Alopecia androgenetica of the male

Last Updated: 2023-07-07

Author(s): Anzengruber F., Navarini A.

ICD11: -

Hippocrates (Calvities / alopecia hippocratica)

  • androgenetic alopecia (AGA)
  • androgenetic alopecia
  • androgenetic effluvium
  • male pattern baldness
  • Alopecia androgenetica of the male
  • Alopecia seborrhoica
  • Calvities hippokratica
  • Pattern baldness
  • Alopecia oleosa
  • common balding
  • hereditary balding/thinning

Polygenetically determined hair loss characterised by the androgen-mediated transition from terminal hair follicles to miniaturised vellus hair follicles and predominantly affects males. In terms of pathophysiology, it is a telogen effluvium. If women are affected, this is always to be considered pathological.

  • Every second man is affected in the course of his life
  • The classification as an actual disease is controversial. Our view is clear: it is a preventable to delayable skin disease.
  • Most common androgen-induced hair loss in both males and females.
  • The prevalence in Asian and African men is lower.
  • Prevalence in European women: 20%
  • Incidence in European women after the age of 65: up to 75%.

The classification is based on gender.

For men, the Hamilton-Norwood classification is used today.

  • Stage I: normal hair pattern
  • Stage II: Forehead-hairline receding, formation of receding hairline at the temples
  • Stage III: Torus-like, occipitoparietal hair thinning, hair bridge still present
  • Stage IV: Almost complete hair loss in the parietal area, remaining is a lateral and posterior hair ring
  • Stage V: thin, crown-shaped, occipital and parietal localised residual hair

In women, the classification is divided into 4 stages according to Ludwig:

  • Stage 0: normal hair growth
  • Stage I: slight hair thinning of the parietal region, but only noticeable when parting the hair, frontal hairline normal, hair plucking test may be positive
  • Stage II: More prominent, visible hair thinning in the parietal region, the frontal hairline is clearly visible
  • Stage III: Pronounced balding fronto-parietal, persisting frontal hairline


Genetic component:

  • Genetic variants in hairless gene and androgen receptor gene (AR gene)
  • Paternal and maternal polygenetic inheritance
  • Genetic variants control the following: Time of manifestation, hairs affected, individual determination of the lifespan of each terminal hair follicle

Under androgen influence, a transition from a terminal to a velus hair follicle takes place. During the genetically determined life span, however, the respective hair follicle is resistant to this influence. The hair follicles of the back of the head are spared the harmful influence of the androgens for a lifetime. The genetic predisposition leads to the affected hair follicles expressing DHT (dihydrogentestosterone) receptors. If DHT is bound, the receptor-ligand complex is transported into the cell nucleus after a structural change, where it functions as a transcription factor. The anagen phase shortens and the affected follicle visibly shrinks. What remains is very fine, barely visible velus hair. It has been shown that androgen-metabolising enzymes (5α-reductases) have a 1.5-fold activity frontally compared to androgen-resistant zones. The enzymes 5α-reductase types I and II metabolise dihydrotestosterone from testosterone


  • Genetics determines the predisposition.
  • The genetic imprinting varies from woman to woman and rarely affects all hair. However, if it is very pronounced, those affected suffer from a clear hair thinning already at the age of 20-30 years.
  • The genetic predisposition and androgens together lead to a reduction of the hair follicle. Since not all follicles are subject to this reduction, a diffuse clinical picture develops. Complete baldness usually remains absent.
  • An increased sensitivity of the testosterone receptors at the hair follicle can also be observed.
  • Shift in the androgen-oestrogen quotient in favour of the androgens during menopause → acceleration of the genetically determined process.
  • Secondary to other underlying diseases that lead to increased androgen levels

Controversial are: Seborrhoea, cholesterol accumulation in the scalp and circulatory disorder


In terms of the clinic, a distinction must again be made between male and female sufferers, even though the respective manifestations can show up in both sexes. It should also be mentioned that hair loss varies from individual to individual.


  • Beginning fronto-temporal with formation of the receding hairline
  • In the course of the disease, most of those affected also show hair thinning at the vertex
  • Somewhat sharply defined areas are possible
  • Diffuse hair loss along the vertex
  • Retention of the velus hair into advanced age can occur
  • Particularly severely affected individuals develop hair loss. severely affected develop hair loss already after puberty diffusely all over the top of the head
  • Slightly increased number of telogen hairs
  • Normal total number of follicles
  • Dandruff and seborrhoeic areas are equally frequent as in healthy individuals
  • The scalp is clinically without findings
  • Manifestation: Before 40 years of age, with a maximum in the 4th decade. Decade.


  • pathological
  • diffuse hair thinning, with mainly the parietal region affected and the frontal hairs persisting
  • beginning between 20 and 40 years


  • Clinical due to the typical presentation of alopecia
  • Hormone or other laboratory tests are not indicated in men
  • Dermoscopy with search for anisotrichosis > 20%!
  • More obsolete: Trichogram to assess hair loss, phototrichogram if necessary

In addition, the following should be performed in female patients:

  • Endocrinological work-up:
  • → Exclusion of hyperandrogenaemia by hormone analysis on the 2-5th day of the cycle, whereby the following parameters should be determined: Testosterone, DHEAs, oestrogen, prolactin, LH and FSH
  • → Exclusion of hyperprolactinaemia, which may also have a drug genesis (neuroleptics or psychotropic drugs)
  • Hair calendar → weekly counting of the hair lost during hair washing, whereby approx. 100 are still within the normal range
  • If necessary, the following additional clarifications: Histology, blood count, blood sugar, ANA, thyroid antibodies, serum zinc and iron, ferritin

Variable from patient to patient.


  • Starting frontally
  • Exclusion of occipital and parietal hair ring until last
  • Diffus in severely affected


  • Partial region affected first
  • Diffuse effluvium
  • Persistent frontal hairline

  • Progression of hair loss
  • Medications
  • Deficiencies
  • Stress episodes
  • New, recent and known illnesses
  • Pregnancy, hormone preparations
  • Family history

Further hair loss can be prevented by starting therapy promptly.

If a high telogen rate of 30-40% (telogen effluvium) is evident in the trichogram at the margin, rapid progression of hair loss is to be expected.