Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).

The present study was designed to investigate the interaction between platelet indices, inflammatory markers and disease activity in rheumatoid arthritis (RA) subjects. The effects of anti-TNF-alpha therapy and conventional treatment on platelet indices were also compared. We studied 97 patients with RA (19 men, 78 women: mean age 51 years) and 33 age and sex-matched healthy subjects as a control group. All RA patients were administered conventional therapy. After 3 months of therapy, 35 subjects who had high disease activity score (DAS28 > 5.1) were grouped as non-responders and were administered infliximab as a TNF-alpha blocker at the standard intravenous dose. Responders to the conventional therapy and non-responders were also compared. At baseline white blood cell (WBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), platelet count and mean platelet volume (MPV) were significantly higher in patients with RA. Mean platelet volume was positively correlated with DAS28 score (r = 0.27; p = 0.007). These markers of inflammation and platelet indices were substantially decreased after therapy. The reductions were similar in responders to conventional therapy and non-responders (TNF alpha group). In conclusion, we found that MPV was correlated with inflammatory markers and disease activity in patients with RA. Both anti-TNF-alpha and conventional therapy decreases markers of inflammation and platelet indices. MPV can reflect both disease activity and response to treatment.

Abdominal obesity is the main determinant of uric acid variance. An increment of 1 SD in serum uric acid levels are associated in both sexes with a 35% higher MS likelihood, independent of 10 risk factors related to MS. After adjustment for waist girth, a more modest but significant likelihood persists, which suggests that serum uric acid is a determinant of MS.

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The present study was designed to investigate the interaction between platelet indices (mean platelet volume (MPV), platelet count (PLC) and platelet mass (PLM)), inflammatory markers and disease activity in ankylosing spondylitis (AS) subjects. The effects of anti-TNF-alpha therapy and conventional treatment on platelet indices were also compared. We studied 68 patients with AS (group I, 46 men, age: 36.4 +/- 6.9 years) and as control group 34 age and sex-matched healty subjects. All patients received conventional therapy (CT) at the beginning (Group I). The patients were reevaluated after 3 months according to Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) score. Group II consisted of 35 subjects who responded to the CT and continued to take the same therapy for 3 months additionally. Group III consisted of 33 subjects who had a high disease activity score (BASDAI > 4) after 3 months and were accepted refractory to the CT therapy. In Group III the treatment was switched to infliximab and continued for 3 months at the standard intravenous dose. Significantly higher baseline MPV, PLC and PLM was reported as compared to controls decreased by therapy (9.12 +/- 1.20 vs. 8.35 +/- 0.94 fl, p < 0.001, 340 +/- 69 vs. 251 +/- 56 (x 10(3)/ microL) p < 0.0001, 3096 +/- 736 vs. 2110 +/- 384; p < 0.0001, respectively). In the same way, they were substantially lowered by both treatments in group II and group III. PLC and PLM were positively correlated with WBC and ESR (r : 0.44; p < 0.0001, r : 0.41; p = 0.001, r : 0.52; p < 0.0001, r : 0.41; p = 0.001), respectively) in AS patients. Additionally, MPV and PLM were positively correlated with BASDAI score (r : 0.41; p < 0.001, r = 0.29; p < 0.001 respectively). We have found that increased platelet activity reduced by therapy in AS patients. Additionally, it was correlated with inflammatory markers and disease activity. According to these results, it can be suggested that both anti-TNF-alpha and conventional therapy might contribute to a decrease in the risk of cardiovascular morbidity and mortality in AS patients.

Objectives: To investigate the role of serum apolipoprotein (apo) B levels in predicting metabolic syndrome (MS), hypertension, atherogenic dyslipidemia and type II diabetes. Methods: Prospective evaluation of 1125 men and 1223 women, aged 28-74 years, participating in the survey 1997/1998 who had serum apo B determinations and were followed-up for a mean 5.9 years. Tertiles of apo B were formed by cut points by 120 and 95 mg/dl. MS was defined by modified ATPIII criteria. Results: Apo B values exhibited no significant difference among sexes. Low-density lipoprotein (LDL)-cholesterol and triglycerides were their leading determinants on linear regression analysis. By logistic regression analyses, the top versus bottom apo B tertile predicted significantly newly developing MS in both sexes separately with two-fold relative risks (RRs) (Po0.02) and the development of high triglyceride/low high-density lipoprotein-cholesterol dyslipidemia with nearly threefold RRs (P ¼ 0.001), after adjustment for waist circumference, C-reactive protein (CRP), physical activity grade and family income category. Development of hypertension was predicted only in women by the apo B top tertile (fully adjusted RR 1.71 [95% CI 1.001; 2.92]), while the significance of the prediction regarding age-adjusted diabetes in women (RR 1.86 [95% CI 1.04; 3.36]) attenuated after adjustment for the stated confounding factors. Conclusions: Apo B concentrations, which reflect the number of small, dense LDL particles in plasma, are a significant predictor of cardiometabolic risk among adults with a high prevalence of MS, independent of waist circumference and CRP.

In the present study, we examined (i) whether C3 (complement C3) was an independent marker of prevalent CHD (coronary heart disease), and (ii) which preferential associations existed between C3 and some cardiovascular risk factors when jointly analysed with CRP (C-reactive protein) and fibrinogen. In a cohort of 756 unselected adults, 39% of whom had the metabolic syndrome, C3 and other risk variables were evaluated in a cross-sectional manner. In a logistic regression model for the likelihood of CHD, a significant OR (odds ratio) of 3.5 [95% CI (confidence intervals), 1.27 and 9.62)] for C3 was obtained after adjustment for smoking status, TC (total cholesterol) and usage of statins. A similar model, also comprising systolic blood pressure, with a cut-off point of >or=1.6 g/l C3 exhibited a 1.9-fold risk (95% CI, 1.01 and 3.58) compared with individuals below the cut-off point. Both analyses displayed an adjusted OR of 1.37 for each S.D. increment in C3. The significant relationship of C3 with a likelihood of CHD also proved to be independent of CRP. In multiple linear regression models, associations were tested for each acute-phase protein with measures of obesity, fasting insulin, triacylglycerols (triglycerides), TC, HDL (high-density lipoprotein)-cholesterol, physical activity, smoking status, diagnosis of metabolic syndrome and family income. When both genders were combined, C3 was independently associated with serum triacylglycerols, waist circumference, BMI (body mass index) and TC. CRP was independently associated with waist circumference, TC, family income (inversely) and physical activity, and fibrinogen with BMI, TC, smoking status and metabolic syndrome. In summary, elevated levels of complement C3 are associated with an increased likelihood of CHD independent of standard risk factors and regardless of the presence of acute coronary events, suggesting that C3 might be actively involved in coronary atherothrombosis. Unlike CRP and fibrinogen, C3 was preferentially associated with waist girth and serum triacylglycerols.