Alopecia and its medical management.

Androgenetic alopecia is the most common form of alopecia. The prevalence in Caucasians is 30% of men by the age of 30, 50% of men by the age of 50, and 50% of women by the age of 60 [1]. It presents as progressive, patterned hair loss. Androgenetic alopecia can begin as early as the teenage years or it can start in later decades of life. It has a different clinical presentation in men and women. In men, it typically begins with a gradual thinning of the hair in the vertex and frontotemporal areas (Fig. 1). With severe involvement, there is progressive frontal recession and involvement of the vertex, eventually resulting in complete loss of hair on the top of the scalp. In women, there is diffuse loss on the vertex, frontal and parietal areas of the scalp. In contrast to men, women usually do not have significant frontal recession, and retain a rim of hair at the frontal hairline. Parting of the hair at the vertex shows a wider area of scalp than parting at the occiput. In both men and women, there are miniaturized hairs and a variation in hair length and diameter. Most women with androgenetic alopecia have normal menses, and in 60% to 70% of patients there is no evidence of an underlying endocrinologic abnormality [2]. If there is evidence of androgen excess such as irregular menstruation, infertility, hirsutism, virilization, galactorrhea, or severe acne, however, then an endocrinologic evaluation is warranted. If an endocrine problem is detected, most commonly it is from polycystic ovary disease, less commonly from congenital adrenal hyperplasia, and rarely from an androgen-secreting tumor. The exact causes of androgenetic alopecia are unknown, although it is believed to be a combination of genetic predisposition inherited as a polygenic autosomal trait [3–5] and the effect of circulating androgens on the hair follicle [6]. Dihydrotestosterone is increased in the scalp of balding individuals, and in congenital 5-a-reductase deficiency baldness does not occur [7]. In addition, the location of the hair follicle determines its response to androgens. During puberty, the vellus follicles in the pubic area, axillae, beard area, and chest develop into terminal hairs. Conversely, the terminal hairs on the nonoccipital scalp will miniaturize in response to androgens [8], whereas the occipital hairs of the scalp do not develop androgenetic alopecia. This geographic patterning of the scalp is associated with differences in 5-a-reductase activity and androgen receptor numbers [9,10]. Transplanted follicles retain their donor site characteristics thus forming the basis for hair transplantation surgery [11]. With successive hair cycles in the susceptible hairs of the scalp, the duration of anagen is shortened and the terminal hairs transform into vellus hairs, which are shorter, finer hairs. On skin biopsy, horizontal sections reveal a reduction in the number of terminal hairs and an increased number of miniaturized hairs. The terminal:vellus ratio is typically less than 4:1 [12]. There might be an increased number of telogen hairs because of the decreased length of anagen and preserved length of telogen. In addition, there is heterogeneity in the diameter of the scalp hairs.