하지 정맥류 환자에서 정맥류 혈관벽의 구조와 조성의 변화에 대한 분석 = Assessment of Wall Structure and Composition of Varicose Veins

다국어 초록 (Multilingual Abstract)

Purpose: Valvular incompetence and venous wall abnormalities have been suggested as primary etiologic factors responible for the development of varicose veins. The valvular theory is known that the continuous gravitational pressure result in varicose vein. There are controversy about this theory. The collagen and elastic fiber have important role of maintaining structure and differentiation of vein. The authors reported on the factor affecting change of venous wall structure in varicose vein. Method: The present study describes the histopathologic aspects of varicose (n=10; mean age, 41.2 years) and normal saphenous veins (n=6 mean age, 55.3 years) of patients using H-E stain, Van-Gieson, Verhoeff stain, and thpe Ⅳ collagen immunohistochemical stain, and examined by light microcopy. Result: In H-E stain, venous wall distension, large amount smooth muscle cell, expansion of extracellular matrix, and a number of endothelial cells were seen. In Van-Gieson stain, the volume of smooth muscle cell increased especially in subendothelial layer and medial layer. The collagen increased in subendothelial and medial layer. The arrangement of smooth muscle cells was broken down due to infiltrations of collagen fiber between the smooth muscle cells. In Verhoeff stain, the elastic fiber was scatterd irregularly in the wall of varicose vein. The elastic fiber increased in small amount within intimal layer, but there was no significant change comparison to control group. In type Ⅳ collagen immunohistochemical stain, there was intense expression of type Ⅳ collagen gradually disappeared from medial layer close to adventitia. Conclusion: The compositions of collagen, elastic fiber, and smooth muscle cell in varicose vein may be different from that of vessel wall in normal vein in same level in the effect of same pressure. The results suggest that the etiology of varicose vein may depend on abnormal response of vessel wall from injury rather than valvular incompetence.