Hirsutism pathophysiology
|
Hirsutism Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Medical Therapy |
|
Case Studies |
|
Hirsutism pathophysiology On the Web |
|
Risk calculators and risk factors for Hirsutism pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: ; Ogheneochuko Ajari, MB.BS, MS [2] Rasam Hajiannasab M.D.[3]
Overview
Androgens are essential for sexual hair and sebaceous gland development. Pilosebaceous unit (PSU) growth and differentiation require the interaction of androgen with numerous other biological factors. In the embryo the pattern of PSU responsiveness to androgen is determined. Hair follicle growth involves close reciprocal epithelial-stromal interactions that recapitulate ontogeny; these interactions are necessary for optimal hair growth in culture.[1] Androgens are responsible for hair follicle size, hair fiber diameter, and the proportion of time terminal hairs spend in the anagen phase.[2] Almost all hirsute women have an increased production rate of androgens specially testosterone. [3]In some women, an increased conversion of testosterone to dihydrotestosterone (DHT) by the enzyme 5-alpha-reductase, is responsible for hirsutism.[4]
Pathophysiology
Hair Growth Cycle
There are approximately 5 million hair follicles at birth in humans with about 80,000 to 150,000 of them on the scalp. The quality of hair is determined by hormones and other intrinsic characteristics of the hair follicle. There are various types of hair which include;
- Vellus hair: These are fine, soft hair that are not pigmented. It covers most of the body before the pubertal period.
- Terminal hair: These are long, coarse and pigmented. Pubertal androgens for example dihydrotestosterone (DHT) convert vellus hair to terminal hair.
The response of hair follicle to androgens and other factors such as local 5 alpha reductase activity determines the level of conversion of hair from the vellus type to terminal hair.
Androgens are essential for terminal hair and sebaceous gland development. Androgens transform the vellus hair into a terminal hair. In androgen-sensitive areas before puberty, the hair is vellus and the sebaceous glands are small. In response to increasing levels of androgens , pilosebaceous units become large terminal hair follicles in sexual hair areas or they become sebaceous follicles (sebaceous glands) in sebaceous areas. Androgens promote growth of sexual hair by recruiting a population of pilosebaceous units to switch from producing vellus hairs to initiating terminal hair growth.[1]
Phases of Hair Growth Cycle
There are 3 phases of hair growth cycle.
- The hair growth phase (termed Anagen phase). This phase varies, depending on the body area affected. It is approximately 4 months for facial hair.
- The involutional phase (Catagen phase). This phase is approximately 2-3 weeks.
- The resting phase (Telogen phase). The hair shaft separates from the dermal papillae at the base of the follicle, which terminates growth.
Growth recommences with the formation of new hair shaft by the reactivation of the dermal papillae, thereby replacing the old hair. The hair growth cycle takes months to years to be completed, causing a delay in hair growth response to changes from effects of androgens. Differences in the activity of DHT, the hormone that acts on the hair follicle to produce terminal hair explains why women with the same plasma level testosterone which is a precursor of DHT, have different degrees of hirsutism.
It is speculated that insulin, at high enough concentration, stimulates the ovarian theca cells to produce androgens. There may also be an effect of high levels of insulin to activate the insulin-like growth factor-I (IGF-1) receptor in those same cells. Again, the result is increased androgen production.
References
- ↑ 1.0 1.1 Deplewski D, Rosenfield RL (2000). "Role of hormones in pilosebaceous unit development". Endocr. Rev. 21 (4): 363–92. doi:10.1210/edrv.21.4.0404. PMID 10950157.
- ↑ Messenger AG (1993). "The control of hair growth: an overview". J. Invest. Dermatol. 101 (1 Suppl): 4S–9S. PMID 8326154.
- ↑ Hatch R, Rosenfield RL, Kim MH, Tredway D (1981). "Hirsutism: implications, etiology, and management". Am. J. Obstet. Gynecol. 140 (7): 815–30. PMID 7258262.
- ↑ Labrie F (1991). "Intracrinology". Mol. Cell. Endocrinol. 78 (3): C113–8. PMID 1838082.