Thrombotic and Atherogenetic Predisposition in Polyglobulic Donors.

This work analyses the results of research regarding the predisposition of genetic hematological risks associated with secondary polyglobulia. The subjects of the study were selected based on shared laboratory markers and basic clinical symptoms. JAK2 (Janus Kinase 2) mutation negativity represented the common genetic marker of the subjects in the sample of interest. A negative JAK2 mutation hypothetically excluded the presence of an autonomous myeloproliferative disease at the time of detection. The parameters studied in this work focused mainly on thrombotic, immunological, metabolic, and cardiovascular risks. The final goal of the work was to discover the most significant key markers for the diagnosis of high-risk patients and to exclude the less important or only complementary markers, which often represent a superfluous economic burden for healthcare institutions. These research results are applicable as a clinical guideline for the effective diagnosis of selected parameters that demonstrated high sensitivity and specificity. According to the results obtained in the present research, groups with a high incidence of mutations were evaluated as being at higher risk for polycythemia vera disease. It was not possible to clearly determine which of the patients examined had a higher risk of developing the disease as different combinations of mutations could manifest different symptoms of the disease. In general, the entire study group was at risk for manifestations of polycythemia vera disease without a clear diagnosis. The group with less than 20% incidence appeared to be clinically insignificant for polycythemia vera testing and thus there is a potential for saving money in mutation testing. On the other hand, the JAK V617F (somatic mutation of JAK2) parameter from this group should be investigated as it is a clear exclusion or confirmation of polycythemia vera as the primary disease.

Plasma levels and leucocyte RNA expression of adipokines in young patients with coronary artery disease, in metabolic syndrome and healthy controls.

OBJECTIVES: Little is known about the role of adipokines in the pathogenesis of coronary artery disease in young patients. The aims of this study were to compare serum levels of adipokines and expression of adipokines in peripheral blood leukocytes in patients with premature coronary artery disease (CAD), metabolic syndrome and healthy individuals. DESIGN AND METHODS: Sixty-five patients with premature CAD (men 18-45years old and women 18-55years old) formed the study group. The control groups were 75 patients with metabolic syndrome and 50 healthy individuals. For each group, RNA expression in peripheral blood leukocytes was determined for 24 different adipokines and 11 adipokines were examined in serum. RESULTS: In individuals with CAD, serum visfatin levels were significantly higher than in metabolic syndrome and healthy controls (2.3 vs. 1.6 vs. 0.7µg/L, P<0.001) while both omentin-1 (92.9 vs. 587.0 vs. 552.3µg/L, P<0.001) and ZAG2 (45.5 vs. 72.5 vs. 77.1mg/L, P<0.001) levels were lower. The receiver operating curve (ROC) analysis for testing the validity of these adipokines in the diagnosis of CAD compared to control groups provided the following areas under the curve (AUC): omentin-1 AUC 0.97 (cut-off ≤222µg/L), ZAG2 AUC 0.89 (cut-off ≤51.7mg/L) and visfatin AUC 0.74 (cut-off ≥1.0µg/L) (P<0.001 in all cases). Visfatin and omentin-1 serum levels did not differ between the acute phase of myocardial infarction and the chronic phase of CAD. In patients with CAD, we found no significant relation between mRNA expression and adipokine concentration. CONCLUSION: Serum omentin-1, visfatin and ZAG2 could serve as biomarkers of premature CAD in young apparently healthy people.

Omentin-1 levels in patients with premature coronary artery disease, metabolic syndrome and healthy controls. Short communication.

OBJECTIVES: Omentin-1 is an adipokine which could have a protective role against the manifestation of atherosclerosis. Only limited data are available on omentin-1 serum values in patients with premature clinical manifestations of atherosclerosis. DESIGN AND METHODS: We tested omentin-1 in human serum by ELISA method in 61 individuals with a premature manifestation of coronary artery disease (CAD), 40 patients with metabolic syndrome and 40 healthy control subjects. RESULTS: Omentin-1 serum levels were significantly lower in patients with CAD (103.1±62.7 mg/L) compared to metabolic syndrome (668.2±339.6 mg/L) and healthy subjects (623.0±373.5 mg/L) (P < 0.01). In CAD patients, omentin-1 serum levels did not differ between patients sampled in the acute phase of myocardial infarction (n = 28; 110.3±82.4 mg/L) and in the chronic phase several months or years after myocardial infarction (n = 33; 97.0±39.3 mg/L) (P = 0.41). We found a weak positive correlation between omentin-1 and body mass index (r = 0.21, P = 0.014). No significant correlation was found between peak cardiac troponin T and omentin-1 (correlation coefficient r = 0.118, P = 0.406). CONCLUSION: Serum omentin-1 seems to be a useful biomarker of coronary artery disease across the whole age spectrum.