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Original Research: Sleep Disorders |

Nonalcoholic Fatty Liver Disease, Nocturnal Hypoxia, and Endothelial Function in Patients With Sleep ApneaNonalcoholic Fatty Liver Disease in Sleep Apnea

Caroline Minville, MD; Marie-Noëlle Hilleret, MD; Renaud Tamisier, MD, PhD; Judith Aron-Wisnewsky, MD; Karine Clement, MD, PhD; Candice Trocme, PhD; Jean-Christian Borel, PhD; Patrick Lévy, MD, PhD; Jean-Pierre Zarski, MD, PhD; Jean-Louis Pépin, MD, PhD
Author and Funding Information

From the Institut universitaire de cardiologie et de pneumologie de Québec (Dr Minville), Quebec City, QC, Canada; Département d’Hépato Gastroentérologie (Drs Hilleret and Zarski), Pôle Digidune, CHU de Grenoble, France; Université Joseph Fourier (Drs Minville, Tamisier, Borel, Lévy, and Pépin), INSERM U 1042, Laboratoire HP2, Hypoxie Physiopathologies, Pôle Locomotion, Rééducation et Physiologie, CHU de Grenoble, France; Assistance Publique-Hôpitaux de Paris (Drs Aron-Wisnewsky and Clement), Département Cœur et métabolisme, Centre de Nutrition Humaine, Hôpital Pitié-Salpétrière, Paris 75613, France; INSERM UMRS 872 team 7 Drs Aron-Wisnewsky and Clement), Nutriomique, Université Pierre et Marie Curie-Paris 6, Centre de Recherche des Cordeliers, Paris 75006, France; and Laboratoire de Biochimie des Enzymes et des Protéines (Dr Trocme), CGD (Institut de Biologie et de Pathologie), CHU de Grenoble, France.

Correspondence to: Jean-Louis Pépin, MD, PhD, Laboratoire EFCR, CHU de Grenoble, BP217X, 38043 Grenoble cedex 09, France; e-mail: jpepin@chu-grenoble.fr


Drs Zarski and Pépin contributed equally to this work.

Funding/Support: This study was supported by the Délégation à la recherche clinique et à l’innovation (DRCI) 2011 in CHU Grenoble and by Agir à dom scientific council grants.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;145(3):525-533. doi:10.1378/chest.13-0938
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Background:  Nocturnal hypoxia, the hallmark of OSA, is a potential contributing factor for nonalcoholic fatty liver disease (NAFLD). NAFLD severity and its implication in OSA-related endothelial dysfunction have not been investigated in a large, unselected OSA population, including nonobese subjects.

Methods:  Noninvasive blood tests (SteatoTest, NashTest, and FibroTest) were used to evaluate steatosis, nonalcoholic steatohepatitis (NASH), and fibrosis in a large cohort of patients with OSA. In the same group, endothelial function and its links with NAFLD severity were assessed.

Results:  Of the 226 subjects included who were referred for suspicion of OSA (men, 55%; median age, 56 years; median BMI, 34.2 kg/m2 [33% with BMI < 30 kg/m2]), 61.5% exhibited moderate or severe steatosis. By multivariate analysis, independent factors for liver steatosis were, as expected, triglyceride levels (P < .0001) and insulin resistance (P = .0004) as well as nocturnal cumulative time spent < 90% of oxygen saturation (CT90) (P = .01). Thirty-eight percent had borderline or possible NASH (N1 or N2 with NashTest). CT90 was significantly associated with borderline or possible NASH (P = .035) in univariate but not in multivariate analysis. The dose-response relationship between the severity of nocturnal hypoxia and liver injury was established only in morbid obesity and not in lean. Multivariate models showed that steatosis was independently associated with endothelial dysfunction after adjustment for confounders.

Conclusions:  In a large, unselected OSA population, the severity of nocturnal hypoxia was independently associated with steatosis. Preexisting obesity exacerbated the effects of nocturnal hypoxemia. NAFLD is a potential mechanism of endothelial dysfunction in OSA.

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