What Role Does PDGFA Gene Polymorphisms Play in Treating Tennis Elbow with PRP? A Prospective Cohort Study.

BACKGROUND: This study aims to identify genotype variants of the platelet-derived growth factor alpha polypeptide gene (PDGFA) that can influence the individual response to the treatment with platelet-rich plasma (PRP) in tennis elbow patients. METHODS: We observed a cohort of 107 patients (132 elbows) with tennis elbow who received treatment with PRP. Patients have been followed-up for two years after PRP injection and the effectiveness of the treatment was measured using universal patient-reported outcome measures (PROMs): visual analog scale (VAS), quick version of disabilities of the arm, shoulder and hand score (QDASH), and patient-rated tennis elbow evaluation (PRTEE). PROMs values, and clinical and platelet parameters were compared between genotype variants of the studied polymorphisms (rs1800814, rs2070958 and rs62433334). RESULTS: The A allele carriers (rs1800814) had significantly lower values of VAS (week 12), QDASH, and PRTEE (weeks 8, 12). The T allele carriers (rs2070958) had significantly lower values of VAS (weeks 8, 12), QDASH, and PRTEE (weeks 4-12). Additional forms of therapy (manual and physical) were necessary significantly more often in GG (rs1800814) and CC (rs2070958) homozygotes. CONCLUSIONS: The PDGFA gene's polymorphisms influences the effectiveness of PRP therapy in tennis elbow treatment. The effectiveness of PRP is greater in A allele (rs1800814) and T allele (rs2070958) carriers.

Effectiveness of Platelet-Rich Plasma for Lateral Epicondylitis: A Systematic Review and Meta-analysis Based on Achievement of Minimal Clinically Important Difference.

Background: The effectiveness of platelet-rich plasma (PRP) injection in the treatment of lateral epicondylitis remains debatable. Purpose: To evaluate the effectiveness of PRP in lateral epicondylitis treatment using minimal clinically important difference (MCID) values as a reference and to investigate if leukocyte content can influence the effectiveness of the therapy. Study Design: Systematic review; Level of evidence, 4. Methods: Following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, the authors searched the Medline and Scopus databases for studies on lateral epicondylitis and PRP therapy that used the following patient-reported outcome measures (PROMs): visual analog scale (VAS) for pain; Disabilities of the Arm, Shoulder and Hand (DASH); Patient-Rated Tennis Elbow Evaluation (PRTEE); and Mayo Clinic Performance Index (MAYO). The weighted arithmetic means for the PROMs were calculated at baseline (week 0) and follow-up weeks 4, 8, 12, 24, 52, and 104. The mean differences in outcomes (ΔVAS, ΔDASH, ΔPRTEE, and ΔMAYO) were compared with the MCID values at each follow-up point. In addition, the effectiveness of leukocyte-rich PRP (LR-PRP) versus leukocyte-poor PRP (LP-PRP) was also compared. The Student t test was used in all analyses. Results: A total of 26 studies were included in the analysis. After PRP injection, all PROM scores improved with time. The scores improved significantly from baseline to each follow-up time (P < .0001), with the exception of the PRTEE (no significant difference at follow-up weeks 12 and 52). The mean difference in scores from baseline exceeded the respective MCIDs from weeks 4 to 104 for the VAS and DASH, from weeks 4 to 52 for the MAYO, and from weeks 8 to 52 for the PRTEE. The MCID for each of the PROMs was exceeded at almost every observation period in both the LR-PRP and the LP-PRP systems. Conclusion: Based on comparisons with the MCID values of commonly used outcome scores, PRP seems to be an effective form of treatment for lateral epicondylitis. Both the LR- PRP and the LP- PRP systems were effective in the context of meeting the MCID.

Family-Based Cohort Association Study of PRKCB1, CBLN1 and KCNMB4 Gene Polymorphisms and Autism in Polish Population.

The aim of the study was to perform family-based association analysis of PRKCB1, CBLN1 and KCNMB4 gene polymorphisms and autism disorder. We comprised 206 Caucasian children with autistic spectrum disorder (ASD) and their biological parents. In transmission/disequilibrium test we observed that T-allele of the rs198198 polymorphism of the PRKCB1 gene was more often transmitted to affected children in the male subgroup (p = 0.010). Additionally, the T carrier state was significantly associated with hypotonia (p = 0.048). In the female subgroup, the T-allele carriers more often showed more mobile/vital behavior (p = 0.046). In conclusion, our study showed that the rs198198 of the PRKCB1 gene may be associated with ASD in men and with some features characteristic for the disorder.

Why PRP works only on certain patients with tennis elbow? Is PDGFB gene a key for PRP therapy effectiveness? A prospective cohort study.

BACKGROUND: There is variability in individual response to platelet-rich plasma (PRP) therapy in tennis elbow treatment. Genetic variation, especially within genes encoding growth factors may influence the observed inter-individual differences. The purpose of this study was to identify polymorphic variants of the platelet-derived growth factor beta polypeptide gene (PDGFB) that determine an improved individual response to PRP therapy in tennis elbow patients. METHODS: This prospective cohort study was designed in accordance with STROBE and MIBO guidelines. A cohort of 107 patients (132 elbows, 25 bilateral) was studied, including 65 females (77 elbows) and 42 males (55 elbows), aged 24-64 years (median 46.00 ± 5.50), with lateral elbow tendinopathy treated with autologous PRP injection. The effectiveness of PRP therapy was recorded in all subjects at 2, 4, 8, 12, 24 and 52 weeks after PRP injection using the Visual Analog Scale (VAS), quick version of Disabilities of the Arm, Shoulder and Hand score (QDASH) and Patient-Rated Tennis Elbow Evaluation (PRTEE). In order to determine the PDGFB variants with the best response to PRP therapy, patient reported outcome measures were compared between individual genotypes within studied polymorphic variants (rs2285099, rs2285097, rs2247128, rs5757572, rs1800817 and rs7289325). The influence of single nucleotide polymorphisms on blood and PRP parameters, including the concentration of PDGF-AB and PDGF-BB proteins was also analyzed. RESULTS: Our analysis identified genetic variants of the PDGFB gene that lead to a better response to PRP therapy. The TT (rs2285099) and CC (rs2285097) homozygotes had higher concentration of platelets in whole blood than carriers of other genotypes (p = 0.018) and showed significantly (p < 0.05) lower values of VAS (weeks 2-12), QDASH and PRTEE (weeks 2-24). The rs2285099 and rs2285097 variants formed strong haplotype block (r2 = 98, D'=100). The AA homozygotes (rs2247128) had significantly lower values of VAS (weeks 4-52), QDASH and PRTEE (weeks 8, 12). CONCLUSIONS: PDGFB gene's polymorphisms increase the effectiveness of PRP therapy in tennis elbow treatment. Genotyping two polymorphisms of the PDGFB gene, namely rs2285099 (or rs2285097) and rs2247128 may be a helpful diagnostic tool while assessing patients for PRP therapy and modifying the therapy to improve its effectiveness.

The relationship between CYP7A1 polymorphisms, coronary artery disease & serum lipid markers.

Polymorphic variants of the CYP7A1 gene can increase the risk of atherosclerosis-based coronary artery disease (CAD) and modify serum lipid markers. Method: We studied haplotype-tagging single nucleotide polymorphisms of CYP7A1 in the Caucasian population and if they are associated with CAD, its symptoms, and any of its risk factors. Results: We did not find the genetic variants of CYP7A1 to be associated with an increased risk of CAD. However, we did find that the common rs3808607 variant is associated with modified concentrations of serum total cholesterol and LDL. We also found that the C allele and the CC genotype of the rs11786580 are more frequent in patients with myocardial infarction. This association was especially strong after the group differentiation by sex.

Analysis of selected promoter polymorphisms and haplotypes of the CYBA gene encoding the p22phox, subunit of NADPH oxidases, in patients with coronary artery disease.

The p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA gene. It was shown that functionally relevant polymorphisms of the CYBA gene -930A > G, -852C > G, -675A > T, -536C > T, 214C > T (previously described as 242C > T), *24A > G (previously described as 640A > G), and *49A > G modulate generation of reactive oxygen species (ROS). To analyse whether the CYBA gene polymorphisms -852C > G, -675A > T, and -536C > T were associated with coronary artery disease (CAD), and to designate haplotype blocks. Four hundred and ninety subjects: 245 patients with CAD and 245 age and sex-matched controls. The polymorphisms were genotyped using the PCR-RFLP method and the TagMan® Pre-designed SNP Genotyping Assay. The analysed polymorphisms do not form haplotype blocks. Case-control study revealed that the -930 G/-675T and -930G/*49G diplotypes were a CAD risk factor. The 675T/*49G diplotype can modulate CAD risk in women. The protective effect reducing CAD risk in women was related to the -930A/-675T and -930A/*49A diplotypes. Carrier state of the -852C allele (-852C > G) was associated with multivessel stenosis while the CC genotype of the -536C > T polymorphism was more frequent in patients with peripheral artery disease. Hypercholesterolemic, cigarette smokers had an increased risk of CAD, especially C - 852 allele (-852C > G) carriers (SIM = 3.54; odds ratios (OR) = 10.01, p < 0.000). The CYBA gene polymorphisms modulate the risk of CAD but do not form a haplotype blocks.

Relationship between CETP gene polymorphisms with coronary artery disease in Polish population.

The cholesteryl ester transfer protein (CETP) gene encodes a hydrophobic glycoprotein that plays a crucial role in the reverse transport of cholesterol. The aim of the present study was to determine whether CETP polymorphisms (rs1532624, rs247616 and rs708272) are associated with coronary artery disease (CAD) in a Polish population. Serum lipid levels and single nucleotide polymorphisms of CETP genes were determined in 494 subjects: 248 patients with premature CAD and 246 blood donors as controls. Selected polymorphisms were examined using TaqMan PCR analysis. We found that CAD risk was significantly higher for CC homozygotes and C allele carriers of the rs247616 polymorphism than for carriers with the T allele (OR 1.89, 95% CI 1.29-2.76, p = 0.001 and OR 1.51, 95% CI 1.14-1.99, p = 0.003) and likewise for the CC genotype of the rs1532624 polymorphism than for those with the A allele (OR 1.59, 95% CI 1.05-2.40, p = 0.026). Moreover, T allele carriers of the rs708272 polymorphism had significantly higher total cholesterol levels compared to CC homozygotes (p < 0.05) in the healthy controls. We also observed an allelic pattern, C(rs2477616)C(rs708272)C(rs1532624), which increased susceptibility to CAD by 43% (OR = 1.43, 95% CI 1.10-1.85, p = 0.006). In conclusion, the rs247616 and rs1532624 polymorphisms of CETP may modulate the risk of CAD in Polish population.

Upstream Stimulating Factor 1 (USF-1) Gene Polymorphisms and the Risk, Symptoms, and Outcome of Pediatric Ischemic Stroke.

BACKGROUND: Pediatric ischemic stroke is an important cause of morbidity and mortality. As previous studies of children after stroke showed, dyslipidemias were very common in Polish and other European populations. Thus, looking for genetic factors predisposing to pediatric stroke, its symptoms, and outcome, we have analyzed 2 polymorphisms of the upstream stimulating factor 1 (USF-1) gene. MATERIALS AND METHODS: The study group consisted of 82 children with stroke, 156 parents, and 146 controls. We used 2 alternative methods: the case-control model and the analysis of families using the transmission disequilibrium test. The 2 polymorphisms, rs2516839 and rs3737787, were genotyped using the TaqMan Pre-Designed SNP Genotyping Assay. The Statistica 10.0 software was used in all statistical analyses. RESULTS: We did not observe any statistical differences in genotype and allele frequencies between patients and controls. There were also no significant differences in the transmission of alleles from the parents to the affected children. However, we have observed that the TT genotype of the rs2516839 polymorphism was more common in patients with epilepsy and dysarthria, whereas the TT genotype of the rs3737787 polymorphism was more frequent in the group of patients with a decrease in intellectual functioning. CONCLUSIONS: Our study did not show any associations between the 2 analyzed polymorphisms of the USF-1 gene and pediatric ischemic stroke. However, we have observed an influence of specific genotypes on the outcome of stroke, including epilepsy, dysarthria, and a decrease in intellectual functioning.

The rs10757278 Polymorphism of the 9p21.3 Locus in Children with Arterial Ischemic Stroke: A Family-Based and Case-Control Study.

BACKGROUND: The association of 9p21.3 locus single nucleotide polymorphisms with arterial ischemic stroke in adults was demonstrated in many studies, but there are no studies in pediatric arterial ischemic stroke patients. We investigated whether the 9p21.3 locus polymorphism, namely rs10757278, is associated with the arterial ischemic stroke risk in children. METHODS: The study group consisted of 335 individuals: 80 children with arterial ischemic stroke, their biological parents (n = 122), and 133 children (age and sex matched) without any symptoms of arterial ischemic stroke as a control group. The rs10757278 polymorphism was genotyped using the TaqMan® Pre-designed SNP Genotyping Assay (Applied Biosystems). Two different study design models were used: family-based association test (transmission-disequilibrium test) and case-control model. RESULTS: There were no statistically significant differences in the distribution of genotypes and alleles of the rs10757278 polymorphism between groups of children with arterial ischemic stroke and controls. The frequency of both transmitted alleles in transmission-disequilibrium test analysis was identical (50%). The A allele carrier state (AA+AG genotype) was more frequent in arterial ischemic stroke children with hemiparesis than in patients without this symptom (94.5% versus 68.0%, P = .004). CONCLUSIONS: There is no evidence to consider the 9p21.3 locus polymorphism as a risk factor for childhood arterial ischemic stroke.

Ultrafast Scavenging of the Precursor of H(•) Atom, (e(-), H3O(+)), in Aqueous Solutions.

Picosecond pulse radiolysis measurements have been performed in several highly concentrated HClO4 and H3PO4 aqueous solutions containing silver ions at different concentrations. Silver ion reduction is used to unravel the ultrafast reduction reactions observed at the end of a 7 ps electron pulse. Solvated electrons and silver atoms are observed by the pulse (electron beam)-probe (supercontinuum light) method. In highly acidic solutions, ultrafast reduction of silver ions is observed, a finding that is not compatible with a reaction between the H(•) atom and silver ions, which is known to be thermally activated. In addition, silver ion reduction is found to be even more efficient in phosphoric acid solution than that in neutral solution. In the acidic solutions investigated here, the species responsible for the reduction of silver atoms is considered to be the precursor of the H(•) atom. This precursor, denoted (e(-), H3O(+)), is a pair constituting an electron (not fully solvated) and H3O(+). Its structure differs from that of the pair of a solvated electron and a hydronium ion (es(-), H3O(+)), which absorbs in the visible region. The (e(-), H3O(+)) pair , called the pre-H(•) atom here, undergoes ultrafast electron transfer and can, like the presolvated electron, reduce silver ions much faster than the H(•) atom. Moreover, it is found that with the same concentration of H3O(+) the reduction reaction is favored in the phosphoric acid solution compared to that in the perchloric acid solution because of the less-efficient electron solvation process. The kinetics show that among the three reducing species, (e(-), H3O(+)), (es(-), H3O(+)), and H(•) atom, the first one is the most efficient.

The CYBA Gene (⁎)49A>G Polymorphism (rs7195830) Is Associated with Hypertension in Patients with Coronary Artery Disease.

Purpose. Single nucleotide polymorphisms of the CYBA gene may modify the risk of coronary artery disease (CAD). The aim of the present study was to investigate whether the (⁎)49A>G (rs7195830) polymorphism is associated with CAD. Materials and Methods. CYBA gene (⁎)49A>G polymorphism was determined in 481 subjects: 242 patients with premature CAD and 239 age and sex matched controls using the fluorescently labeled allele-specific oligonucleotides method. Results. The frequency of the (⁎)49G allele carrier state was significantly higher in patients than in controls (84.8% versus 76.6%, resp., P = 0.020), as well as the frequency of the (⁎)49G allele (62.2% versus 54.0%, P = 0.009). Both factors were associated with CAD in the analyzed population (OR = 1.70, 95% CI: 1.04-2.76 for GG+AG versus AA and OR = 1.40, 95% CI: 1.08-1.83 for (⁎)49G versus (⁎)49A). Carrier state of the (⁎)49G allele was a stronger and independent risk factor for CAD among women (OR = 4.35, 95% CI: 1.50-13.20, P = 0.002), as well as the (⁎)49G allele (OR = 2.25, 95% CI: 1.34-3.77, P = 0.001). The (⁎)49G allele carrier state was also associated with left ventricular hypertrophy in patients with coronary artery disease (P = 0.015). Conclusion. The CYBA gene (⁎)49A>G polymorphism modifies the risk of coronary artery disease.

Unexpected Ultrafast Silver Ion Reduction: Dynamics Driven by the Solvent Structure.

Picosecond pulse radiolysis measurements have been performed in neutral and highly acidic aqueous solutions containing silver ions at different concentrations. Silver ion reduction is used to understand the ultrafast chemistry of irradiated water and aqueous solutions. The absorption band measured at the end of the 7-ps electron pulses has an intense band with a maximum at 360 nm due to the formation of silver atoms. Kinetics shows that the amount of silver atom formed at the end of the electron pulse in phosphoric acid solutions is greater than that in neutral water. This unexpectedly high yield of silver atom formation cannot be explained solely by the reaction between silver ions and solvated electrons in neutral solutions nor by the reaction with hydrogen atoms in phosphoric acid solutions. To explain the observed ultrafast reduction of silver ions, the presolvated electron, be it free or paired to the hydronium cation, must react very quickly with a silver ion, potentially competing with geminate recombination of the electron and its sibling radical cation.

The rs2516839 Polymorphism of the USF1 Gene May Modulate Serum Triglyceride Levels in Response to Cigarette Smoking.

Single nucleotide polymorphisms (SNPs) of the USF1 gene (upstream stimulatory factor 1) influence plasma lipid levels. This study aims to determine whether USF1 SNPs interact with traditional risk factors of atherosclerosis to increase coronary artery disease (CAD) risk. In the present study serum lipid levels and USF1 gene polymorphisms (rs2516839 and rs3737787) were determined in 470 subjects: 235 patients with premature CAD and 235 controls. A trend of increasing triglycerides (TG) levels in relation to the C allele dose of rs2516839 SNP was observed. The synergistic effect of cigarette smoking and C allele carrier state on CAD risk was also found (SIM = 2.69, p = 0.015). TG levels differentiated significantly particular genotypes in smokers (1.53 mmol/L for TT, 1.80 mmol/L for CT and 2.27 mmol/L for CC subjects). In contrast, these differences were not observed in the non-smokers subgroup (1.57 mmol/L for TT, 1.46 mmol/L for CT and 1.49 mmol/L for CC subjects). In conclusion, the rs2516839 polymorphism may modulate serum triglyceride levels in response to cigarette smoking. Carriers of the C allele seem to be particularly at risk of CAD, when exposed to cigarette smoking.

CYP7A1 gene polymorphism located in the 5' upstream region modifies the risk of coronary artery disease.

BACKGROUND: 7-Alpha cholesterol hydroxylase (CYP7A1), the first enzyme of classic conversion pathway leading from cholesterol to bile acids synthesis, is encoded by CYP7A1 gene. Its single nucleotide polymorphisms (SNPs) influence serum lipid levels and may be related to impaired lipid profile leading to coronary artery disease (CAD). The aim of the present study was to analyze the possible association between the rs7833904 CYP7A1 polymorphism and premature CAD. MATERIAL AND METHODS: Serum lipid levels and rs7833904 SNP were determined in 419 subjects: 200 patients with premature CAD and 219 age and sex matched controls. RESULTS: The A allele carrier state was associated with CAD (OR = 1.76, 95% CI; 1.14-2.71, P = 0.014). The effect was even stronger in the male subgroups (OR = 2.16, 95% CI; 1.28-3.65, P = 0.003). There was no effect in the females. Risk factors of CAD and clinical phenotype of atherosclerosis were not associated with genotype variants of the rs7833904 SNP. Lipid profiles also did not differ significantly between individual genotypes. CONCLUSION: The CYP7A1 rs7833904 polymorphism may modify the risk of CAD. This effect is especially strong in male subjects. The studied polymorphism does not significantly influence serum lipid levels, in the present study.

Methylenetetrahydrofolate reductase gene A1298C polymorphism in pediatric stroke--case-control and family-based study.

Moderate hyperhomocysteinemia is one of the risk factors of pediatric stroke. Methylenetetrahydrofolate reductase (MTHFR) is an important enzyme, which regulates homocysteine metabolism, and some polymorphisms of gene encoding this enzyme are associated with a decreased activity of the enzyme. The aim of the study was to assess an association between the A1298C polymorphism and pediatric stroke. We also evaluated a possible synergistic effect of A1298C and C677T polymorphisms of this gene. The study group consisted of 88 children after ischemic stroke, 142 of their parents and 111 controls. The A1298C polymorphism was genotyped using the restriction fragment length polymorphism method. We used 2 study designs: a case-control model and a family-based association test. The Statistica 7.1 and EpiInfo 6 softwares were used in all analyses. We did not observe any statistically significant differences either in the transmission of the A allele in the family-based test or in the frequency of the A allele in the patients group compared with the controls. We also did not notice any significant additive or synergistic effects between the A1298C and C677T polymorphisms. An analysis of the results obtained in this study and a critical review of previously published studies indicate that the A1298C polymorphism of the MTHFR gene is not related to ischemic stroke in children.

CYP3A5*3 and C3435T MDR1 polymorphisms in prognostication of drug-resistant epilepsy in children and adolescents.

Drug-resistant epilepsies still remain one of the most profound problems of contemporary epileptology. Several mechanisms of drug resistance are possible; among them, genetic factors have a prominent place. Much importance is attached to genes, which encode enzymes that metabolize antiepileptic drugs CYP 3A, which belong to the family of cytochromes P450 and the genome of multidrug resistance, such as multidrug resistance 1 (MDR1) that expresses P-glycoprotein (P-gp), a drug transporter protein. The aim of the study was to assess the relation between polymorphism of gene CYP3A5 and polymorphism C3435T of MDR1 gene with the occurrence of focal, drug-resistant epilepsy in children and youths up to 18 years of age. The study comprised 85 patients, and their age range was from 33 months to 18 years of age, suffering from epilepsy, partly responding well to treatment, partly drug resistant. The polymorphism of both genes has been analysed using the PCR-RFLP method. The study failed to corroborate association between polymorphism CYP3A5*3 and C3435T polymorphism in MDR1 gene and pharmacoresistant epilepsy. The results of our research do not confirm the prognostic value of the polymorphisms examined in the prognostication of drug resistance in epilepsies.

Spur reactions observed by picosecond pulse radiolysis in highly concentrated bromide aqueous solutions.

The formation of the well-known product Br3(-), observed in the steady-state radiolysis of highly concentrated Br(-) aqueous solutions, has now been directly observed at ultrashort times corresponding to the relaxation of the spur. The transient absorption induced by picosecond pulse radiolysis of 6 M Br(-) aqueous solution was probed simultaneously at 260 nm with the third harmonic laser wave and from 350 to 750 nm with a supercontinuum generated by the fundamental laser wave. This approach allows several transient radiolytic species to be followed in parallel, particularly the solvated electron, BrOH(-•), Br2(-•), and Br3(-). The kinetics measured within 4 ns at 260 and 370 nm clearly exhibit that the decay of Br2(•-) is correlated with the formation of Br3(-). In highly concentrated Br(-) solutions, the OH(•) radical is fully replaced by Br2(•-), and the spur kinetics of OH(•) radical in pure water is comparable with that of Br2(-•). Model calculations indicate that the main OH(•) radical combination product H2O2 in pure water has formation kinetics similar to that of Br3(-) in 6 M Br(-) solutions. Moreover, they point out that oxidation of Br(-) occurs within the electron pulse both by direct energy absorption and by scavenging of the water radical cation, H2O(•+).

Polymorphisms of genes encoding coagulation factors II, V, VII, and XIII in relation to pediatric ischemic stroke: family-based and case-control study.

BACKGROUND: The investigation of a possible association between the FII, FV, FVII, and FXIII genes polymorphisms and pediatric ischemic stroke (IS). METHODS: The study group consisted of 392 individuals, including 81 children with IS, their biological parents (n=162), and 149 control children. The polymorphisms were genotyped using polymerase chain reaction-restriction fragments length polymorphism method. The relation between analyzed polymorphisms and the disease was tested by 2 independent methods: family-based association test-transmission/disequilibrium test (TDT) and classic case-control model. RESULTS: We did not observe any preferential distribution of any analyzed allele from parents to the affected children. For the FVII gene polymorphism, there was a trend toward a higher frequency of the R allele. In a case-control model, the differences between the patients and controls in the frequency of the Q allele, Q allele carriers, and RR homozygotes lay close to the border of statistical significance (P=0.08). There were no significant differences in genotype and allele distribution between patients and controls in case of other polymorphisms. CONCLUSIONS: Analyzed polymorphisms of coagulation factors are not significant determinants of pediatric IS in the studied population; however, these findings require a confirmation in a larger group of participants.