No relationship between lipoprotein-associated phospholipase A2, proinflammatory cytokines, and neopterin in Alzheimer's disease.

OBJECTIVE: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a reported risk factor for dementia. However, the relationship between Alzheimer's disease (AD) and Lp-PLA2 is still debatable and, to the best of our knowledge, no study has evaluated the associations between levels of Lp-PLA2, proinflammatory cytokines, and neopterin in AD. METHODS: In total, 59 patients with AD and 38 non-demented individuals were included in the case-control study. Fasting serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), neopterin, and Lp-PLA2 were determined using ELISA. The associations between AD and each of the variables were analyzed by logistic regression. RESULTS: The median Lp-PLA2 levels in AD and controls were similar (P=0.29, not significant). Median serum neopterin and IL-6 levels were significantly higher in patients with AD than in controls (P=0.0001 and P=0.03, respectively). In regression analyses, median neopterin levels, a lower level of education, and female gender were significantly associated with AD when compared with controls (OR, 31.44, 95% CI 3.59-275.28, P=0.002; OR, 4.35, 95% CI 1.13-16.61, P=0.032; OR, 7.25, 95% CI 1.88-28.00, P=0.004, respectively). CONCLUSION: In contrast to previous evidence suggesting its role in dementia and AD, Lp-PLA2 enzyme levels were higher in the controls, and no relationship between Lp-PLA2 and either proinflammatory cytokines or neopterin was identified in AD. Elevated neopterin levels may be considered inflammatory markers of AD.

Association of uric acid and carotid artery disease in patients with ischemic stroke.

BACKGROUND AND PURPOSE: Some previous studies reported an independent association between uric acid and coronary artery disease, while little is known on the association among uric acid and carotid artery disease (CAD). To address this issue, we investigated the association between CAD and higher uric acid level because of the well-known importance of the carotid artery pathologies for ischemic stroke. METHODS: Between 2009 and 2012, we conducted a study among 406 consecutive first-ever ischemic stroke patients to assess the relationship between uric acid and carotid artery. A mean intima-media thickness IMT was calculated for the wall of the left and right common carotid arteries (CCA) and IMT of the bifurcation of the carotid arteries. CAD was assessed by neuroimaging techniques in patients with carotid artery stenosis more than 50%. Logistic regression models were used to determine the relation among pathological changes of the carotid artery and higher uric acid level. RESULTS: In patients with hyperuricemia, the frequency of age (>60 years), hypertriglyceridemia, higher apo B, renal failure were significantly higher than those with normal uric acid level. CAD was more frequent in patients with hyperuricemia than those with normal uric acid level (OR, 1.8, 95% CI, 1.1-3.1; P = 0.01). In patients with higher uric acid level, the mean of the IMT of the CCA and of the bifurcation of the carotid artery were higher than those with normal uric acid level (P = 0.001 for each). Covariance matrix analysis displayed a strong correlation between CAD and age (>60 years) (P < 0.05), sex (P < 0.01), hyperuricemia (P < 0.01), hypertension (P < 0.05), and hypercholesterolemia (P < 0.05). In the models of regression analysis, a strong association was found among patients with CAD and sex, renal failure, hyperuricemia, number of plaques, and size of plaques. CONCLUSION: Our study demonstrated that higher uric acid level is strongly associated with CAD. Elevated uric acid might be injurious for large cerebral arteries with some probable confounding risk factors. Further prospective large clinical trials will determine whether lowering uric acid level reduces the frequency of CAD and ischemic stroke.

Effect of different levels of cigarette smoking on lipid peroxidation, glutathione enzymes and paraoxonase 1 activity in healthy people.

The purpose of this study was to examine the effect of different levels of cigarette smoking on lipid peroxidation, glutathione enzymes and paraoxonase 1 (PON1) activity in a healthy population. The study included 130 subjects who were classified as mild (20 cigarettes daily, Group III, n=33) and never smokers (controls, Group IV, n=32). Malondialdehyde (MDA) levels, PON1 and erythrocyte glutathione enzyme activities were measured. MDA levels were significantly higher in smokers than never smokers (P<0.05 for Group I, P<0.001 for Group II and III). PON1 activity was significantly lower in heavy smokers (P<0.001). Glutathione peroxidase (GSH-Px) activity was significantly lower in the smokers (P<0.0001). Glutathione reductase (GR) activity was significantly higher in smokers (P<0.0001). MDA levels negatively correlated with PON1 and GSH-PX activities (P<0.01), whereas they positively correlated with GR activities (P<0.001). At every level, cigarette smoking is associated with increased lipid peroxidation and causes an impairment in antioxidant systems.

Increased thickness of the carotid artery intima-media assessed by ultrasonography in Behçet's disease.

OBJECTIVE: Behçets disease (BD), is a unique systemic vasculitis, which affects almost all types and sizes of blood vessels. Carotid intima-media thickness (IMT) is an endothelial cell dysfunction (ECD) parameter which may also be associated with atherosclerosis. We aimed to search carotid IMT and plaque formation in BD, using high-resolution B-mode Doppler ultrasonography (USG). METHODS: We studied 114 BD patients (M/F: 68/46; mean age 38.15 +/- 9.44 years; disease duration 121 +/- 79 months), being followed up by Ege University Rheumatology Department. Age and sex-matched, 77 healthy controls, and as the disease control group 46 non-matched SLE patients were also included. Exclusion criteria for all the study participants were hypertension, hyperlipidemia, diabetes mellitus, obesity and history of cardiovascular or cerebrovascular disease. Comparison of the three groups were made by ANOVA and for post-hoc confirmation, Bonferoni test was used. RESULTS: The carotid IMT in BD (mean +/- SD, 0.55 +/- 0.14 mm) was significantly higher than in healthy controls (0.48 +/- 0.09 mm) (p = 0.004), but significantly lower than in SLE (0.66 +/- 0.24 mm) (p = 0.001). Likewise, plaque frequency in BD (5/114) was significantly higher than in healthy controls (0/77), but significantly lower than in SLE (8/46) (p < 0.001). CONCLUSION: Despite significantly higher carotid IMT and plaque frequency in BD compared with healthy controls, these parameters in BD were not as marked as in SLE. Less severe carotid artery abnormalities in BD, may partially explain why cardiovascular morbidity and mortality do not seem to be increased in BD, unlike in SLE.