慢性静脉病的新病理生理学方面

IF 0.1 Q4 MEDICINE, GENERAL & INTERNAL Romanian Journal of Military Medicine Pub Date : 2022-11-01 DOI:10.55453/rjmm.2022.125.4.24
Nicuța Manolache, G. Stoleriu, D. Brǎnișteanu, S. Robu, C. Diaconu, D. Costache
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引用次数: 1

摘要

“随着时间的推移,慢性静脉病一直是人们非常感兴趣的病理学。它在世界人口中广泛流行(成年女性占10-33%,男性占10-20%)通过影响患者生活质量的深刻社会职业影响,慢性静脉病是一个真正的公共卫生问题,是导致发病和致残的重要原因,是医学制药领域的一个永久性研究领域。现在特别注意确定疾病发展的机制和阶段。从强调静脉性高血压作为疾病发展中一个重要因素的重要性的研究到今天,它已经证明了静脉内皮和糖盏在引发和发展慢性静脉疾病中的基本作用。生化、免疫组织化学和功能研究使我们能够评估细胞代谢中发生的变化,并有证据表明某些免疫血管因子导致慢性静脉疾病中的血管变化:特异性受体、粘附分子、细胞因子、基质和金属蛋白酶。慢性静脉病的病理生理学分析仍然是一个有待科学研究的广阔领域。“
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New pathophysiological aspects in chronic venous disease
"Chronic venous disease has been pathology of great interest over time. With its large prevalence among the world population (10-33% adult woman and 10-20% of men) through profound socio-professional implications that affect the quality of life of patients, chronic venous disease is a real public health problem, being an important cause of morbidity and disability, a permanent area of research in the medical-pharmaceutical field. Special attention is now given to identifying the mechanisms and stages of disease development. From studies that have highlighted the importance of venous hypertension as an essential element in the development of the disease, to this day it has come up to demonstrating the fundamental role of the venous endothelium and glycocalyx in triggering and progressing of chronic venous disease. Biochemical, immunohistochemical, and functional investigations have allowed the evaluation of changes that occur in cellular metabolism and evidence of some immune-vascular factors responsible for vascular alterations in chronic venous disease: specialized receptors, adhesion molecules, cytokines, matrix and metalloproteinases. The analysis of the pathophysiology of chronic venous disease is still a vast area open to scientific research."
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来源期刊
Romanian Journal of Military Medicine
Romanian Journal of Military Medicine MEDICINE, GENERAL & INTERNAL-
自引率
33.30%
发文量
2
审稿时长
12 weeks
期刊最新文献
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