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In men, the thick, pigmented terminal hairs in the affected area of the scalp eventually are replaced by the fine, unpigmented vellus hairs. Women, however, rarely become completely bald but usually experience thinning charac- terized by an intermixing of the normal terminal hairs with finer vellus hairs (7). In both men and women, the hair growth cycle is altered, with fewer hairs in the anagen stage and more hairs in the telogen stage for longer periods of time (7). Although scalp hair growth is not androgen-dependent, androgens are nec- essary for the full expression of androgenetic alopecia whereby they diminish 60 Trancik the size of the hair follicle and diameter of the hair fiber, as well as shift hairs from the growing to resting state (6). The main androgen circulating in the plasma of men is testosterone, whereas the most important androgen in women is andro- stenedione. This finding may explain the different clinical presentation of androgenetic alopecia in men and women. Clinical Presentation The clinical presentation of androgenetic alopecia is different for men and women. It may occur as early as 17 years of age in normal males and by 25 to 30 years of age in endocrinologically normal females (6). There is no evidence, however, to suggest that there is an age at which the onset of the balding process is no longer initiated or a threshold age at which the progression of baldness ceases to continue (7,10). Invariably, both men and women see increased shed- ding of hair, which prompts them to seek out medical advice. In men, androgenetic alopecia is usually progressive, typically receding from the normal hairline in an M-shaped pattern with an enlarging balding vertex (6). Several classification systems have been used to characterize the balding state of men, the most popular being the Hamilton scale as modified by Norwood (Fig. Women often do not present with a distinct pattern, but rather have diffuse hair loss or thinning of the temporal and parietal areas with retention of the frontal hairline in most cases.

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Decreased level Moisturizers 93 of ceramides in stratum corneum of atopic dermatitis: An etiologic factor in atopic dry skin? Decreased stratum corneum ceramides in atopic individuals—a pathobiochemical factor in xerosis? Lipid composition of outer stratum corneum and nails in atopic and control subjects. Studies of the barrier in ‘‘dry’’ and clinically normal skin of patients with atopic dermatitis. Quantification of stratum corneum ceramides and lipid envelope ceramides in the hereditary ichthyosis. The effect of 4 barrier creams on the absorption of water, benzene, and formaldehyde into excised human skin. Effect of long-term use of moisturizers on skin hydration, barrier function and susceptibility to irritants. Efficacies of a barrier cream and an afterwork emollient against cutting fluid dermatitis in metalworkers: a prospective study. Regula- tion of epidermal sphingolipid synthesis by permeability barrier function. Transepidermal water loss: the signal for recovery of barrier structure and function. Transepidermal water loss and absorption of hydro- cortisone in widespread dermatitis. In vivo relationship be- 94 Loden´ tween percutaneous absorption and transepidermal water loss according to ana- tomic site in man. Basal transepidermal water loss, skin thickness, skin blood flow and skin colour in relation to sodium-lauryl-sulphate-induced irritation in normal skin. Improvement in skin barrier function in patients with atopic dermatitis after treatment with a moisturizing cream (Cano- derm). The effect of two urea-containing creams on dry, eczematous skin in atopic patients. Assessment of efficacy and side-effects by non-invasive techniques and a clinical scoring scheme.

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