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The purpose of this study was to determine whether there is a correlation between CPAP usage and corneal thickness in patients with sleep disordered breathing. Full-night polysomnography (PSG) recordings were collected. Ten patients had undergone PSG recordings with continuous positive airway pressure (CPAP), and seven patients had undergone PSG recordings without CPAP. We measured corneal thickness by ultrasonic pachymeter before sleep and ten minutes after waking. We also measured visual acuity with a routine ophthalmologic eye chart before and after sleep. We asked patients to fill out a post-sleep questionnaire to get their subjective opinions. In the without-CPAP group, corneal thickness increased significantly during sleep in both eyes (left, p = 0.0025; right, p<0.0001). In the with-CPAP group, corneal thickness did not increase significantly (p>0.05 for both left and right cornea). There was no significant difference in visual acuity tests (p>0.05 for both left and right eye) between the two groups. According to our results, there is a significant increase in corneal thickness in the without-CPAP group. Our data show that a low percentage of Rapid Eye Movement (REM) sleep may cause an increase in corneal thickness, which can indicate poor corneal oxygenation. In fact, many sleep-disordered breathing (SDB) patients have low REM. Since a contact lens may cause low corneal oxygenation, SDB patients with contact lenses should be monitored carefully for their corneal thickness.

Background: In the present study, we want to demonstrate the correlation between obstructive sleep apnea syndrome (OSAS) whose independent effect on carotid artery intima-media thickness (IMT) was demonstrated, with Framingham risk score (FRS) showing the overall cardiovascular risk., Methods: IMT of the carotid artery was measured with ultrasonography and 10-year risk of coronary heart disease (CHD) was defined with FRS in 90 consecutive patients referred to our sleep clinic and who underwent polysomnography (PSG), with vascular risk factors and without a clinical atherosclerotic disease., Results: IMT and FRS were found to be statistically significantly increased in the severe OSAS group compared to the other two groups. Carotid IMT was found to be significantly positively correlated with, apnea-hypopnea index (AHI), oxygen desaturation index (ODI) and time duration with oxygen saturation (SpO2) <90%, and negatively correlated with minimum oxygen saturation at sleep (minimum SpO2) and mean SpO2. In control and mild OSAS group IMT and FRS have significantly positive correlation (r: 0.501, P: 0.027; r: 0.625, P<0.001), while in severe OSAS group no significant correlation was detected between IMT and FRS (r: 0.321, P: 0.06). In the regression analysis AHI and ODI were found to be an independent predictor of carotid IMT. ODI was found to have an independent effect on the progression of atherosclerosis., Conclusions: Increased carotid IMT in severe OSAS group could not be explained with the classical risk factors. In this respect, FRS might be insufficient to determine correctly the cardiovascular risk and protection strategies against the disease in OSAS patients.

YKL-40 (chitinase-3-like-1) has been introduced as a marker of inflammation in asthma. The aim of this study was to determine the role of YKL-40 in asthma and to evaluate the relationship between YKL-40 and asthma severity.In the study, 60 non-smoker asthma patients without additional diseases (aged between 20-60 years, female: 34) were grouped [Group I: Well controlled asthma patients (n: 30), Group II: Patients during acute exacerbation of asthma (n: 30)]. Healthy non-smoker female individuals were included in Group III (n: 30) as a control group. The level of serum YKL-40 of all groups were determined by ELISA. Also, serum YKL- 40 level was correlated with age, asthma duration in years, body mass index (BMI), forced expiratory volume in first second/ forced vital capacity (FEV1/FVC, %), FEV1 (%), and total IgE levels of asthma patients. Mean serum YKL-40 level was highest in patients during acute exacerbation of asthma (36.36±10.49 ng/ml) while mean serum YKL-40 level was the lowest (13.20±5.60 ng/ml) in the control group. There was a negative significant correlation between the serum YKL-40 levels and FEV1 (%) in patients during acute exacerbation of asthma. There were no significant correlations between the serum YKL-40 levels and other variables in group II.We found that increased serum YKL-40 levels may be used as a marker for evaluation of asthma severity and genetic polimorphism.