Wall Structure and Composition Changes of Primary Varicose Veins of the Legs: A Histopathologic Study.
- Author:
Bong Seok JANG
1
;
Chang Keun OH
;
Jae Bong LEE
;
Mun Bum KIM
;
Ho Sun JANG
;
Kyung Sool KWON
Author Information
1. Department of Dermatology, College of Medicine, Pusan National University, Busan, Korea. ckoh@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
Varicose vein;
Collagen;
Smooth muscle cell
- MeSH:
Actins;
Collagen;
Collagen Type IV;
Coloring Agents;
Connective Tissue;
Dilatation;
Endothelium;
Eosine Yellowish-(YS);
Hematoxylin;
Hemodynamics;
Humans;
Hyperplasia;
Hypertrophy;
Leg*;
Metabolism;
Microscopy;
Muscle, Smooth;
Myocytes, Smooth Muscle;
Varicose Veins*;
Veins
- From:Korean Journal of Dermatology
2003;41(7):873-880
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Many factors have been implicated in the etiology of varicose veins. Among them, the most widely advanced are weakness of the vascular wall due to defective smooth muscle and connective tissue metabolism, dysfunction of the endothelium, valvular incompetence, and hemodynamic stress. However, the etiology remains unclear. OBJECTIVE: This study was performed to analyze the wall structure and composition changes of primary varicose veins of the legs. METHODS: Varicose vein samples were collected from 13 patients having primary varicose veins who underwent ambulatory phlebectomy. Control veins(below the age of 50 years) were collected from 2 patients with no history or clinical evidence of varicose vein. Samples were stained with hematoxylin and eosin, Masson's Trichrome, Van Gieson stains and immunohistochemical stains for collagen type IV, alpha-smooth muscle actin antigen were performed. Tissue samples were examined by light microscopy for comparative histological changes and different components of the varicose vein wall as compared to control veins. RESULTS: In the varicose vein, there was intimal hypertrophy in almost all the sections examined. The thickness of intima varied at different places. There were hyperplasia of smooth muscle cell and collagen in the varicose vein. Collagen type IV exhibited an accumulation especially in the subendothelial region of varicose vein. CONCLUSION: Dilatation and varicosities are not due to deficiency in the vein wall components, but rather to hemodynamic response. Modulation in the extracellular proteins may be the cause for the development of varices.
