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2 results on '"MBL genetic variant"'

1. High rate of in-stent restenosis after coronary intervention in carriers of the mutant mannose-binding lectin allele.

Author

Bagyura, Zsolt, Kiss, Loretta, Berta, Balázs, Szilágyi, Ágnes, Hirschberg, Kristóf, Széplaki, Gábor, Lux, Árpád, Szelid, Zsolt, Soós, Pál, and Merkely, Béla

Subjects
CORONARY restenosis, MANNOSE-binding lectins, ATHEROSCLEROSIS, SINGLE nucleotide polymorphisms, POLYMERASE chain reaction, LOGISTIC regression analysis
Abstract

Background: In-stent restenosis occurs in 10-30% of patients following bare metal stent (BMS) implantation and has various risk factors. Mannose-binding lectin (MBL) is known to have effect on the progression of atherosclerosis. Single nucleotide polymorphisms (SNP) of the MBL2 gene intron 1 (codon 52, 54, 57) are known to modulate the bioavailability of the MBL protein. Our aim was to identify the association of these polymorphisms of the MBL gene in the occurrence of in-stent restenosis after coronary artery bare metal stent implantation.Methods: In a non-randomized prospective study venous blood samples were collected after recoronarography from 225 patients with prior BMS implantation. Patients were assigned to diffuse restenosis group and control group based on the result of the coronarography. MBL genotypes were determined using quantitative real-time PCR. Proportion of different genotypes was compared and adjusted with traditional risk factors using multivariate logistic regression.Results: Average follow-up time was 1.0 (+ - 1.4) year in the diffuse restenosis group (N = 117) and 2.7 (+ - 2.5) years in the control group (N = 108). The age, gender distribution and risk status was not different between study groups. Proportion of the MBL variant genotype was 26.8% (29 vs. 79 normal homozygous) in the control group and 39.3% (46 vs. 71 normal homozygous) in the restenosis group (p = 0.04). In multivariate analysis the mutant allele was an independent risk factor (OR = 1.96, p = 0.03) of in-stent restenosis.Conclusions: MBL polymorphisms are associated with higher incidence of development of coronary in-stent restenosis. The attenuated protein function in the mutant allelic genotype may represent the underlying mechanism. [ABSTRACT FROM AUTHOR]

Published
2017
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2. High rate of in-stent restenosis after coronary intervention in carriers of the mutant mannose-binding lectin allele

Author

Pál Soós, Zsolt Bagyura, Kristóf Hirschberg, Balázs Berta, Ágnes Szilágyi, Zsolt Szelid, Árpád Lux, Loretta Kiss, Gábor Széplaki, and Béla Merkely

Subjects
0301 basic medicine, Bare-metal stent, Male, Pathology, Time Factors, medicine.medical_treatment, Coronary Artery Disease, 030204 cardiovascular system & hematology, Coronary Angiography, Gastroenterology, Coronary artery disease, 0302 clinical medicine, Restenosis, Gene Frequency, Risk Factors, Odds Ratio, Prospective Studies, Mannan-binding lectin, Homozygote, Middle Aged, Phenotype, Metals, Female, Stents, Cardiology and Cardiovascular Medicine, Research Article, Bare metal stent, In-stent restenosis, medicine.medical_specialty, Heterozygote, MBL genetic variant, Cardiology, Gene association, Single-nucleotide polymorphism, Prosthesis Design, Real-Time Polymerase Chain Reaction, Mannose-Binding Lectin, Polymorphism, Single Nucleotide, Risk Assessment, Coronary Restenosis, 03 medical and health sciences, Percutaneous Coronary Intervention, Internal medicine, medicine, Humans, Genetic Predisposition to Disease, Risk factor, Allele frequency, Genetic Association Studies, Aged, Chi-Square Distribution, business.industry, Percutaneous coronary intervention, medicine.disease, 030104 developmental biology, Logistic Models, Case-Control Studies, Multivariate Analysis, business
Abstract

Background In-stent restenosis occurs in 10–30% of patients following bare metal stent (BMS) implantation and has various risk factors. Mannose-binding lectin (MBL) is known to have effect on the progression of atherosclerosis. Single nucleotide polymorphisms (SNP) of the MBL2 gene intron 1 (codon 52, 54, 57) are known to modulate the bioavailability of the MBL protein. Our aim was to identify the association of these polymorphisms of the MBL gene in the occurrence of in-stent restenosis after coronary artery bare metal stent implantation. Methods In a non-randomized prospective study venous blood samples were collected after recoronarography from 225 patients with prior BMS implantation. Patients were assigned to diffuse restenosis group and control group based on the result of the coronarography. MBL genotypes were determined using quantitative real-time PCR. Proportion of different genotypes was compared and adjusted with traditional risk factors using multivariate logistic regression. Results Average follow-up time was 1.0 (+ − 1.4) year in the diffuse restenosis group (N = 117) and 2.7 (+ − 2.5) years in the control group (N = 108). The age, gender distribution and risk status was not different between study groups. Proportion of the MBL variant genotype was 26.8% (29 vs. 79 normal homozygous) in the control group and 39.3% (46 vs. 71 normal homozygous) in the restenosis group (p = 0.04). In multivariate analysis the mutant allele was an independent risk factor (OR = 1.96, p = 0.03) of in-stent restenosis. Conclusions MBL polymorphisms are associated with higher incidence of development of coronary in-stent restenosis. The attenuated protein function in the mutant allelic genotype may represent the underlying mechanism.

Published
2016

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