基于免疫组化的精索静脉曲张与下肢静脉曲张转化发病机制平等的研究

L. Severgina, V. V. Studennikova, L. Rapoport, I. Korovin, D. Korolev
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引用次数: 0

摘要

背景。精索静脉曲张和下肢静脉曲张分布广泛。迄今为止,静脉曲张转化的机制仍不完全清楚。研究免疫组化谱,以证实精索静脉曲张与下肢静脉曲张转化的共同发病机制;目的:确认未分化结缔组织发育不良综合征在这些疾病发生发展中的关键作用。材料和方法。将24例6-35岁男性患者的静脉壁碎片分为相应组:1-12组精索静脉曲张患者,2-12组下肢静脉曲张患者。对照组——5名基本健康的男子(16-32岁)。采用ⅲ型、ⅳ型胶原、α-SMA、纤维连接蛋白、层粘连蛋白、MMP-2和MMP-9、TGF-β1单克隆抗体进行免疫组化研究。结果和讨论。两组静脉壁活检标本的组织学和免疫组织化学研究显示,形态学变化与对照组相似。在评估两组小鼠α-SMA表达水平时,肥大的平滑肌细胞束(在纤维化最小的壁增厚区)中有显著表达,结缔组织套套“缠结”的平滑肌细胞束中表达较弱。在两个研究组中,III型胶原蛋白在内膜下区和表面平滑肌细胞束之间的表达均较弱。平滑肌细胞壁增厚和肥大区可见ⅳ型胶原的表达。在两组中,纤维连接蛋白在静脉壁变化最大的部分,特别是在平滑肌细胞束周围的中间层有明显的表达。MMP-2在各壁层均有明显表达,MMP-9在壁薄区(内膜下区和肌层)过表达。在两组的静脉活检标本中也检测到TGF-β1过表达,主要是在变薄和明显的肌间纤维化区域。考虑到精索静脉曲张和下肢静脉曲张的静脉壁免疫组化表现的相似性,我们可以谈谈它们重塑的共同形态发生机制。因此,我们认为有可能将各种形式的静脉曲张合并为一种单一的疾病-静脉曲张疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Immunohistochemical basing of the pathogenesis equality of varicose vein transformation in varicocele and varicose veins of the lower extremities
Background. Varicocele as well as varicose veins of the lower extremities are quite widespread. To date, the mechanisms of variceal transformation remain not completely clear.Aim. To study the immunohistochemical profile in order to substantiate the common pathogenesis of varicose veins transformation in varicocele and varicose veins of the lower limbs; to confirm the key role of undifferentiated connective tissue dysplasia syndrome in the development of these diseases.Materials and methods. Vein wall fragments from 24 male patients aged 6–35 years old divided into the corresponding groups: group 1–12 patients with varicocele, group 2–12 patients with varicose veins of the lower limbs. Control group – 5 practically healthy men (age 16–32 years). Immunohistochemical study was performed with monoclonal antibodies to collagen types III, IV, α-SMA, fibronectin, laminin, MMP-2 and MMP-9, TGF-β1.Results and discussion. Histological and immunohistochemical studies of vein wall biopsy specimens in both groups revealed similar morphological changes, different from the control group. When assessing the expression level of α-SMA in both study groups, there was marked expression in the bundles of hypertrophic smooth muscle cells (in the zone of wall thickening where fibrosis was minimal) and weak expression in the bundles of smooth muscle cells “enmeshed” in connective tissue sleeves. Collagen type III showed weak expression in the subintimal zone and between the bundles of superficially located smooth muscle cells in both study groups. Expression of type IV collagen was detected in the areas of wall thickening and hypertrophy of smooth muscle cells. In both groups there was a pronounced expression of fibronectin in the most altered sections of the vein walls, especially in the middle layer, around the bundles of smooth muscle cells. There was marked expression of MMP-2 in all layers of the wall, and overexpression of MMP-9 in the areas of wall thinning (in the subintimal zone and muscular layer). TGF-β1 overexpression was also detected in vein biopsy specimens from both groups, predominantly in areas of thinning and pronounced intermuscular fibrosis.Conclusion. Taking into account the similarity of immunohistochemical manifestations in the vein walls in varicocele and varicose veins of the lower limbs we can speak about the common morphogenetic mechanisms of their remodeling. Thus, we consider it possible to combine various forms of varicosity into a single disease – varicose vein disease.
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