Alopecia androgenetica of the male

Last Updated: 2021-08-20

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.

It is essential to start treatment as early as possible. The patient should be informed that any medication is only effective as long as it is used regularly.

Therapy for men:


  • 2-5% solution (e.g. Regaine, Alopexy, Lonolox, Magistral formulation)
  • Application 2 times/day
  • Requires a prescription
  • Effects by inducing vascular growth factors such as VEGF at the papilla
  • Stops hair loss or at least delays progression in most users
  • In approx. 50% find thickening of scalp hair after 4-6 months
  • Side effects in 5-10% of users include: local redness and itching

Finasteride (e.g. Propecia):

  • Testosterone-like steroid
  • Selective, competitive inhibition of 5α-reductase type II, thereby lowering DHT levels by up to 70%
  • 1time/daily. taken orally
  • In 90% of cases, the progression of hair loss is blocked
  • 50% of patients can enjoy visible hair thickening
  • The greatest impact on hair thickening takes place in the 1st-2nd years of treatment.
  • Side effects include a subjective weakening of libido or potency in 1-2% of patients
  • Off-label use
  • Nicotinic acid p.o. (e.g. Nicobion Tbl.) and vitamin B complexes can be supportive

17α-estradiol solutions are not suitable for male patients, as side effects such as gynaecomastia or potency disorders may occur.

Hair transplantation:

  • An option in very severe alopecia
  • Based on the observed androgen resistance of occipital hair follicles, which is also maintained at the new location (donor dominance)
  • Transplanted are micro(1-2 hairs)- or minigrafts (3-5 hairs)
  • Artificial hair is not implanted due to a foreign body reaction
  • Positive is the durability of this method
  • Negative can be seen the fact, that the result does not achieve the naturalness as the hair regrown by medication
  • Also robot-guided transplants available

Cosmetic options: Wig, second hairpiece, concealer spray or highlights.

Therapy for women:

Therapy in general: promotion of blood circulation via scalp massage or external therapy

Medication for female patients:

  • Minoxidil in a 2% solution (Regaine Women 2% solution) or Regaine 5% 1 time/day each. If dandruff or seborrhoea occurs, it is recommended to use additional degreasing shampoos (e.g. Sebiprox, Nizoral). Tar-containing shampoos are also an option.
  • Oestrogen-containing tinctures for application to the scalp such as 17-α-estradiol (R087,R088) or alfatradiol (e.g. Ellcarnell alpha). Estradiol or glucocorticoids can be administered topically over a short period of time (e.g. Crinohermal fem). Also salicylic acid (e.g. Alpicort F) and antiphlogistic or hyperaemic additives. The efficacy of these is controversial. A subjective improvement is already possible in 50% of cases with external therapy methods such as tinctures or shampoos.
  • Administer antiandrogens only in cooperation with the gynaecologist. Contraindications are: Gravidity, liver tumours, previous thromboembolism, smokers >35 years, cardiovascular diseases, diseases of the lipid metabolism, liver metabolism disorders and severe obesity.
  • For premenopausal mild to moderate alopecia: ethylestradiol and cyproterone acetate (e.g. Diane 35 and e.g. Androcur) 50mg/day on day 1.-10. During therapy, additionally prescribe a cyproterone acetate depot of 300mg i.m. 1 time/month on the 4th-7th cycle day. Alternatives to cyproterone acetate for combination with Diane 35 are Dienogest (Valette) and Drospirenon (Yasmin)
  • Perimenopausal and 4 years after menopause: continuous cyproterone actetate (e.g. Androcur) 25-100mg/day
  • Supportive is biotin (vitamin H) e.g. Bio-H Tin (improvement of hair and nail quality, reduced effluvium), intake p.o. for at least 6-8 weeks. If necessary, mixed preparations such as Pantovigar 3 times/day 1 capsule for 3-6 months. However, the effectiveness here is controversial.
  • In case of iron or zinc deficiency, substitution should take place, e.g. with zinc orotate 20 mg 1 time/day or ferrosanol duodenal 1 time/day 100 mg p.o.