The aim of this study was to investigate the relation of serum monocyte to serum HDL cholesterol ratio with obstructive sleep apnea syndrome (OSAS). A total of 336 patients who underwent polysomnography (PSG) were included in this study. The individuals with an apnea hypopnea index (AHI) <5/h were included in the study as controls while the patients with an AHI > 5 and excessive daytime sleepiness were included in the study as OSAS patients. OSAS patients were compared with the control group for serum monocyte count, high density lipoprotein (HDL) levels, and monocyte to HDL ratio (MHR). Mild, moderate and severe OSAS subgroups were compared for the same parameters. Additionally, correlations of serum monocyte count, HDL level and MHR with other PSG parameters were analyzed. The mean MHR of control and OSAS groups were 12.90 ± 6.64 and 4.91 ± 6.98, respectively, and the difference was statistically significant ( = 0.041). Mean HDL level of the control group was 47.25 ± 13.61 mg/dL while it was 43.14 ± 13.61 mg/dL in OSAS group ( < 0.001). Comparison of OSAS subgroups for MHR and HDL levels revealed statistically significant differences ( < 0.001 and = 0.020, respectively). MHR was higher in OSAS patients compared to the controls. MHR may be a new, useful predictor for OSAS.

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Sleep deprivation, which is a type of sleep disorder, generates oxidative stress in an organism and has acute and chronic adverse effects on well-being by causing biochemical changes. Although the acute manifestations mainly include disturbed neuromediator homeostasis in the central nervous system, changes in hormonal regulation and alterations in sympathetic and parasympathetic system activity, eating disorders, psychosocial disorders, thermoregulation disorders and a disturbed blood lipid profile occur in the chronic period and can result in morbidity and mortality (Pilcher & Huffcutt 1999). Disorders of connective tissue elements and impairments in the regulation of connective tissue mediators associated with sleep deprivation may lead to prolonged wound healing and deterioration of immunity, and induce negative regulation systems in ageing physiology (Opp & Toth 2003).

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