Alopecia androgenetica in men L64.-

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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alopecia oleosa; alopecia seborrhoica; Androgenetic alopecia; androgenetic effluvium; Androgenetic hair loss; Balding; Balding male; Calvities hippocratica; male; Male pattern alopecia; male pattern baldness; Male type hair loss; Pattern baldness; receding hairline of a man

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Most common type of hair loss realized by androgens in men and women. Emergence of the genetically determined characteristic pattern of the hair coat. Frequently accompanying seborrhoea (hence also Alopecia oleosa, Alopecia seborrhoica).

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Prevalence in European men about 50%; prevalence in Asian and African men low.

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  • Associations with polygenic hereditary factors, which are unknown so far, are discussed. Genes involved in the androgen-hair follicle interaction are assumed. Described in connection with alopecia are the hairless gene (see also Alopecia congenitalis universalis) and the androgen-receptor gene (AR gene), which is located on the region Xq12-22 of the X chromosome. Possible associations with the A. androgenetica are still controversially discussed.
  • The interaction of genetic disposition and hormonal manifestation factors leads to a shortening of the anagen phase and to the miniaturization of the hair follicles with vellus hair formation ("regressive metamorphosis"). Due to their genetic predisposition, hair follicles express DHT receptors. The natural ligand of these receptors is DHT (dihydrotestosterone), which is formed by conversion of testosterone into DHT by the enzyme 5α reductase. 2 isoemzymes of 5α reductase are known: type 1 and type 2 (predominating in hair follicles of scalp and beard). The intracellular binding of DHT to DHT receptors leads to a change in the androgen-receptor complex, which is transported into the cell nucleus and acts as a transcription factor. The distribution of androgen-metabolizing enzymes (5α-reductase type 1 and 2, aromatase, hydroxysteroid dehydrogenase) may be responsible for the development of androgenetic alopecia. In men, a 1.5-fold higher activity of androgen-metabolizing enzymes was detected frontally.
  • Secondary factors (associations are controversial!):
    • Seborrhoea
    • Cholesterol accumulation in the scalp (5α-Reductase expression from cholesterol after contact with sunlight in the scalp!)
    • Circulatory disorders in the scalp.

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Variable, usually before the 40th LJ; first signs often already after puberty, usually in the 3rd decade of life. Maximum in the 4th decade.

Clinical features
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Variable clinic according to the stage of the disease:

  • Stage I: Normal hair pattern.
  • Stage II: receding of the forehead-hair borders, especially at the temples with formation of receding hairline.
  • Stage III: Tonsure-like, occipitoparietal hair thinning with existing hair bridge.
  • Stage IV: Almost complete loss of hair in the parietal region; remaining lateral and posterior hair crown.
  • Stage V: Thin occipital and parietal crown-shaped hair.

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Regressive transformation of terminal hair follicles to miniature follicles.

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Clinic; medical history; trichogram: telogenic effluvium; if necessary phototrichogram.

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Association with coronary heart disease, benign prostatic hypertrophy and prostate CA are described.

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Remember! Treatment should be given as early as possible to stop irreversible follicular regressions!

General therapy
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In the case of a pronounced desire for therapy, detailed consultation and information about possible therapy options. It is important to dampen the usually too high expectations of a successful therapy. The primary treatment goal is to stop the progression of hair loss.

Notice! Important for all therapy approaches: Therapy success can only be expected after several weeks or several months of application.

External therapy
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ApplyMinoxidil 5% solution (e.g. Regaine 5%, Lonolox) 2 times/day to the affected areas. Long-term therapy is necessary, as hair loss occurs again in men after weaning, about 3 months later.

Caffeinated Exteriors: In vitro and penetration studies on the influence of caffeine on the hair follicle demonstrate the penetration and accumulation of topical caffeine (Otberg N et al. 2008). However, penetration and accumulation are not equivalent to stimulation (Dressler C 2017).

Smaller predominantly positive studies exist on combinations of caffeine+minoxidil (Golpur et al. 2013), caffeine (1.5%)+minoxidil (5%)+azelaic acid (1.5%) (Pazoki-Tourodi et al. 2013)

The knowledge about the effects of topical caffeine also in combination with other active agents such as minoxidil and aelaic acid at the hair root is currently insufficient (Fischer TW et al. 2014). The European S3-guideline for the treatment of AGA mentions caffeine as a treatment option, however, due to a lack of evidence it does not pronounce an indication for a treatment (cited in Dressler C 2017).

Thymuskin is said to have shown a beneficial effect on hair growth in small study cohorts.

Internal therapy
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  • Finasteride (e.g. Propecia®: 4-azasteroid = selective 5-alpha-reductase-type 2-inhibitor) 1 time a day 1 mg p.o. for at least 6 months ( off-label use; finasteride is available only on prescription but not reimbursable). Studies comparing finasteride with minoxidil show a significantly superior efficacy of finasteride (Arca E et al. 2004). It has been shown that finasteride is a long-term therapy approach (>6 months). Patients should be informed that possible therapeutic success will decrease if the therapy is discontinued.
  • Alternatively, dutasteride (e.g. Avodart, selective 5-alpha-reductase type I and type 2 inhibitors): once/day 0.5 mg p.o. for at least 6 months ( off-label use).
  • Please note the possible side effects caused by the antiandrogenic effect.
  • Nicotinic acid p.o. (e.g. Nicobion Tbl.) and vitamin B-complex (withoutB1) can be used as support.

Operative therapie
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If necessary, transplantation of mini- or micrografts from the occipital parts of the head, see hair transplantation. Donor dominance, micrografts 1-2 hairs, minigrafts 3-5 hairs. After 3-6 months normal growth should occur.

Notice! Artificial hair transplants are obsolete because of foreign body reactions!

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Currently, further studies are expected in male androgenetic alopecia with extracts of green tea (epigallocatechin-3-gallate), extracts of saw palmetto fruit (Serenoa repens) as well as Citrullus colocynthis and Cuscuta reflexa (Rondanelli M et al. 2016).

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Cosmetics: Wig, second hair pieces, masking spray (dyes scalp), highlights.

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  1. Bader U, Trueb RM (2002) Androgenetic alopecia in the man. Ther Umsch 59: 211-216
  2. Dressler C (2017) Efficacy of topical cocaffeine in male androgenetic aloepsia. J Dtsch Dermatol Ges 15: 734-741.
  3. Feldmann KA et al (2002) Recent therapeutic progress in alopecia and hypertrichosis. dermatologist 53: 293-295
  4. Pazoki-Toroudi H et al (2013) The efficacy and safety of minoxidil 5% in combination with azelaic acid 1/5% and caffeine 1% solution on male pattern hair loss. Journal Investigative Dermatology 2013; 133: Suppl 1
  5. Hanneken S et al (2003) Androgenetic alopecia. Current aspects of a familiar phenotype dermatologist 54: 703-712
  6. Hillmer AM et al (2005) Genetic variation in the human androgen receptor gene is the major determinant of common early-onset androgenetic alopecia. Am J Hum Genet 77: 140-14811
  7. Hoffmann R (2002) TrichoScan. A new instrument for digital hair analysis. dermatologist 53: 798-804
  8. Paus R, Cotsarelis G (1999) The biology of hair follicles. N Engl J Med 341: 491-497
  9. Price VH (1999) Treatment of hair loss. N Engl J Med 341: 964-973
  10. Prieto VG et al (2002) Androgenetic alopecia: analysis of proliferation and apoptosis. Arch Dermatol 138: 1101-1102
  11. Rondanelli M et al (2016) A bibliometric study of scientific literature in Scopus on botanicals for treatment of androgenetic alopecia. J Cosmet Dermatol 15:120-130.


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Last updated on: 29.10.2020