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Clinical Investigations: SLEEP AND BREATHING |

Tissue Hypoxia in Sleep Apnea Syndrome Assessed by Uric Acid and Adenosine*

Hiroshi Saito, MD, FCCP; Masaharu Nishimura, MD; Eiji Shibuya, MD; Hironi Makita, MD; Ichizo Tsujino, MD; Kenji Miyamoto, MD; Yoshikazu Kawakami, MD, FCCP
Author and Funding Information

Affiliations: *From the First Department of Medicine (Drs. Saito, Nishimura, Shibuya, Makita, Tsujino, and Kawakami), Hokkaido University School of Medicine; and Department of Physical Therapy (Dr. Miyamoto), College of Medical Technology, Hokkaido University, Hokkaido, Japan.,  Currently at Kohnan Hospital, Kohnan, Japan.

Correspondence to: Masaharu Nishimura, MD, First Department of Medicine, Hokkaido University School of Medicine, North 15, West 7, Kita-ku, Sapporo, 060-8638, Japan; e-mail: ma-nishi@med.hokudai.ac.jp



Chest. 2002;122(5):1686-1694. doi:10.1378/chest.122.5.1686
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Study objective: Although the overnight increase in urinary uric acid/creatinine ratio (ΔUA/Cr) is considered by some to be a marker of tissue hypoxia in patients with obstructive sleep apnea-hypopnea syndrome (OSAS), this index is not universally accepted. The purpose of this study was to confirm the validity of ΔUA/Cr as a marker of tissue hypoxia by measuring the plasma level of adenosine during sleep, and also to test the hypothesis that the heart rate (HR) response to apnea is a determinant of tissue hypoxia.

Design: Intergroup comparative study.

Setting: A university hospital, Sapporo, Japan.

Patients: Eighteen patients with OSAS who had apnea-associated, moderate-to-severe arterial desaturation. The patients were classified into two groups: the ΔUA/Cr-positive group, who were considered to have tissue hypoxia, and the ΔUA/Cr-normal group, who were not.

Measurements and results: Although there were no significant differences between two groups of the patients in either arterial desaturation parameters or the apnea-hypopnea index, the plasma level of adenosine during sleep was significantly higher in the ΔUA/Cr-positive group than in the ΔUA/Cr-normal group. Successful treatment with nasal continuous positive airway pressure significantly decreased both ΔUA/Cr and the plasma level of adenosine only in the ΔUA/Cr-positive group. The magnitude of the HR increase after the termination of apnea was significantly smaller in the ΔUA/Cr-positive group.

Conclusions: ΔUA/Cr is a marker of tissue hypoxia, which does not necessarily parallel arterial desaturation indexes in OSAS. Intersubject variability in the HR response to apnea may explain the discrepancy between tissue hypoxia and arterial desaturation indexes.

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