Increased platelet activation and aggregation are central processes in the pathophysiology of atherosclerosis. Increased platelet activity is associated with increased platelet volume. Mean platelet volume (MPV), a determinant of platelet function, is a newly emerging risk factor for atherothrombosis. Familial Mediterranean Fever (FMF) is an autosomal recessive disease characterized by recurrent inflammatory febrile attacks of serosal and synovial membranes. Recently few studies have shown that FMF is associated with increased atherosclerosis risk. The present study was designed to evaluate levels of MPV in FMF patients compared with healthy subjects. We selected 35 FMF patients and 35 healthy control subjects matched for age, gender, and body mass index. Metabolic parameters and MPV levels were measured in all groups. Metabolic parameters were not different among the study groups (p > 0.05). The levels of MPV were significantly higher in the FMF group than in the control group (8.6 +/- 0.9 fl vs 7.8 +/- 0.5 fl, p = 0.001). The MPV levels were negatively correlated with duration of colchicine treatment (r = -0.40, p = 0.017). Also MPV levels showed positive correlation with delay of diagnosis (r = 0.58, p = 0.001). In conclusion, our results suggest that patients with FMF tend to have an increased platelet activation. Increased platelet activity could contribute to increasing the atherosclerotic risk in FMF patients.

The pathophysiological mechanism of hypertensive retinopathy (HR) is not fully established. Elevated blood pressure alone does not fully account for the extent of retinopathy so other pathogenic mechanisms may be involved, such as increased platelet activation. Mean platelet volume (MPV) is a marker of platelet activation. Therefore, this study was designed to answer the following questions: Do MPV levels change in HR? and is there any relation between degree of HR and MPV levels? This study included newly diagnosed and 57 untreated essential hypertensive patients with HR. The hypertensive patients were divided into two groups according to the Keith, Wagener classification. Group 1 comprised 29 hypertensive patients with grade 1 HR with a mean age of 56.8 +/- 9.7 years. Group 2 comprised 28 hypertensive patients with grade 2 HR with a mean age of 58.1 +/- 10.3 years. Twenty-seven normotensive subjects who were the healthy participants and had undergone the check-up program were used as the control group. Fundoscopic examination, metabolic parameters and MPV levels were measured in all groups. The level of MPV in group 2 was significantly higher than in group 1 (8.9 +/-0 0.8 fl vs. 8.3 +/- 0.8 fl, p = 0.02) and the normotensive control group (8.9 +/- 0.8 fl vs 7.8 +/- 0.7 fl, p < 0.001). It was also higher in group 1 than in normotensive control group (8.3 +/- 0.8 fl vs.7.8 +/- 0.7 fl, p < 0.01). In addition, MPV showed a positive correlation with the degree of HR in the hypertensive group (r = 0.41, p = 0.015). Our study suggests that platelet activation, a mechanism known to be involved in vascular lesions, may promote the development of HR.

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There have been few studies concerning the cytokine profiles in gastric mucosa of Helicobacter pylori–infected patients with normal mucosa, chronic gastritis, and gastric carcinoma (GAC).In the present study, we aimed to elucidate the genomic expression levels and immune pathological roles of cytokines—interferon (IFN)-γ, tumor necrosis factor (TNF)-α, interleukin (IL)-4, IL-6, IL-10, transforming growth factor (TGF)-β, IL-17A, IL-32—in H pylori–infected patients with normal gastric mucosa (NGM; control), chronic active gastritis (CAG), and GAC. Genomic expression levels of these cytokines were assayed by real-time PCR analysis in gastric biopsy specimens obtained from 93 patients.We found that the genomic expression levels of IFN-γ, TNF-α, IL-6, IL-10, IL-17A mRNA were increased in the CAG group and those of TNF-α, IL-6, IL-10, IL-17A, TGF-β mRNA were increased in the GAC group with reference to H pylori–infected NGM group.This study is on the interest of cytokine profiles in gastric mucosa among individuals with normal, gastritis, or GAC. Our findings suggest that the immune response of gastric mucosa to infection of H pylori differs from patient to patient. For individual therapy, levels of genomic expression of IL-6 or other cytokines may be tracked in patients.