OSA: severe (44 patients), moderate (84 patients), or non-existent (35 patients). This last group, who did not have OSA, was used as the control group. Elevated liver enzymes were found in 32 patients, 29 of whom were in the severe or moderate group. Liver biopsies were performed in 18 of these patients: 9 with severe OSA, 6 with moderate OSA and 3 with no OSA. Patients with severe OSA had a significantly higher percentage of steatosis (fatty liver disease), lobular necrosis and fibrosis (two signs of liver damage) than patients in the other two groups, regardless of body mass index (BMI), which itself is a known risk factor for fatty liver disease. They also had significantly higher levels of insulin and were more insulin resistant than the other patients.
Although the authors note that the results should be considered with caution due to the limited number of patients who underwent liver biopsy, they conclude that severe OSA, independent of being overweight, is a risk factor for liver disease. In addition, they postulate that OSA may contribute to insulin resistance and fatty liver disease, since insulin responsiveness improves after treating OSA. They suggest that the striking relationship between the severity of sleep apnea and liver damage indicates that OSA may play a role in how fatty liver disease develops.
"In conclusion," the authors state, "OSA is a risk factor for abnormal liver enzymes independently from BMI, and should be investigated in patients without other cause of liver disease." They conclude: "Further studies are needed to assess the prevalence of OSA in patients with NASH [nonalcoholic steatohepatitis, or fatty liver disease with inflammation] and to evaluate whether treatment of OSA may improve liver injury."
John Wiley & Sons, Inc.
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