Hair Loss (Alopecia): Causes

The following forms of alopecia are distinguished:

  • Alopecia areata* (ICD-10: L63.-) – this is a round, localized pathological hair loss.
  • Alopecia androgenetica* (AGA, synonym: male-type alopecia) (ICD-10: L64.-) – Leads in about 80% of men to “Geheimratsecken” or in the pronounced case to a “bald head”; in women, androgenetic alopecia can also occur; causes are:
    • Increased androgen production (see below Adrenogenital syndrome (AGS), congenital; PCO syndrome).
    • Hyperprolactinemia (increase in prolactin levels in the blood), shift in the testosterone-estrogen ratio in favor of testosterone.
    • Taking androgens or anabolic steroids (muscle building drugs).
    • Increased sensitivity of testosterone receptors at the hair follicle or density of androgen receptors (possibly of greater importance than serum concentrations of androgens)
  • Other hair loss without scarring (ICD-10-GM L65.-).
    • Telogen effluvium (ICD-10-GM L65.0): increased hair loss or thinning of hair growth due to premature entry of hair cells into the telogen phase (resting phase of the hair cell)
    • Anageneffluvium (ICD-10-GM L65.1): increased hair loss or thinning of hair growth due to anagen shutdown of hair cells (growth phase of the hair cell).
  • Alopecia cicatrica (scarring alopecia) (ICD-10: L66.-) – associated with inflammation, fibrosis and loss of hair follicles; irreversible.

* Non-scarring alopecia – much more common – reversible.

Different growth phases see below “hair root status (trichogram)”

Non-scarring alopecia

Alopecia androgenetica (AGA)/hormonal hereditary hair loss – [most common form]

Pathogenesis (disease development)

Until now, alopecia androgentica was thought to be caused by elevated hormone (androgen) levels. However, evaluation of the SHIP-TREND population study revealed no association between sex hormones such as testosterone, androstenedione, or DHEAS and alopecia. Alternatively, it is discussed that besides genetic factors (see below), the hormone dihydrotestosterone (DHT, more precisely 5α-dihydrotestosterone), a potent downstream product of testosterone, as well as the tissue hormone prostaglandin D2 (PGD2) are possible causes for alopecia. In men, this form of hair loss can occur at a very early age, leading to the formation of a bald patch with a ring of hair at the back of the head. This is called alopecia climacteria. The hair in women usually becomes thinner around the crown.

Etiology (causes)

Biographic causes – men

  • Genetic burden from parents, grandparents: genome-wide association studies show that genetic alterations are associated with an increased risk of androgenetic alopecia (AGA); polygenic inheritance is thought to occur; since the androgen receptor is inherited on the X chromosome, this explains the maternal influence in male androgenetic alopecia.
    • Genetic risk dependent on gene polymorphisms:
      • Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
        • Genes: AR (androgen recepto8r), LINC01432.
        • SNP: rs2223841 in gene AR
          • Allele constellation: A (high risk).
          • Allele constellation: G (lower risk)
        • SNP: rs1160312 in gene LINC01432
          • Allele constellation: AA (1.6-fold).
          • Allele constellation: AG (1.6-fold)
  • Age – increasing age
  • Body size – small men
  • Skin type – fair complexion
  • Hormonal factors – androgenic hormones
  • Bone density – increased bone density (due toMen with hair loss can sunlight better for vitamin D synthesis).

Behavioral causes

Biographical causes – women

  • Genetic burden from parents, grandparents (see above); in the case of strong genetic penetrance, it can begin to develop AGA at the age of 20 to 30 years.
  • Age – increasing age
  • Hormonal factors – gravidity (pregnancy), menopause (menopause; here: Decrease in estrogens associated with a relative androgen oversupply).

Disease-related causes.

Endocrine, nutritional and metabolic diseases (E00-E90).

  • Adrenogenital syndrome (AGS) – autosomal recessive inherited metabolic disease characterized by disorders of hormone synthesis in the adrenal cortex. These disorders lead to a deficiency of aldosterone and cortisol.
  • Hyperandrogenemia (excess of male sex hormones in women), manifested

Neoplasms – tumor diseases (C00-D48).

  • Androgen-producing neoplasms, unspecified.

Alopecia areata (circular hair loss)

Pathogenesis (disease development)

Circular hair loss occurs in familial cluster. It is an autoimmune disease in which T lymphocytes directed against the hair follicle occur in the area surrounding the hair bulb (hair bulb). As a result, round bald patches form on the head, either isolated or multiple. It is an inflammatory, usually reversible hair loss in alopecia areata.

Etiology (causes)

Disease-related causes.

Blood, hematopoietic organs – immune system (D50-D90).

  • Alopecia areata is associated with autoimmune diseases such as Addison’s disease; but also with trisomy 21

Other forms of alopecia without scarring

Diffuse hair loss

Normal condition: physiologically, up to 100 (150) hairs fall out daily. By means of morphologic characteristics of the hairs that fall out, it is possible to distinguish whether telogen effluvium (cob hairs) or anagen effluvium (papillary hairs) is present. Telogen effluvium

Pathogenesis (disease development)

This type is a diffuse loss of normal hair. Causes include severe stress (e.g. high fever, infections), micronutrient deficiencies (iron deficiency, zinc deficiency; crash diets emotional stress), endocrinological disorders/thyroid disorders, hyperprolactinemia, medications, and others. Increased hair loss typically occurs with a latency of 3 months. If the increased hair loss occurs over a period of more than 6 months, it is called chronic telogen effluvium. Diffuse hair loss is usually reversible after elimination of the underlying causes. Anagen effluvium

Pathogenesis (disease development)

Increased hair loss or thinning of hair growth due to anagen shutdown of the hair cells (growth phase of the hair cell). This type is the diffuse loss of normal hair. This follows either severe stress (e.g. high fever, infections), hormonal fluctuations (delayed anagen shutdown: e.g. after childbirth/postpartum hair loss) or induced by chemotherapy, radiotherapy or other toxins/intoxications. Increased hair loss typically occurs 2-4 weeks after exposure. It is usually reversible after resolution of the underlying causes. Hypoestrogenemic effluvium/estrogen deficiency-related hair loss.

Pathogenesis (disease development)

Increased hair loss or thinning of hair growth. Hair loss occurs with the onset of a hormonal disorder (e.g. menopause). The cause is hypoestrogenemia (deficiency of estrogens).

Traumatic alopecia

Pathogenesis (disease development)

Traction alopecia: This type of hair loss can be caused by the pull of a curling iron, rubber bands, exposure to heat or chemicals, or trichotillomania (hair plucking) – the compulsive plucking of one’s own head hair, eyebrows, eyelashes & body hair.

Fungal diseases – tinea capitis

Pathogenesis (disease development)

In fungal infections of the hairy head, a distinction is made between superficial and deep forms of progression. Children are preferentially affected. The pathogens differ depending on the area.The superficial form has one or more scaly scalp foci within which no hair or only broken hairs are visible. In the deep form, inflammatory redness and thickening of the skin is also found. The deep form heals partially with scars. Therefore, prompt treatment with an antifungal agent is indicated.

Alopecia cicatrica (scarring alopecia)

Scarring hair loss is often the result of primary diseases of the skin.

Etiology (causes)

Disease-related causes.

Blood, hematopoietic organs – immune system (D50-D90).

  • Sarcoidosis (Besnier-Boeck-Schaumann disease) – inflammatory systemic disease affecting mainly the skin, lungs and lymph nodes.

Skin and subcutaneous (L00-L99).

Neoplasms – tumor diseases (C00-D48)

  • Skin metastases, unspecified

Other

  • Skin injury
  • Injuries, burn injuries, radiation damage

Frontal fibrosing alopecia (FFA)

The cause of FFA is unknown.

Alopecia, in general

Etiology (causes)

Biographic causes

  • Genetic burden from parents, grandparents.
  • Age of life – so-called alopecia senilis (it is normal that hair falls out more in old age)

Behavioral causes

  • Nutrition
  • Pleasure food consumption
    • Tobacco (smoking) – Smokers and ex-smokers are 80% more likely to suffer from androgen-related hair loss compared with nonsmokers of the same age; for heavy smokers who consume more than 20 cigarettes per day, the risk was even increased by about 130 percent.
  • Drug use
  • Psycho-social situation
    • Stress – can lead to diffuse hair loss.

Causes due to disease

The conditions listed below are themselves treatable, but if the condition has resulted in the loss of hair follicles, the loss of those hair follicles is not reversible!

  • Autoimmune diseases
  • Chronic infections
  • Chronic discoid lupus erythematosus
  • Folliculitis decalvans
  • Lichen follicularis
  • Linear scleroderma
  • Brocq’s pseudopelade
  • Sarcoidosis
  • Rarely skin metastases

Laboratory diagnoses – laboratory parameters considered independent risk factors/causes.

Medications that can cause hair loss; hair loss typically occurs 2 to 3 months after starting the medication

* Mild alopecia* * Moderate alopecia* * * Strong alopecia.

X-rays

  • Radiatio (radiotherapy)

Environmental pollution – intoxications (poisonings).

  • Air pollutants: particulate matter (PM10) and diesel exhaust (→ decrease in the concentration of the protein beta-catenin in hair follicles; beta-catenin is required for hair growth).