Impact of long-term continuous positive airway pressure on liver fat in male obstructive sleep apnea patients with fatty liver
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Obstructive sleep apnea (OSA) is an established factor in the pathogenesis and exacerbation of fatty liver disease. However, randomized controlled trials have failed to demonstrate decreases in liver fat content in OSA patients by continuous positive airway pressure (CPAP) performed for several months. The aim of this study is to investigate the impact of long-term CPAP therapy on liver fat content in OSA patients with fatty liver. Liver fat content in 61 male OSA patients was evaluated by computed tomography performed because of abdominal obesity before and after CPAP initiation. At baseline, there were 25 participants with fatty liver. Their apnea–hypopnea index and percent sleep time with oxygen saturation < 90% were greater than those in the 36 participants who did not have fatty liver (52.3 vs. 41.8/h and 30.4 vs. 14.8%, respectively). The average therapy duration was 31 months. In the analysis of the entire participant group, liver fat content did not change after CPAP therapy. In those without fatty liver, liver fat content increased accompanied by increases in BMI, whereas in the participants with fatty liver, liver fat content decreased despite stable BMI, abdominal fat distribution, and insulin resistance. In male OSA patients with abdominal obesity, decreases in liver fat content were observed after long-term CPAP therapy only when fatty liver was present at baseline. This implies that there are some conditions, such as OSA-related hypoxemia and others, which may exacerbate fatty liver and that fatty liver may improve with CPAP therapy.
KeywordsSleep apnea syndromes NAFLD Liver steatosis CPAP ventilation Long-term effects Hypoxia
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Conflict of interest
Kimihiko Murase, Kiminobu Tanizawa, Toru Oga, and Kazuo Chin belong to the Department of Respiratory Care and Sleep Control Medicine which is funded by endowments from Philips-Respironics, Teijin Pharma, Fukuda Denshi, and Fukuda Lifetec Keiji to Kyoto University. Other authors certify that they have no affiliations with or involvement in any organization or entity with any financial interest (such as honoraria; educational grants; participation in speakers’ bureaus; membership, employment, consultancies, stock ownership, or other equity interest; and expert testimony or patent-licensing arrangements), or non-financial interest (such as personal or professional relationships, affiliations, knowledge, or beliefs) in the subject matter or materials discussed in this manuscript.
Kyoto University Graduate School and Faculty of Medicine Ethics Committee (IRB approval number: E-1307). All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
This study was supported by Grants (26293198 and 17H04182) from the Japanese Ministry of Education, Culture, Sports, Science and Technology, the Intractable Respiratory Diseases and Pulmonary Hypertension Research Group, the Ministry of Health, Labor and Welfare, Japan, and Health, Labor and Welfare Sciences Research Grants, Research on Region Medical, the Ministry of Health, Labor and Welfare, Japan and the Japan Vascular Disease Research Foundation. The Department of Respiratory Care and Sleep Control Medicine is funded by endowments from Philips-Respironics, Teijin Pharma, Fukuda Denshi and Fukuda Lifetec Keiji to Kyoto University. The sponsor had no role in the design or conduct of this research.
Informed consent was obtained from all individual participants included in the study.
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