Increase and Redistribution of Sex Hormone Receptors in Premenopausal Women Are Associated with Varicose Vein Remodelling.

Natalio García-Honduvilla,Julia Buján,Gemma Pascual,Pedro Lopez-Hervas,Miguel A Ortega,Javier Leal,Ángel Asúnsolo,Felipe Sainz

doi:10.1155/2018/3974026

Abstract

In chronic venous insufficiency of the lower limbs, data show that the clinical manifestation is varicose veins (VVs), and VV epidemiology suggests that sex hormones directly influence disease development through intracellular receptors. This study aimed to determine the presence and localization of oestrogen receptors (ERs), progesterone receptors (PRs), and androgen receptors (ARs) in both healthy and VV wall cells and their relationship with gender. In this study, samples from patients without a history of venous disease (CV) (n = 18) and with VV (n = 40) were used. The samples were divided by gender: CV women (CVw) = 6, CV men (CVm) = 12, VV women (VVw) = 25, and VV men (VVm) = 15. RT-qPCR and immunohistochemical techniques were performed, and increased ER and PR protein expression was found in VVw in all tunica layers. ARs were localized to the adventitial layer in the CV and were found in the neointima in VVs. mRNA expression was increased for ER and PR in VVw. AR gene expression was significantly decreased in VVm. The increase in the number of these receptors and their redistribution through the wall reinforces the role of sex hormones in varicose vein development.

Highlights

Varicose veins are the most common form of primary venous insufficiency, with a high prevalence of 20–60% in the Western population [1]
Previous clinical and epidemiological studies have shown a predominance of varicose veins in women [12, 14, 15]; this study aimed at verifying whether steroid receptors and progesterone, oestrogen, and androgen receptors are involved in varicose vein development and whether this occurs differently in men and women
Quantifying the ER-positive cells showed that the mean was 9.03 ± 0.55 in the CV men (CVm) group and 16.23 ± 1.38 in the varicose vein (VV) men (VVm) group, which was a statistically significant difference (∗∗p = 0 005)

Summary

Introduction

Varicose veins are the most common form of primary venous insufficiency, with a high prevalence of 20–60% in the Western population [1]. The primary cause of varicose vein (VV) formation has not been established; both valvular dysfunction and venous pressure seem to play key roles in disease onset and progression [2,3,4]. Macroscopic changes in the veins occur at a microscopic level through modifications to the extracellular matrix (ECM) and cellular components. Oxidative Medicine and Cellular Longevity (especially of smooth muscle cells (SMCs)) [7]. Several studies implicate variations in ECM components (collagen fibres, elastic fibres, matrix metalloproteinase (MMP), and glycosaminoglycans) and in SMCs in varicose vein pathology [7,8,9]

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