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  • Author: Tatjana Jevtović-Stoimenov x
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Open access

Tatjana Jevtović-Stoimenov, Danica Marković, Milena Despotović, Dušica Pavlović and Gordana Kocić

Summary

TNF-alpha and LT-alpha are involved in the pathogenesis of established lymphoproliferative diseases. Both molecules bind to TNFRI and TNFRII. TNFRI is the major mediator of the TNF pro-apoptotic and proliferative effects and TNFRII might enhance these effects. TNF receptors I and II are normally present on hematopoetic cells. TNFR II is characteristic only on immune cells, especially on peripheral leukocytes. Neoplastic B cells and activated B lymphocytes have increased expression of surface TNFR I. In this study, we have analyzed polymorphisms in the TNFRI gene (TNFRI+36A/G SNP) and polymorphism in the TNFRII gene (TNFRII + 676 T/G). All these polymorphisms were studied in patients with chronic lymphocytic leukemia (CLL), patients with non-Hodkin’s lymphoma (NHL) and in healthy controls. The present study was undertaken to investigate the genetic association of these polymorphisms with lymproproliferative disease development.

A total of 68 patients (49-CLL, 19-HNL) were diagnosed at the Clinic of Hematology, Clinical centre Niš, Serbia, using clinical findings and conventional morphological, cytochemical and immunological tests. Genomic DNA was isolated from isolated lymphocytes by proteinase K/phenol/chloroform method, and genotyped for TNFR I (A36G) and TNFR II (T676G) using the PCR-RFLP method.

No significant differences in allele frequencies of TNFR1 polymorphism were found between the patients with lymphoproliferative disease and healthy individuals. In a group of healthy individuals, the study has revealed for the first time significantly higher TNFRI G/G genotype compared to the patients with lymphoproliferative disease (χ22 = 5.66; p = 0.017). Also, we reported the implication of TNFRII T allele in NHL pathogenesis, respectively (χ22 = 10.77; p = 0.001; Mantel-Haenszel: χ22 = 10.64; p = 0.0011).

Our data showed that TNFRII T676G polymorphisms have an important role in NHL pathogenesis but not in CLL patients. A/A polymorphism in TNFRI was not associated with CLL and NHL patients in the Serbian population. Investigated polymorphisms on TNFR genes in leukemic cells of CLL and NHL patients have not showed a correlation with increased proliferation of B lymphocytes and increased expression of TNF R II on B CLL lymphocytes.

Open access

Sonja Stojanović, Bojana Stamenković, Jovan Nedović, Tatjana Jevtović-Stoimenov and Dušica Pavlović

Summary

To examine whether the presence of the rare A allele of the TNF-Alpha-308 G/A gene polymorphism is associated with erosive arthritis and rapid radiological progression of the disease.

The examined group included 131 patients with early RA. Using the PCR-RFLP method, the TNF-Alpha-308 G/A gene polymorphism was determined for all patients. In relation to the presence of the A allele of the examined polymorphism, the patients were divided into two subgroups: subgroup A (G/A and A/A genotypes) and subgroup G (G/G genotype). Based on the presence of the destructive changes in joints found in the initial radiographs, the findings were classified as erosive and non-erosive RA. Radiological progression was assessed on the basis of the annual change in the Larsen score – LS (0-200).

Group A comprised 62 (47.33%) patients, while group G comprised 69 (52.67%) patients. The presence of cysts and erosions in subgroups A and G was compared before the start of the methotrexate therapy. It was determined that erosions (erosive RA) were statistically significantly more frequent in group A (83.87% of patients) in comparison with group G (44.93% of patients), p < 0,001. Group A patients had a higher value of the Larsen score in relation to the group G both before and after methotrexate was administered for a year (before therapy, LS in group A: 48.58 ± 20.54; in group G 20.73 ± 12.31; p < 0.01; after MTX therapy, LS in group A: 58.32 ± 22.25; in group G 25.35 ± 14.57; p < 0.001). The average value of the annual LS change in group A was statistically significantly greater than the change in group G patients (9.98 ± 4.95 to 5.23 ± 2.72) (p < 0.05).

The presence of the A allele of the TNF-Alpha-308 G/A gene polymorphism is associated with the occurrence of early erosive joint changes and more rapid radiological progression of the disease.

Open access

Milena Despotović, Tatjana Jevtović Stoimenov, Ivana Stanković, Jelena Bašić, Branka Đorđević and Dušica Pavlović

Summary

Bronchial asthma (BA) is a chronic inflammatory disease of the airways in the pathogenesis of which oxidative stress has a very important role. Single nucleotide polymorphisms (SNPs) in catalase gene may result in decreased antioxidative defense capacity, and thus a higher risk for BA development. Since oxidative stress has an important role in the pathogenesis of BA and catalase has a key role in antioxidant defense, the aim of this study was to examine the association of CAT C-262T polymorphism with BA in Serbian patients with BA.

A total of 170 subjects (79 patients with BA and 91 controls) were screened for CAT C-262T SNP using PCR-RFLP method.

The analysis of genotype distribution did not show statistically significant differences between BA patients and controls (p > 0.05). Moreover, no differences were detected when comparison was performed based on dominant or recessive model. The distribution of CAT-262C and CAT-262T alleles did not show differences between patients and healthy controls (p = 0.715; OR = 1.091; 95% CI = 0.684–1.741). Further analysis of genotype and allele distributions, based on stratification by sex, did not show significant differences between BA patients and controls (p > 0.05).

This is the first study that examined CAT C-262T (rs1001179) SNP in Serbian patients with BA. The results obtained in this study showed that biallelic SNP at the position-262 in the catalase gene is not associated with BA in the Serbian population.

Open access

Olivera Andrejić, Rada Vučić, Svetlana Apostolović, Milan Pavlović, Dragana Stokanović, Valentina Nikolić, Tatjana Jevtović-Stoimenov and Stefan Momčilović

Summary

The aim of our study was to determine the factors influencing galectin-3 levels in patients with acute coronary syndrome and decreased left ventricular ejection fraction. We collected material from 37 successive patients with acute coronary syndrome and decreased left ventricular ejection fraction, of which 19 patients had atrial fibrillation, and 18 patients who were without atrial fibrillation constituted a control group. Blood samples used for the biochemical measurements were obtained on the third day from acute coronary syndrome. We used Statistical Package for Social Sciences for data analysis. A p-value less than 0.05 was considered to be a measure of statistical significance. Galectin-3 concentration is directly correlated with age and B-type natriuretic peptide level. Also, our results showed an inverse correlation between galectin-3 and total body weight, body mass index, body surface area and creatinine clearance. The following variables were found to be significant predictors of galectin-3 level: decreased left ventricular ejection fraction, total body weight, LDL concentration and body mass index. We identified factors that can predict a decrease in the left ventricular ejection fraction below 45% after acute coronary syndrome: atrial fibrillation increases the risk by almost six times, and urea concentration increases the risk by 1.2 times for each unit. Left ventricular ejection fraction below 45%, TBW, body mass index and LDL level are good predictors of galectin-3 concentration in patients with ACS and decreased left ventricular ejection fraction. Atrial fibrillation could be a predictive marker of decreased left ventricular ejection fraction.