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)
- Genes/SNPs (single nucleotide polymorphism; English : single nucleotide polymorphism):
- Genetic risk dependent on gene polymorphisms:
- 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
- Consumption of stimulants
- Tobacco (smoking) + obesity
- Overweight (BMI ≥ 25; obesity) + smoking.
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).
- Chronic discoid lupus erythematosus – autoimmune disease leading to skin lesions.
- Folliculitis decalvans – inflammation of hair follicles leading to hair loss.
- Lichen follicularis – lichen that affects the hair follicles.
- Lichen ruber planus (nodular lichen).
- Linear scleroderma – connective tissue hardening of the skin.
- Pseudopelade Brocq – form of alopecia.
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
- Malnutrition and malnutrition with accompanying micronutrient deficiency, see micronutrient therapy (vital substances) for details.
- Pleasure food consumption
- Drug use
- Amphetamines (indirect sympathomimetic).
- 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.
- Ferritin serum level (due toexclusion of iron deficiency).
- Endocrine changes
- After childbirth
- After puberty
- During menopause
- Endocrine disorders:
- Diabetes mellitus
- Hyperprolactinemia
- Hypo- and hyperthyroidism (hypo- and hyperthyroidism)
- Addison’s disease (primary adrenocortical insufficiency; NNR insufficiency).
- Polycystic ovary syndrome (PCO syndrome).
- Disease of the parathyroid gland
- After discontinuation of hormonal contraceptives.
Medications that can cause hair loss; hair loss typically occurs 2 to 3 months after starting the medication
- ACE inhibitors (captopril, enalapril).
- Analgesics/antirheumatics – ibuprofen, naproxen, piroxicam.
- Anthelmintics (albendazole, mebendazole).
- Antiarrhythmics – Amiodarone
- Antidepressants
- Lithium (e.g., quoilinonum)
- Selective serotonin reuptake inhibitors (SSRIs) – fluoxetine, sertraline.
- Tetracyclic antidepressants
- Tricyclic antidepressants (TCAs) – amitriptyline, desipramine, imipramine.
- Antiepileptic drugs – carbamazepine, gabapentin, valproate, valproic acid.
- Angiogenesis inhibitors (sorafenib, sunitinib).
- Anticoagulants
- Coumarin derivatives – indandiones, phenprocoumon (product names: Marcumar, Falithrom), warfarin.
- Heparin (enoxaparin)
- Low-molecular-weight heparins (NMH) (certoparin, dalteparin, enoxaparin, nadroparin, reviparin, tinzaparin).
- Synthetic. Heparin analogue (Fondaparinux).
- Antimalarials – e.g. chloroquine
- Antifungals
- Azoles (voriconazole)
- Triazole derivatives (fluconazole)
- Antipsychotics (neuroleptics) – haloperidol.
- Antiretroviral drugs – e.g., indinavir
- Beta-blockers – e.g., metoprolol, propranolol; also for topical beta-receptor blockers: pindolol.
- Biologicals (adalimumab)
- Coumarins
- Gout remedy – colchicine
- Guanethidine
- H2 blockers – e.g., ranitidine, cimetidine
- Heparin
- Hormones
- Anabolic steroids
- Androgens (testosterone, testosterone antate, testosterone undecanoate).
- Progestins
- Hormone antagonists
- Aldosterone antagonists (e.g., spironolactone).
- Aromatase inhibitors (anastrozole, testolactone) → alopecia androgenetica in women undergoing mammary carcinoma (breast cancer) therapy.
- Estrogen antagonists (antiestrogens) – tamoxifen → alopecia androgenetica in women under breast carcinoma therapy.
- Octreotide
- Prolactin antagonist (bromocriptine)
- Thyrostatic agents (carbimazole, propylthiouracil).
- Estrogens
- Immunosuppressants
- Azathioprine
- Ciclosporin (cyclosporin A)
- Interferons (Interferon-α)
- Immunotherapeutics (fingolimod).
- Lipid-lowering agents
- Fibrates
- HMG-CoA reductase inhibitors (statins) – atorvastatin, cerivastatin, fluvastatin, lovastatin, mevastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin.
- Nicotinic acid
- Mesalazine
- Metals
- Gold
- Arsenic
- Metal binder – D-penicillamine (chelating agent).
- Monoclonal antibodies – pertuzumab
- Proton pump inhibitors (PPI; acid blockers) – esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazole.
- Uricosurics (benzbromarone, probenecid).
- Antivirals
- Vitamins and their derivatives
- Vitamin A
- Vitamin A derivatives: retinoids (acitretin, isotretinoin).
- Cytostatics
- Alkylants (busulfan* * , carmustine* , chlorambucil, cycophosphamide* * * , dacarbazine* , ifosfamide, melphalan* , procarbazine, thiotepa* ).
- Anthracyclines (adriamycin* * * , daunorubicin* * * , daunorubicin, epirubicin).
- Antimetabolites (cytarabine* , fluorouracil* , mercaptopurine* , methotrexate (MTX)* * ).
- Mitomycins (Mitomycin C* * )
- Platinum derivatives (carboplatin, cisplatin* , oxaliplatin).
- Purine analogues (thioguanine* )
- Taxanes (paclitaxel, taxoids* * * )
- Topoisomerase inhibitors (mitoxanthrones).
- Other cytostatic drugs (actinomycin* * , bleomycin* , camptothecin* * , capecitabine, cytarabine, estramustine, etoposide* * * , floxuridine* * , hexamethylmelamine* , Hydroxyurea* , Ifosfamide* * * , L-asparaginase* , Nitrogen mustard* * , Mitomycins, Streptozotocin* , Teniposide* * , Vincristine* * * , Vinblastine* * * , Vindesine* * * ).
* 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).