**1. Introduction**

Androgenetic alopecia is the common type of hair loss in men and women since puberty. Typically, AA is the complex result of an androgen-dependent process and this process is located to androgen receptor (AR) areas (frontal and vertex zone). Number of androgen receptors is genetic transmission. The polymorphism involving the CAG triple repeat expan‐ sion of the AR protein has been revealed in men with AA. This male pattern hair loss may represents from influence of minimal androgen excess basing on genetically sensitive hair papilla.

Dihydrotestosterone (DHT) is derived from circulating testosterone (T) inhibits cell prolifer‐ ation in the dermal papilla and local production of vascular endothelial growth factor [1]. As a result, the DHT-dependent process leads to the miniaturization of sensitive hair follicles and progressive thinning the scalp hair. It is known that the follicular dermal papilla controls hair growth. Steroid hormones, including androgens, estrogens and glucocorticoids may influence on timing of hair cycle [2].

More recent studies have focused on androgen-regulated hair growth. But, studies of action of other steroids in the hair follicle have been relatively limited. There are two estrogen receptors (ERα and ERβ) which bind to 17β-estradiol. The effects of estrogens seem complex whereby estrogen prolongs the anagen phase of the hair follicle and stimulates hair shaft elongation [2]. ERβ expression was found in outer root shaft and epithelial matrix. In contrast, ERα and AR were expressed in dermal papilla [3].Therefore, the ratio of ERα to ERβ in dermal papilla cells is extremely important. Estrogen also modifies androgen metabolism. The local production of estrogens from androgen precursors has been converted by the aromatase cytochrome P 450 enzyme complex. It is now clear there is aromatase expression in the dermal papilla and the outer root sheath. The activity of aromatase is higher in women in occipital

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**Figure 1.** The hair shaft

scalp area compared to the frontal scalp and it has been diminished in AA [4]. Some researchers found that estradiol inhibited 5 alpha-reductase activities [5]. The effects on estrogens might be explained by an increased conversion of T to the weaker androgens such as androstendione and androstendiol. Progesterone is able to modulate activity of DHT in dermal papilla by 75% [4, 6]. Also, progesterone is widely recognized as a marker of estrogen action and has antiinflammatory properties. Progesterone regulates the expression of matrix metalloproteinases (MMPs) by transforming growth factor-β [7].

by application of Ludwig scales (II–III). Exclusion criteria were: replacement hormone therapy (RHT) with estrogens, progesterone, testosterone, L-thyroxin or corticoids during last 6 months. Women's group was divided by 5 subgroups: women with excess of androgens, ages before 40 and after 40 y.o. (22 and 19 correspondently), women with excess of estrogens before and after 40 y.o. (24 and 17) and women with obesity at age of 20-40 year (16 patients). Women had both AA and the other sings of elevated androgens level (hirsutism and acne) were included in group with excess of androgens (HA 1 and 2). Women in group with excess of estrogens had endometriosis, uterine leiomyoma or combining both of these (HE 1 and 2). Childbearing aged women with abdominal obesity (waist >88 cm.) and excess of ALT con‐ centration in blood were enrolled in group with obesity (O1). Control group included in agematched men and women (76 and 32 patients correspondently) who presented no diseases at the time of examine. The concentration of TE has been analyzed by ICP mass-spectrometer Nexion-300D and Elan-9000 (Perkin Elmer Corp., USA). Reference materials of serum and hair samples were used. The level of FSH (follicle-stimulated hormone), LT (leuteotpophic), 17βestradiol (E2), progesterone (PR), prolactin, androstendione (A), dihydrotestosterone (DHT)

Copper Deficiency a New Reason of Androgenetic Alopecia?

http://dx.doi.org/10.5772/58416

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**Figure 2.** The timing of the hair cycle

and sex hormone bound globulin (SHPG) was tested by routine laboratory methods.

Statistical analyses were performed with the ANOVA software (Statistics version 7). We applied non parametrical statistics: median, 25 and 75 percentiles. Student's t-test was used to

However, in women hair loss is not limited to only this location and combined with diffuse alopecia. Except in some cases, treatment of 5 alpha reductase inhibitors is ineffective in women. The origin and mechanisms of AA in women are different and more complicated than in men and remain a challenge.

The aim of the work was to estimate a possible role of trace elements (TE) changes in AA in man and women.
