Nocturnal change of circulating intercellular adhesion molecule 1 levels in children with snoring.

Hypoxia promotes adherence of leukocytes to endothelial cells by inducing expression of adhesion molecules like intercellular adhesion molecule 1 (ICAM-1). Increased serum levels of circulating ICAM-1 (cICAM-1) have been reported in adults with sleep apnea and associated hypoxemia. This investigation assessed the hypothesis that the overnight change of cICAM-1 levels in children with snoring is correlated with the severity of obstructive sleep-disordered breathing. Evening and morning serum levels of cICAM-1 were measured in children with snoring referred for polysomnography. Twenty-five children with an apnea-hypopnea index greater than or equal to 5 episodes/h (5.5 +/- 1.8 years), 30 subjects with an index less than 5 and greater than 1 (6.3 +/- 2 years), and 19 children with an index less than or equal to 1 (7.1 +/- 3 years) were recruited. Overnight change in cICAM-1 (log-transformed ratio of morning-to-evening levels) was similar in subjects with an apnea-hypopnea index greater than or equal to 5 episodes/h compared to those with an index less than 5 and greater than 1 or to children with an index less than or equal to 1 (-0.001 +/- 0.08 vs -0.03 +/- 0.09 vs -0.06 +/- 0.1; p > 0.05). When multiple regression analysis was applied, apnea-hypopnea index, respiratory arousal index, and oxygen saturation of hemoglobin nadir were not significant predictors of overnight change in cICAM-1 levels. Thus, in children with snoring, overnight change in cICAM-1 levels is not related to severity of obstructive sleep-disordered breathing.

Hemodialysis procedure does not affect the levels of sICAM-1 and sVCAM-1 in patients with end stage renal disease.

Atherosclerosis is by far the leading cause of mortality and morbidity in patients with end stage renal disease undergoing chronic hemodialysis (HD). Vascular endothelial cell adhesion molecules like the intercellular adhesion molecule-1 (ICAM-1) and the vascular cell adhesion molecule-1 (VCAM-1) are involved in the pathogenesis of atherosclerosis. Their soluble forms (sICAM-1, sVCAM-1) are considered potential serum markers of endothelial activation and atherosclerosis. The aim of this study was to clarify the influence of the HD procedure on the levels of sICAM-1 and sVCAM-1 in patients with end stage renal disease. We evaluated 35 clinically stable patients (18 males, 17 females, mean age 61 +/- 12) on chronic HD treatment. Diabetes mellitus coexisted in eight patients and arterial hypertension in 23 patients. Blood was drawn before, every hour during, and after a single HD session in each patient. Low-flux cuprophane dialyzers (GFS 12, Gambro, Lund, Sweden) were used in 22 and high-flux polysulfone dialyzers (Hemoflow F 60S, Fresenius, Oberursel, Germany) in 13 cases. At 30 min into the HD session (n=31, 20 low-flux HD, 11 high-flux HD) blood was drawn simultaneously from the entrance and the exit line of the dialyzer. From all these samples, serum concentrations of sICAM-1 and sVCAM-1 were determined by commercially available enzyme immunoassays (ELISA, R&D Systems, Minneapolis, USA). Results were corrected according to hemoconcentration, where appropriate. Plasma levels of sVCAM-1 were elevated in patients with end stage renal disease before the beginning of the dialysis session when compared to healthy controls (1449 +/- 497 ng/mL vs. 691 +/- 118 ng/mL). On the contrary, such an elevation was not found in the case of sICAM-1 (231 +/- 58.5 ng/mL vs. 236.4 +/- 96.8 ng/mL in healthy controls). These levels remained stable in all measurements throughout the dialysis procedure. Furthermore, serum sICAM-1 and sVCAM-1 levels remained unaltered after the passage of the dialyzer. The levels of sICAM-1 and sVCAM-1 were not influenced by the existence of diabetes mellitus, hypertension, or by the utilization of biocompatible, high flux dialyzers. Our study confirms that in chronic HD patients serum levels for sVCAM-1 are elevated. The levels of adhesion molecules are not affected by the HD procedure. These findings probably can be attributed to a decreased renal clearance or catabolism of sICAM-1 and sVCAM-1 and to the different sources of the two molecules. Neither coexisting diabetes mellitus nor arterial hypertension influences the circulating levels of these adhesion molecules. The functional role of sVCAM-1 and sICAM-1, the exact renal contribution to their metabolism, and their role as markers of atherosclerosis in chronic renal disease need further evaluation.