Hirsutism pathophysiology

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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

The growth of hair on sex-specific areas of the body occurs due to androgens. Androgens induce vellus follicles in sex-specific areas to develop into terminal hairs, which are larger and more heavily pigmented.

Pathophysiology

The growth of hair on sex-specific areas of the body occurs due to androgens. Androgens stimulate the growth of vellus follicles in sex-specific areas to develop into terminal hairs, which are larger and have increased pigmentation (darker).[1][2][3][4]

Types of hair

  • 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:
    • Lanugo hair: The soft hair which covers the fetal skin and it disappears within the first three months after the fetus delivery.
    • Vellus hair: This is fine, soft hair that is not pigmented. It covers most of the body before the pubertal period.
    • Terminal hair: This is long, coarse and pigmented. Pubertal androgens for example dihydrotestosterone (DHT) convert vellus hair to terminal hair.

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.

Pathogenesis

  • The growth of sexual hair is dependent on the presence of androgens.
  • Androgens induce vellus follicles in sex-specific areas to develop into terminal hairs, which are larger and more heavily pigmented.
  • Hirsutism is caused by increased androgen production and/or an increased sensitivity of the hair follicles to androgens.
  • Hyperandrogenism, resulting from any factors, prolongs the anagen(growth) phase of androgen-sensitive hairs, resulting in their conversion from fine, light, vellus hairs to coarse, dark, terminal hairs.
  • 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.[1]
Hair Follicle[5]
Courtesy to WikiMedia
  • 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.
  • DHT is a hormone that acts on the hair follicle to produce terminal hair.
  • Differences in the activity of DHT explains why women with the same plasma level testosterone, 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 resulting in increased androgen production.

Associated Conditions

Common conditions associated with hirsutism include:

References

  1. 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.
  2. Messenger AG (1993). "The control of hair growth: an overview". J. Invest. Dermatol. 101 (1 Suppl): 4S–9S. PMID 8326154.
  3. Hatch R, Rosenfield RL, Kim MH, Tredway D (1981). "Hirsutism: implications, etiology, and management". Am. J. Obstet. Gynecol. 140 (7): 815–30. PMID 7258262.
  4. Labrie F (1991). "Intracrinology". Mol. Cell. Endocrinol. 78 (3): C113–8. PMID 1838082.
  5. "Category:Hair follicle - Wikimedia Commons".

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