H Sahebjani1. 1. Veterans Affairs Medical Center, Department of Medicine, University of Cincinnati College of Medicine, Ohio 45220, USA.
Abstract
STUDY OBJECTIVE: To assess the utility of urinary uric acid excretion as a marker of nocturnal hypoxia in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) before and after the institution of nasal continuous positive airway pressure (CPAP). DESIGN: Prospective, open. SETTING: Sleep Disorders Laboratory, Veterans Affairs Medical Center. PARTICIPANTS: Thirty consecutive male subjects, 20 with OSAHS and 10 without OSAHS. MEASUREMENTS AND METHODS: Spot morning urine and venous blood samples were obtained in all subjects; samples were also obtained after the application of CPAP in those with OSAHS. Uric acid excretion, normalized to creatinine clearance, was calculated as the product of urinary uric acid and serum creatinine concentrations divided by urine creatinine concentration. In patients with OSAHS, uric acid excretion was 0.55+/-0.1 mg/dL before CPAP therapy and decreased to 0.30+/-0.01 mg/dL after CPAP therapy (p < 0.001). The latter value did not differ significantly from the mean value (0.32+/-0.03 mg/dL) in the control group. Uric acid excretion in OSAHS patients correlated significantly with the apnea-hypopnea index (r=0.42; p<0.0003). CONCLUSION: Uric acid excretion is increased in OSAHS patients and normalizes after CPAP treatment, most likely reflecting differences in tissue oxygenation between the two conditions. Further studies in large number of patients may confirm the usefulness of this simple test for diagnosis and follow-up of patients with OSAHS.
STUDY OBJECTIVE: To assess the utility of urinary uric acid excretion as a marker of nocturnal hypoxia in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) before and after the institution of nasal continuous positive airway pressure (CPAP). DESIGN: Prospective, open. SETTING: Sleep Disorders Laboratory, Veterans Affairs Medical Center. PARTICIPANTS: Thirty consecutive male subjects, 20 with OSAHS and 10 without OSAHS. MEASUREMENTS AND METHODS: Spot morning urine and venous blood samples were obtained in all subjects; samples were also obtained after the application of CPAP in those with OSAHS. Uric acid excretion, normalized to creatinine clearance, was calculated as the product of urinary uric acid and serum creatinine concentrations divided by urine creatinine concentration. In patients with OSAHS, uric acid excretion was 0.55+/-0.1 mg/dL before CPAP therapy and decreased to 0.30+/-0.01 mg/dL after CPAP therapy (p < 0.001). The latter value did not differ significantly from the mean value (0.32+/-0.03 mg/dL) in the control group. Uric acid excretion in OSAHS patients correlated significantly with the apnea-hypopnea index (r=0.42; p<0.0003). CONCLUSION:Uric acid excretion is increased in OSAHS patients and normalizes after CPAP treatment, most likely reflecting differences in tissue oxygenation between the two conditions. Further studies in large number of patients may confirm the usefulness of this simple test for diagnosis and follow-up of patients with OSAHS.
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