6533b82dfe1ef96bd129121f

RESEARCH PRODUCT

Veränderungen der extrazellulären Matrix in der Venenwand – Ursache der primären Varikosis?

Th. BöttgerD. KirschW. WahlTh. JungingerR. KüchleH.-p. DienesH. Duschner

subject

Pathologymedicine.medical_specialtybiologybusiness.industryVascular diseaseTenascinAnatomymedicine.diseaseExtracellular matrixFibronectinPathogenesismedicine.anatomical_structureLamininVaricose veinsmedicinebiology.proteinmedicine.symptomCardiology and Cardiovascular MedicineVeinbusiness

description

Background: Conflicting theories on the development of primary varicosis have led to the molecular biological investigation of the vein wall or, more accurately, of the extracellular matrix. It was the aim of this study to quantify matrix expression and to compare pathological changes in the vein wall with valve-orientated staging of varicosis, in order to determine indicators of the primary cause of varicosis. Materials and methods: Three hundred seventy-two tissue specimens of greater saphenous veins were obtained from 17 patients with varicosities and categorised according to Hach stage and procurement site. The specimens were compared with 36 specimens collected from six patients without varicosities, incubated with fluorescence-stained antibodies for collagen 4, laminin, fibronectin and tenascin prior to being assessed with confocal laser scan microscopy. In addition, 22 vein specimens (16 varicose, 6 normal veins) serving as negative controls were investigated. Results: Image analysis and statistical evaluation showed that compared with normal veins, varicose veins are associated with a significant increase in matrix protein expression for collagen 4, laminin and tenascin. A trend towards an increase in matrix expression was further observed for fibronectin. There was, however, no difference between varicose veins and clinically healthy vein segments inferior to a varicose segment. Conclusion: If the findings of the present investigation can be confirmed by other studies, alterations in the vein wall may be regarded as the primary cause of varicosis and valvular insufficiency as the result of these changes.

https://doi.org/10.1024/0301-1526.29.3.173