Basics

Description

  • Alopecia: Absence of hair from areas where it normally grows:
    • Anagen phase: Growing hairs, 90% scalp hair follicles at any time, lasts 2–6 years
    • Catagen phase: Regression of follicle, <1% follicles, lasts 3 weeks
    • Telogen phase: Resting phase, lasts 2–3 months, 50–150 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. Onset in females prior to 40 years, affecting as many as 70% of women over 65 years (1)
  • Alopecia areata: Onset usually prior to 30 years; men and women are equally effected. 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 over 65 years of age (1)


Prevalence
  • Androgenic alopecia: In males, 30% Caucasian by 30 years, 50% by 50 years and 80% by 70 years.
  • Alopecia areata: 1/1000 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, 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 (2)
    • 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 (3).
      • Increased androgen receptors, increased 5-alpha reductase leads to increased testosterone conversion in follicle to DHT. This leads to decreased follicle size and vellus hair (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).
      • Polycystic ovarian syndrome, adrenal hyperplasia, 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 2–3 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, etc. 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

Diagnosis

History

  • Description of hair loss problem: Rate of loss, duration, location, degree of hair loss, other symptoms including pruritus, infection, hair care, and treatments
  • Medications
  • Medical illness including chronic disease, recent illness, surgeries, pregnancy, thyroid disorder, iron deficiency, poisonings, exposures
  • Psychological stress
  • Dietary history and weight changes
  • Family history of hair loss or autoimmune disorders

Physical Exam

  • Pattern of hair loss:
    • Generalized, patterned, focal
    • Assess hair density, vellus vs. terminal hairs, broken hair
  • Scalp scaling, inflammation, papules, pustules
  • Presence of follicular ostia to determine class of alopecia
  • Hair pull test:
    • Pinch 25–50 hairs between thumb and forefinger and exert slow, gentle traction while sliding fingers up:
      • Normal: 1–2 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 nigrans, truncal obesity

Differential Diagnosis

Search for type of alopecia and then for reversible causes.

Diagnostic Tests and 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

Diagnostic Procedures/Other
  • Light hair-pull test: Pull on 25–50 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)

Treatment

General Measures

  • Stop any possible medication causes if possible; this will often resolve telogen effluvium (5)[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 (Drugs)

Non-scarring:

  • Androgenic alopecia: Treatment must be continued indefinitely. Can use in combination.
  • Minoxidil (Rogaine): 2% topical solution (1 mL b.i.d.) for women, 5% topical solution (1 mL b.i.d.) or foam (daily) for men. Works in 60% of cases (3,4)[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 (3,4)[A]
  • Finasteride(Propecia): 1 mg/d for men and women (1)[A],(4)[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 (3)[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 (6)[A]
  • Spironolactone(Aldactone): 100–200 mg/d (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 (6)[A]
  • Alopecia areata: No FDA-approved treatment; high rate of spontaneous remission in patchy AA.

Intralesional steroids:

  • Triamcinolone: 2.5–5 mg/mL (4,6)[C]:
    • First line if <50% scalp involved
    • Inject 0.1 mL into deep dermal layer at 0.5–1 cm intervals with ½ in 30-gauge needle, every 4–6 weeks. Max. 20 mg/session (2)[C]
    • Adverse effects: Local burning, pruritus, skin atrophy
  • Topical steroids: Very limited evidence for efficacy
  • Betamethasone: 0.1% foam shows limited hair regrowth (2)[C]:
    • Adverse effects: Folliculitis, high relapse rate after discontinuation
  • Systemic glucocorticoids: Use in extensive AA. May induce regrowth, but requires long-term monthly treatment to maintain growth (2)[B]:
    • Adverse effects: Hyperglycemia, adrenal insufficiency, osteoporosis, cataracts, obesity
    • Psychiatric: SSRIs, psychiatric care, support groups
  • 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 (3)[A]

Complementary and Alternative Therapies

  • Many herbal medications are available; no clear evidence at this time.
  • Volumizing shampoos can help remaining hair look fuller.

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 (2)[A].
  • Telogen effluvium: Maximum shedding 3 months after the inciting event and recovery following correction of the cause. Usually subsides in 3–6 months but takes 12–18 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 (7).
  • Tinea capitis: Excellent prognosis with treatment

Codes

ICD-9

  • 704.0 Alopecia
  • 704.00 Alopecia, unspecified
  • 704.01 Alopecia areata
  • 704.02 Telogen effluvium
  • 704.09 Other alopecia

ICD-10

  • L63.0 Alopecia (capitis) totalis
  • L63.1 Alopecia universalis
  • L63.9 Alopecia areata, unspecified
  • L64.9 Androgenic alopecia, unspecified
  • L65.0 Telogen effluvium
  • L65.9 Nonscarring hair loss, unspecified

SNOMED

  • 19754005 Alopecia totalis
  • 238725004 non-scarring alopecia (disorder)
  • 39479004 Telogen effluvium (disorder)
  • 400088006 Scarring alopecia
  • 56317004 Alopecia (disorder)
  • 68225006 Alopecia areata (disorder)
  • 86166000 Alopecia universalis (disorder)
  • 87872006 Male pattern alopecia (disorder)

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.

Authors


Amy M. Zack, MD, FAAFP

Figures

Figure 10-4

Alopecia areata. Note black, flecklike "exclamation mark" hairs at the periphery.
Figure 10-5

Alopecia areata. This man's alopecia areata is limited to his beard.
Figure 10-6

Alopecia areata (alopecia universalis). This patient has lost most of her eyebrows, which she colors in with an eyebrow pencil. She also lacks eyelashes, pubic hair, axillary hair, and hair on her extremities.
Figure 10-7

Alopecia areata (regrowing hair). In this patient with alopecia areata, clusters of hair regrew after intralesional triamcinolone acetonide injections. Some of the regrown hairs are white (vitiliginous).
Figure 10-8

Trichotillomania. This condition is seen most often in young girls. Hairs tend to be broken at different lengths. The areas of alopecia are not completely devoid of hair.
Figure 10-11

Traction alopecia. This woman's alopecia is the result of the use of tight curlers: Note the symmetric loss of hair in a frontotemporal distribution. Also note the "relaxed" curl that was chemically straightened.
Figure 10-12

Traction alopecia. Note the fringe of residual hairs at the distal margin of alopecia. These hairs were too short to be "grabbed" by the hair curlers.

Bibliography

  1. BMJ Best Practice. Accessed 5/30/2013. http://bestpractice.bmj.com/best-practice/monograph/223/basics/epidemiolog...
  2. Alkhalifah A. Alopecia areata update. Dermatol Clin. 2013;31:93–108.  [PMID:23159179]
  3. Banka N, Bunagan K, Shapiro, J. Pattern hair loss in men: Diagnosis and medical treatment. Dermatol Clin. 2013;31:129–140.  [PMID:23159182]
  4. Rathnayake D, Sinclair R. Innovative use of spironolactone as an antiandrogen in the treatment of female pattern hair loss. Dermatol Clin. 2010;20:611–618.
  5. Harrison S, Bergfeld W. Diffuse hair loss: Its triggers and management. Cleve Clin J Med. 2009;76:361–367.  [PMID:19487557]
  6. Mesinkovska N, Bergfled W. Hair: What's new in diagnosis and management? Female pattern hair loss update: Diagnosis and treatment. Dermatol Clin. 2013;31:119–127.  [PMID:23159181]
  7. Otberg N. Primary cicatricial alopecias. Dermatol Clin. 2013;31:155–166.  [PMID:23159184]


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