Cytokine gene single nucleotide polymorphisms associated with infectious endocarditis

E. Samoylenko, N. Kolesnikova
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Abstract

Infectious endocarditis is a disease with the primary pathogen localization on the heart valves and the mural endocardium, occurring with the possible generalization of the septic process and the immunopathological changes that are very significant in the disease manifestation and course. Based on the fact that 30–50% of cases concerning infectious endocarditis develop without the obvious involvement of standard risk factors (invasive procedures or endovascular disorders), it can be assumed that molecular genetic factors are involved in the disease pathogenesis and its complications. There is reason to believe that the activation of inadequate inflammation in response to the microbial invasion may be due to polymorphism in the genes controlling the cytokine activity. However, the information available today on the various cytokines level and the gene polymorphism in various clinical variants of infectious endocarditis is very limited and commonly contradictory, which requires a deeper study of the pathogenetic association of infectious endocarditis with cytokine genetic defects. In this regard, the expansion of ideas concerning the of cytokine gene polymorphisms in the form of point mutations (SNP), capable of regulating the intensity of cytokine expression and their biological effects, will allow to predict the risk of infectious endocarditis, the severity of its course, the risk of possible complications, as well as the individual treatment tactics for patients. KEYWORDS: infectious endocarditis, clinical variants, complications, cytokines, cytokine genes, genetic polymorphism, pathogenesis, diagnosis. FOR CITATION: Samoylenko E.S., Kolesnikova N.V. Cytokine gene single nucleotide polymorphisms associated with infectious endocarditis. Russian Medical Inquiry. 2023;7(7) (in Russ.). DOI: 10.32364/2587-6821-2023-7-7-2.
细胞因子基因单核苷酸多态性与感染性心内膜炎相关
感染性心内膜炎是一种原发病原体定位于心瓣膜及心内膜壁的疾病,其发生可能伴随脓毒过程的普遍化和免疫病理改变,在疾病的表现和病程中具有非常重要的意义。基于30-50%的感染性心内膜炎病例的发展没有明显的标准危险因素(侵入性手术或血管内病变)参与,可以假设分子遗传因素参与了疾病的发病机制及其并发症。有理由相信,在对微生物入侵的反应中,炎症的激活不足可能是由于控制细胞因子活性的基因的多态性。然而,目前关于感染性心内膜炎各种临床变异体中各种细胞因子水平和基因多态性的信息非常有限,而且往往相互矛盾,这就需要对感染性心内膜炎与细胞因子遗传缺陷的发病关系进行更深入的研究。在这方面,关于细胞因子基因多态性以点突变(SNP)形式的扩展思想,能够调节细胞因子表达的强度及其生物学效应,将允许预测感染性心内膜炎的风险,其病程的严重程度,可能的并发症的风险,以及患者的个体治疗策略。关键词:感染性心内膜炎,临床变异,并发症,细胞因子,细胞因子基因,基因多态性,发病机制,诊断。引用本文:Samoylenko e.s., Kolesnikova N.V.与感染性心内膜炎相关的细胞因子基因单核苷酸多态性。俄罗斯医学调查。2023;7(7)(俄文)。DOI: 10.32364 / 2587-6821-2023-7-7-2。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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