Abstract

The aim of the research. To expand the knowledge about immunohistochemical changes in female patients with androgenetic alopecia (AGA) focusing on non-androgenic co-factors of pathogenesis of the disease, as this may serve as a basis for improving therapeutic regimens.
 Materials and methods. Scalp biopsies of female patients with androgenetic alopecia were examined by immunohistochemical method. The study included two groups: the main group of 30 female patients aged 22 to 40 years, average age 32,13±5,03 years, and the control group that included 20 skin samples from women aged 25–40 years (average age 34,75±4,19 years) who underwent autopsies.
 Results. It was found that AGA in women is characterized by a number of immunomorphological manifestations: the inflammatory infiltrate that consists of immunocompetent T-lymphocytes CD3+, CD4+ and CD8+, macrophages (CD68+); imbalance of growth polypeptides VEGF, TGF-β1, EGFR; accumulation of oxidative stress enzymes eNOS and iNOS; accumulation of pathological fraction of Collagen IV.
 Conclusions. The data obtained by this study helps to improve the concept of morphogenesis of AGA, and also can become a base to improve the standards of treatment of the disease. The pathological triade “oxidative stress-microinflammation- fibrosis” should be considered as a possible treatment target, as well as the imbalance of growth peptides.

Highlights

  • IntroductionHair loss could cause significant psychological trauma to both female and male patients [1, 2]

  • Hair is an important part of our appearance and social communication

  • Recent studies show that oxidative stress, micro-inflammation, premature apoptosis and fibrosis can be considered as non-androgenic cofactors of its development [6]

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Summary

Introduction

Hair loss could cause significant psychological trauma to both female and male patients [1, 2]. This problem is further exacerbated by the limited treatment options available, which give only temporary results with many chances of side effects [3]. One of the main areas of research in trichology is the study of various aspects of AGA. The aggressive effect of androgens on the hair follicle in androgen-dependent areas of the scalp under conditions of genetic predisposition is considered as the main etiopathogenetic mechanism of AGA [4, 5]. Recent studies show that oxidative stress, micro-inflammation, premature apoptosis and fibrosis can be considered as non-androgenic cofactors of its development [6]

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