Mehmet Ali Demirkıran1, Cüneyt Köksoy2, Aylin Okçu Heper3, Uğur Bengisun2. 1. Clinic of General Surgery, Şehitkamil State Hospital, Gaziantep, Turkey. 2. Department of General Surgery, Division Peripheral Vascular Surgery, Ankara University Faculty of Medicine, Ankara, Turkey. 3. Department of Pathology, Ankara University Faculty of Medicine, Ankara, Turkey.
Abstract
OBJECTIVE: The etiology and pathophysiology of chronic venous disease is not fully understood. This study aimed to determine the variation of the extracellular matrix proteins in varicose vein wall according to clinical stage. MATERIAL AND METHODS: Forty varicose and 10 control veins were sampled from the saphenofemoral junction. The Clinical Etiologic Anatomic Pathophysiologic (CEAP) classification was used in patients with varicose veins. Samples were stained with hematoxylin-eosin, Masson's trichrome, EVG (Elastica-van Gieson) stain and with laminin, fibronectin, tenascin antibodies. Stained samples were examined immuno-histochemically. Changes in extracellular matrix were determined semi-quantitatively using light microscopy. RESULTS: It was observed that in the early stages (C2-C3) of chronic venous disease, fibrosis is increased in the intima and media layers, with fragmentation in lamina elastica interna, and increased tenascin expression in the intima layer. In advanced stages (C4-C6), the accumulation of tenascin in the intima continued along with fibrosis in the media layer, the thickness of the media layer increased and fibronectin deposition was observed. CONCLUSION: This study showed that changes first occur in the intima during the early stages of the disease with addition of alterations in the media layer at later stages.
OBJECTIVE: The etiology and pathophysiology of chronic venous disease is not fully understood. This study aimed to determine the variation of the extracellular matrix proteins in varicose vein wall according to clinical stage. MATERIAL AND METHODS: Forty varicose and 10 control veins were sampled from the saphenofemoral junction. The Clinical Etiologic Anatomic Pathophysiologic (CEAP) classification was used in patients with varicose veins. Samples were stained with hematoxylin-eosin, Masson's trichrome, EVG (Elastica-van Gieson) stain and with laminin, fibronectin, tenascin antibodies. Stained samples were examined immuno-histochemically. Changes in extracellular matrix were determined semi-quantitatively using light microscopy. RESULTS: It was observed that in the early stages (C2-C3) of chronic venous disease, fibrosis is increased in the intima and media layers, with fragmentation in lamina elastica interna, and increased tenascin expression in the intima layer. In advanced stages (C4-C6), the accumulation of tenascin in the intima continued along with fibrosis in the media layer, the thickness of the media layer increased and fibronectin deposition was observed. CONCLUSION: This study showed that changes first occur in the intima during the early stages of the disease with addition of alterations in the media layer at later stages.
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