Serum sCD40L
r-Spearman’s
p
Age
0.12
ns
BMI
0.16
ns
AHI
0.24
0.01
DI
0.17
ns
Mean SaO2
−0.13
ns
Mean of min. SaO2
−0.18
<0.05
CRP
0.21
<0.05
Uric acid
0.32
<0.001
Total cholesterol
−0.02
ns
LDL cholesterol
0.05
ns
HDL cholesterol
−0.08
ns
Triglycerides
0.15
ns
Uric acid negatively correlated with the mean SaO2 during sleep (r = −0.25; p = 0.005) and the mean minimal SaO2 at the end of the sleep apnea/hypopnea episodes (r = −0.29; p = 0.001), and positively with oxygen DI (r = 0.21; p < 0.005), AHI (r = 0.18; p < 0.05), and BMI, but did not correlate with age or cholesterol lipid profile.
sCD40L concentrations were higher in the OSA patients with hyperuricemia compared with those having uric acid within a normal range (sCD40L: 9.0 ng/ml vs. 8.0 ng/ml; p < 0.05), although the two groups did not differ appreciably regarding the BMI or lipid profile (Table 2). There was a higher prevalence of hypertension and ischemic heart disease in the patients with hyperuricemia compared with those without it: 88 vs. 60 % (Chi2 = 6.5; p = 0.01) and 31 vs. 11 % (Chi2 = 4.52; p < 0.05), respectively.
Table 2
Comparison of OSA patients with elevated and normal levels of serum uric acid
OSA with uric acid within the norm (n = 26) | OSA with uric acid above the norm (n = 53) | p | |
|---|---|---|---|
Age (year) | 53.7 ± 9.8 | 55.7 ± 6.9 | ns |
BMI (kg/m2) | 33.5 ± 8.0 | 35.4 ± 7.8 | ns |
sCD40L (ng/ml) | 8.0 ± 3.7 | 9.0 ± 3.7 | <0.05 |
CRP (mg/l) | 5.8 ± 6.4 | 7.0 ± 4.1 | <0.05 |
AHI | 34.5 ± 20.8 | 34.3 ± 21.6 | ns |
DI | 32.4 ± 2.8 | 34.4 ± 26.6 | ns |
Total cholesterol (mg/dl) | 210.2 ± 3.6 | 210.0 ± 49.0 | ns |
LDL cholesterol (mg/dl) | 138.4 ± 38.8 | 136.88 ± 46.4 | ns |
HDL cholesterol (mg/dl) | 44.2 ± 19.4 | 49.07 ± 20.3 | ns |
Triglycerides (mg/dl) | 156.8 ± 63.8 | 202.11 ± 131.6 | ns |
4 Discussion
The major finding of the present study was that pro-atherogenic sCD40L is increased in OSA patients and the increase is associated with the severity of OSA, as indicated by the AHI and the dip in arterial oxygen saturation toward the end of breathless episodes. Moreover, we found a positive association between sCD40L and such biomarkers of pro-atherogenic state as uric acid and CRP, and a higher prevalence of cardiovascular diseases in patients with hyperuricemia. Taken together, the assessment of sCD40L, uric acid, and CRP might be helpful in predicting the cardiovascular risk in OSA patients.
An increase in sCD40L in OSA patients has been observed in some previous studies. Akinnusi et al. (2009) examined a small group of 12 OSA patients and found an increased sCD40L compared with a group of 12 controls. Barcelo et al. (2009) compared the plasma level of sCD40L in 41 OSA patients with and without cardiovascular diseases and found an increased level of sCD40 in all, regardless of cardiovascular problems, compared with controls. Minoguchi et al. (2007) demonstrated a higher sCD40L concentration in patients with moderate-to-severe OSA than that in patients with mild OSA or in obese control subjects. However, the association of sCD40L with the severity of OSA has not been obvious. Only in a study of Minoguchi et al. (2007) a connection of sCD40L with AHI has been observed; while the other studies outlined above failed to substantiate it, although a decline of sCD40L after CPAP-treatment was described. Neither has an association between sCD40L and the Epworth Sleepiness Scale (ESS) or arousal index been found (Akinnusi et al. 2009). We found not only a positive correlation of sCD40L with AHI, but also a negative one with the mean minimal SaO2 present at the end of breathless hypoxic episodes. The finding is in line with the influence of hypoxemia on sCD40L observed in other studies, where a positive association of sCD40L with the amount of time spent with a saturation of less than 90 % was described (Akinnusi et al. 2009; Minoguchi et al. 2007; Kobayashi et al. 2006).
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