Alopecia
Basics
Basics
Basics
Description
Description
Description
- Alopecia: absence of hair from areas where it normally grows
- Anagen phase: growing hairs, 90% scalp hair follicles at any time, lasts 2 to 6 years
- Catagen phase: regression of follicle, <1% follicles, lasts 3 weeks
- Telogen phase: Resting phase lasts 2 to 3 months, 50 to 150 telogen hairs shed per day.
- Classified as scarring (cicatricial), nonscarring (noncicatricial), or structural
- Scarring (cicatricial) alopecia
- Inflammatory disorders leading to permanent hair loss and follicle destruction
- Includes lichen planopilaris, frontal fibrosing alopecia, and discoid lupus erythematosus
- Nonscarring (noncicatricial) alopecia
- Lack of inflammation, no destruction of follicle
- Includes androgenic alopecia, alopecia areata (AA), telogen effluvium, anagen effluvium
- Structural hair disorders
- Brittle or fragile hair from abnormal hair formation or external insult
Epidemiology
Epidemiology
Epidemiology
Prevalence
- Androgenic alopecia:
- In males, 30% Caucasian by 30 years of age, 50% by 50 years of age, and 80% by 70 years of age
- In females, 70% of women >65 years of age
- AA: 1/1,000 with lifetime risk of 1–2%, men and women affected equally
- Scarring alopecia: rare, 3–7% of all hair disorder patients
Etiology and Pathophysiology
Etiology and Pathophysiology
Etiology and Pathophysiology
- Scarring (cicatricial) alopecia
- Inflammatory disorders leading to permanent destruction of the follicle
- Slick smooth scalp without follicles evident
- Three major subtypes based on type of inflammation: lymphocytic, neutrophilic, and mixed
- Primary scarring includes discoid lupus, lichen planopilaris, dissecting cellulitis of scalp, primary fibrosing, among others.
- Secondary scarring from infection, neoplasm, radiation, surgery, and other physical trauma, including tinea capitis
- Central centrifugal cicatricial alopecia most common form of scarring hair loss in African American women; etiology unknown but likely secondary to hair care practices
- Nonscarring (noncicatricial) alopecia
- Focal alopecia
- AA
- Patchy hair loss, usually autoimmune in etiology, T cell–mediated inflammation resulting in premature transition to catagen then telogen phases
- May occur with hair loss in other areas of the body (alopecia totalis [entire scalp]), alopecia universalis (rapid loss of all body hair)
- Nail disease frequently seen
- High psychiatric comorbidity (1)
- Alopecia syphilitica: “moth-eaten” appearance, secondary syphilis
- Postoperative, pressure-induced alopecia: from long periods of pressure on one area of scalp
- Temporal triangular alopecia: congenital patch of hair loss in temporal area, unilateral or bilateral
- Traction alopecia: patchy, due to physical stressor of braids, ponytails, hair weaves
- Pattern hair loss
- Androgenic alopecia: hair transitions from terminal to vellus hairs
- Male pattern hair loss: androgen-mediated hair loss in specific distribution; bitemporal, vertex occurs where androgen sensitive hairs are located on scalp. This is a predominantly hereditary condition (2).
- Increased androgen receptors, increased 5-α reductase leads to increased testosterone conversion in follicle to dihydrotestosterone (DHT). This leads to decreased follicle size and vellus hair (2).
- Norwood Hamilton classification type I to VII
- Female pattern hair loss: thinning on frontal and vertex areas (Ludwig classification, grade I to III). Females with low levels of aromatase have more testosterone available for conversion to DHT (3). This carries an unclear inheritance pattern (2).
- Polycystic ovarian syndrome, adrenal hyperplasia, and pituitary hyperplasia all lead to androgen changes and can result in alopecia.
- Medications (hormone replacement therapy, oral contraceptive pills)
- Drugs (testosterone, progesterone, danazol, adrenocorticosteroids, anabolic steroids)
- Trichotillomania: intentional pulling of hair from scalp; may present in variety of patterns
- Diffuse alopecia
- Telogen effluvium: sudden shift of many follicles from anagen to telogen phase resulting in decreased hair density but not bald areas
- May follow major stressors, including childbirth, injury, illness; occurs 2 to 3 months after event
- Can be chronic with ongoing illness, including SLE, renal failure, IBS, HIV, thyroid disease, pituitary dysfunction
- Adding or changing medications (oral contraceptives, anticoagulants, anticonvulsants, SSRIs, retinoids, β-blockers, ACE inhibitors, colchicine, cholesterol-lowering medications, etc.)
- Malnutrition from malabsorption, eating disorders; poor diet can contribute.
- Anagen effluvium
- Interruption of the anagen phase without transition to telogen phase; days to weeks after inciting event
- Chemotherapy is most common trigger.
- Radiation, poisoning, and medications can also trigger.
- Structural hair disorders
- Multiple inherited hair disorders including Menkes disease, monilethrix, and so forth. These result in the formation of abnormal hairs that are weakened.
- May also result from chemical or heat damaging from hair processing treatments
Genetics
Family history of early patterned hair loss is common in androgenic alopecia, also in AA.
Risk Factors
Risk Factors
Risk Factors
- Genetic predisposition
- Chronic illness including autoimmune disease, infections, cancer
- Physiologic stress including pregnancy and childbirth
- Poor nutrition
- Medication, chemotherapy, radiation
- Hair chemical treatments, braids, weaves/extensions
General Prevention
General Prevention
General Prevention
Minimize risk factors where possible.
Commonly Associated Conditions
Commonly Associated Conditions
Commonly Associated Conditions
- See “Etiology and Pathophysiology.”
- Vitiligo—4.1% patients with AA, may be the result of similar autoimmune pathways (4)
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