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May 20th, 2012:

What Causes Androgenetic Areata?

Hair follicles contain androgen receptors. In the presence of androgens, genes that shorten the anagen phase are activated, and hair follicles shrink or become miniaturized. With successive anagen cycles, the follicles become smaller (leading to shorter, finer hair), and nonpigmented vellus hairs replace pigmented terminal hairs. In women, the thinning is diffuse, but more marked in the frontal and parietal regions. Even persons with severe androgenetic alopecia almost always have a thin fringe of hair frontally. The remaining hair configuration may resemble a monk’s haircut.

Women with androgenetic alopecia do not have higher levels of circulating androgens. However, they have been found to have higher levels of 5a-reductase (which converts testosterone to dihydrotestosterone), more androgen receptors, and lower levels of cytochrome P450 (which converts testosterone to estrogen).

Most women with androgenetic alopecia have normal menses, normal fertility, and normal endocrine function, including gender-appropriate levels of circulating androgens. Therefore, an extensive hormonal work-up is unnecessary. If a woman has irregular menses, abrupt hair loss, hirsutism, or acne recurrence, an endocrine evaluation is appropriate. In this situation, total testosterone, free testosterone, dehydroepiandrosterone sulfate, and prolactin levels should be obtained.

Because the hair loss in androgenetic alopecia is an aberration of the normal hair cycle, it is theoretically reversible. Advanced androgenetic alopecia, however, may not respond to treatment, because the inflammation that surrounds the bulge area of the follicle may irreparably damage the follicular stem cell.