Effects of an In-Patient Individualized Rehabilitation Program on Severity and Symptoms of Obstructive Sleep Apnea Syndrome (OSAS):Results of a Randomized Controlled Pilot Study

The obstructive sleep apnea/hypopnea syndrome (OSAS), with an estimated prevalence of between 2 and 4% (1) is characterized by repetitive obstructions of the upper airway that generate intermittent hypoxemia and sleep fragmentation. The typical clinical profile of the apneic patient is an middle aged (50-55 years) obese male, snoring and drowsy. Moreover, OSAS is a risk factor for hypertension independent of obesity (2, 3) and it is now clear evidence that untreated apnea patients have high cardiovascular morbidity / mortality (CVM) higher than subjects treated with CPAP (4-6).

Clinically, excessive daytime sleepiness (EDS) is the main symptom (7) but the attentional and cognitive disorders (8.9), depression or simply a state of fatigue are other possible manifestations of OSAS. The impact on quality of life (QoL) (10-12) are significant and underestimated. The origins of this drowsiness are multiple: one finds the fragmentation of sleep (13,14), intermittent hypoxia, respiratory effort, obesity (15) and certain cytokines such as TNF-alpha and IL-6 involved in sleep regulation (16-19).

On the pathophysiology, the investigators find in the obstructive apneic oxidative stress (20-24) and systemic inflammation (25-27). CRP and levels of some cytokines (IL-1 beta, IL-6, IL-8 and TNF-alpha) are increased and their levels are correlated with the severity of disease as the increase of CVD (28-30 ). Intermittent hypoxia appears to play an essential role in the genesis of these abnormalities (31).

On the metabolic dysregulation of many coexist. Found abnormal fasting blood glucose, a state of insulin resistance, dyslipidemia, and hyperleptinemia. Insulin resistance increases with body weight independent of the index of apnea / hypopnea (AHI) (18, 32-34). Intermittent hypoxia appears to be the cause. Leptin secreted by adipocytes, regulates weight by controlling appetite and energy expenditure. The hyperleptinemia found in OSA is controversial. Obesity appears to be primarily responsible for some (36) while others suggest the role of nocturnal hypoxemia (37). In fact, it is more the state of leptin resistance that hyperleptinemia alone that seems to be involved.

Treatment with continuous positive airway pressure (CPAP) has clearly demonstrated its effectiveness to suppress apneas and sleep fragmentation associated. A meta-analysis (38) has confirmed the improvement of IDS by the PPC. However, in less severe forms, improving the SDE is less clear (39) and the PPC is sometimes not easily accepted, not tolerated and limiting its effectiveness is its poor compliance (40,41). From a pathophysiological point of view, CSF improves systemic inflammation (26,27) and diminishes the CVD (5.6). For cons, the metabolic dysregulation (insulin resistance, hyperleptinemia, dyslipidemia) are improving somewhat CPAP except in patients without obesity (42-44).