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Alopecia
Amy M. Zack, MD, FAAFP
image BASICS
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, or structural
  • Scarring (cicatricial) alopecia
    • Inflammatory disorders leading to permanent hair loss and follicle destruction
    • Includes lymphocytic, neutrophilic, and mixed subtypes
  • Nonscarring alopecia
    • Lack of inflammation, no destruction of follicle
    • Includes focal, patterned, and diffuse hair loss such as androgenic alopecia, alopecia areata, telogen effluvium, anagen effluvium, syphilitic hair loss
  • Structural hair disorders
    • Brittle or fragile hair from abnormal hair formation or external insult
EPIDEMIOLOGY
  • Androgenic alopecia: onset in males between 20 and 25 years of age. Onset in females prior to 40 years of age, affecting as many as 70% of women >65 years of age
  • Alopecia areata: onset usually prior to 30 years of age; men and women are equally affected. Well-documented genetic predisposition
Incidence
Incidence greatest in Caucasians, followed by Asians, African Americans, and Native Americans. In females, 13% premenopausal, with as many as 70% females >65 years of age
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
  • Alopecia areata: 1/1,000 with lifetime risk of 1-2%
  • Scarring alopecia: rare, 3-7% of all hair disorder patients
ETIOLOGY AND PATHOPHYSIOLOGY
  • Scarring (cicatricial) alopecia
    • Slick smooth scalp without follicles evident
    • Inflammatory disorders leading to permanent destruction of the follicle; it is not known what causes inflammation to develop.
    • 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
  • Nonscarring alopecia
    • Focal alopecia
    • Alopecia areata
      • 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 predominately-hereditary condition (2,3).
      • Increased androgen receptors, increased 5-alpha reductase leads to increased testosterone conversion in follicle to dihydrotestosterone (DHT). This leads to decreased follicle size and vellus hair (2,3).
      • Norwood Hamilton classification type I-VII
      • Female pattern hair loss: thinning on frontal and vertex areas (Ludwig classification, grade I-III). Females with low levels of aromatase have more testosterone available for conversion to DHT (4). This carries an unclear inheritance pattern (3).
      • Polycystic ovarian syndrome, adrenal hyperplasia, and pituitary hyperplasia all lead to androgen changes and can result in alopecia.
    • 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 alopecia areata.
  • Rare structural hair disorders may be inherited.
RISK FACTORS
  • Genetic predisposition
  • Chronic illness including autoimmune disease, infections, cancer
  • Physiologic stress including pregnancy
  • Poor nutrition
  • Medication, chemotherapy, radiation
  • Hair treatments, braids, weaves
GENERAL PREVENTION
Minimize risk factors where possible.
COMMONLY ASSOCIATED CONDITIONS
  • See “Etiology and Pathophysiology.”
  • Vitiligo—4.1% patients with alopecia areata (AA), may be the result of similar autoimmune pathways (5).
image DIAGNOSIS
PHYSICAL EXAM
  • Pattern of hair loss
    • Generalized, patterned, focal
    • Assess hair density, vellus versus terminal hairs, broken hair.
  • Scalp scaling, inflammation, papules, pustules
  • Presence of follicular ostia to determine class of alopecia
  • Hair pull test
    • Pinch 25 to 50 hairs between thumb and forefinger and exert slow, gentle traction while sliding fingers up.
      • Normal: 1 to 2 dislodge
      • Abnormal: ≥6 hairs dislodged
      • Broken hairs (structural disorder)
      • Broken-off hair at the borders patch that are easily removable (in alopecia areata)
  • Hair loss at other sites, nail disorders, skin changes
  • Clinical signs of thyroid disease, lupus, or other diseases
  • Clinical signs of virilization: acne, hirsutism, acanthosis nigricans, truncal obesity
DIFFERENTIAL DIAGNOSIS
Search for type of alopecia and then for reversible causes.
DIAGNOSTIC TESTS & INTERPRETATION
Initial Tests (lab, imaging)
  • No testing may be indicated depending on clinical appearance.
  • Nonandrogenic alopecia
    • TSH, CBC, ferritin
    • Consider: LFT, BMP, zinc, VDRL, ANA, prolactin all depending on clinical history and exam
  • Androgenic alopecia: especially in females
    • Consider free testosterone and dehydroepiandrosterone sulfate.
P.37

Diagnostic Procedures/Other
  • Light hair-pull test: Pull on 25 to 50 hairs; ≥6 hairs dislodged is consistent with shedding (effluvium, alopecia areata).
  • Direct microscopic exam of the hair shaft
    • Anagen hairs: elongated, distorted bulb with root sheath attached
    • Telogen hairs: rounded bulb, no root sheath
    • Exclamation point hairs: club-shaped root with thinner proximal shaft (alopecia areata)
    • Broken and distorted hairs may be associated with multiple hair dystrophies.
  • Biopsy: most important in scarring alopecia
  • Ultraviolet light fluorescence and potassium hydroxide prep (to rule out tinea capitis)
image TREATMENT
GENERAL MEASURES
  • Consider potential harms and benefits to the patient prior to treatment. Many will gain an improved quality of life that is of benefit (3)[A].
  • Stop any possible medication causes if possible; this will often resolve telogen effluvium (6)[C].
  • Treat underlying medical causes (e.g., thyroid disorder, syphilis).
  • Traction alopecia: Change hair care practices; education.
  • Trichotillomania: often requires psychological intervention to induce behavior change
MEDICATION
  • Nonscarring Androgenic alopecia: Treatment must be continued indefinitely. Can use in combination
    • Minoxidil (Rogaine): 2% topical solution (1 mL BID) for women, 5% topical solution (1 mL BID) or foam (daily) for men. Works in 60% of cases (2,4)[A]
      • Unclear mechanism of action; appears to prolong anagen phase (2)[A]
      • Adverse effects: skin irritation, hypertrichosis of face/hands, tachycardia. Category C in pregnancy (2,4)[A]
    • Finasteride (Propecia): 1 mg/day for men and women (off label) (7,8)[A] 30-50% improvement in males, poor data in females (3)[A].
      • 5-alpha reductase inhibitor, reduces DHT in system, increases total and anagen hairs, slows transition of terminal to vellus hairs
      • Works best on vertex, least in anterior, temporal areas (2)[A]
      • Adverse effects: loss of libido, gynecomastia, depression. Caution in liver disease. Absolutely no use or contact during pregnancy, category X, reliable contraception required in female use (8)[A]
    • Spironolactone (Aldactone): 100 to 200 mg/day (off-label) (4)[C]
      • Aldosterone antagonist, antiandrogen; blocks the effect of androgens, decreasing testosterone production
      • Adverse effects: dose-dependent, hyperkalemia, menstrual irregularity, fatigue; Category D in pregnancy
    • Ketoconazole: decreases DHT levels at follicle, works best with minoxidil in female androgenic alopecia (8)[A]
    • Combination: Finasteride + minoxidil has superior efficacy to monotherapy (3)[A]. Alopecia areata: no FDA-approved treatment; high rate of spontaneous remission in patchy AA. Treatments all focus on symptom management rather than etiology (9)[B].
  • Intralesional steroids
    • Triamcinolone: 2.5 to 5 mg/mL (4)[C]
      • First line if <50% scalp involved
      • Inject 0.1 mL into deep dermal layer at 0.5 to 1 cm intervals with 1/2 in 30-gauge needle, every 4 to 6 weeks. Maximum 20 mg/session (1)[C]
      • Adverse effects: local burning, pruritus, skin atrophy
    • Topical steroids: very limited evidence for efficacy
    • Betamethasone: 0.1% foam shows limited hair regrowth (1)[C].
      • Adverse effects: folliculitis, high relapse rate after discontinuation
    • Systemic glucocorticoids: use in extensive, multifocal AA. May induce regrowth but requires long-term monthly treatment to maintain growth (1,9)[B].
      • Adverse effects: hyperglycemia, adrenal insufficiency, osteoporosis, cataracts, obesity
      • Psychiatric: SSRIs, psychiatric care, support groups
    • PUVA light therapy + prednisone: moderate effectiveness in diffuse AA (9)[B]
    • Tinea capitis: see “Tinea (Capitis, Corporis, Cruris)”
SURGERY/OTHER PROCEDURES
  • Hair transplantation
  • Wigs, hairpieces, extensions
  • Surgical: graft transplantation, flap transplantation, or excision of the scarred area; used primarily in scarring alopecia
  • Laser therapies to promote growth: lacks evidence (2)[A]
COMPLEMENTARY & ALTERNATIVE MEDICINE
  • Many herbal medications are available; no clear evidence at this time.
  • Volumizing shampoos can help remaining hair look fuller.
image ONGOING CARE
DIET
If nutritional deficit noted, supplementation may be necessary.
PATIENT EDUCATION
National Alopecia Areata Foundation: www.naaf.org
PROGNOSIS
  • Androgenic alopecia: Prognosis depends on response to treatment.
  • Alopecia areata: Often regrows within 1 year even without treatment. Recurrence common. 10% have severe, chronic form. Poor prognosis more likely with long duration, extensive hair loss, autoimmune disease, nail involvement, and young age
  • Telogen effluvium: maximum shedding 3 months after the inciting event and recovery following correction of the cause. Usually subsides in 3 to 6 months but takes 12 to 18 months for cosmetically significant regrowth. Rarely, permanent hair loss, usually with long-term illness
  • Anagen effluvium: Shedding begins days to a few weeks after the inciting event, with recovery following correction of the cause. Rarely, permanent hair loss
  • Traction alopecia: Excellent prognosis with behavior modification
  • Cicatricial alopecia: hair follicles permanently damaged; prognosis depends on type of alopecia and available treatments
  • Tinea capitis: Excellent prognosis with treatment
REFERENCES
1. Alkhalifah A. Alopecia areata update. Dermatol Clin. 2013;31(1):93-108.
2. Banka N, Bunagan MJ, Shapiro J. Pattern hair loss in men: diagnosis and medical treatment. Dermatol Clin. 2013;31(1):129-140.
3. Blumeyer A, Tosti A, Messenger A, et al. Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men. J Dtsch Dermatol Ges. 2011;9(Suppl 6):S1-S57.
4. Rathnayake D, Sinclair R. Innovative use of spironolactone as an antiandrogen in the treatment of female pattern hair loss. Dermatol Clin. 2010;28(3):611-618.
5. Kumar S, Mittal J, Mahajan B. Colocalization of vitiligo and alopecia areata: coincidence or consequence? Int J Trichology. 2013;5(1):50-52.
6. Harrison S, Bergfeld W. Diffuse hair loss: its triggers and management. Cleve Clin J Med. 2009;76(6):361-367.
7. BMJ Best Practice. Epidemiology. http://bestpractice.bmj.com/best-practice/monograph/223/basics/epidemiology.html. Accessed 2013.
8. Atanaskova Mesinkovska N, Bergfeld WF. Hair: what is new in diagnosis and management? Female pattern hair loss update: diagnosis and treatment. Dermatol Clin. 2013;31(1):119-127.
9. Brzezińska-Wcisło L, Bergler-Czop B, Wcisło-Dziadecka D, et al. New aspects of the treatment of alopecia areata. Postepy Dermatol Alergol. 2014;31(4):262-265.
Additional Reading
Otberg N. Primary cicatricial alopecias. Dermatol Clin. 2013;31(1):155-166.
See Also
  • Tinea (Capitis, Corporis, Cruris); Syphilis; Lupus Erythematosus, Systemic (SLE); Polycystic Ovarian Syndrome (PCOS); Lichen Planus; Hyperthyroidism
  • Algorithm: Alopecia
Codes
ICD10
  • L65.9 Nonscarring hair loss, unspecified
  • L64.9 Androgenic alopecia, unspecified
  • L63.9 Alopecia areata, unspecified
Clinical Pearls
  • History and physical are necessary in determining type of alopecia for appropriate treatment.
  • Treatment of underlying medical condition or removal of triggering medication will often resolve hair loss.
  • Educating the patient about the nature of the condition and expectations is key to care.
  • Alopecia can affect the psychological condition of the patient, and it may be necessary to address this in any type of hair loss.