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Tuesday, December 30, 2008

ALOPECIA

ALOPECIA - Aubrey L.Knight, MD
BASICS
DESCRIPTION
• Absence of the hair from skin areas where it normally is present. Anagen hairs are growing hairs. Telogen hairs are dead "resting" hairs.
• Telogen effluvium: Diffuse hair loss that (usually) results in temporarily decreased hair density but does not progress to complete baldness.
• Anagen effluvium: Diffuse shedding of hairs, including growing hairs, that may progress to complete baldness.
• Cicatricial alopecia: Also known as scarring alopecia; characterized by slick, smooth scalp without any evidence of follicular openings of hair.
• Androgenic alopecia: Hair loss occurring in either sex, caused by stimulation of the hair roots by male hormones, more common after age 50.
• Alopecia areata: Patchy, nonscarring hair loss.
• Traction alopecia: Patchy, initially nonscarring hair loss due to pulling on the hair.
• Tinea capitis: Patches of hair broken off close to the scalp ("Black dot"), with/without associated inflammation, caused by fungus infection.
• Trichotillomania: Intentional pulling out of otherwise healthy hair; is usually due to habit.
ALERT
Pediatric Considerations
Tinea capitis is the only common form of alopecia.
Pregnancy Considerations
Postpartum hair loss is due to altered physiology during pregnancy.
EPIDEMIOLOGY
• Predominant age
- Incidence of androgenic alopecia increases with age.
- Tinea capitis and traction alopecia more common in children
• Predominant sex: Male > Female
Prevalence
• 50% of white men have noticeable male-pattern baldness by 50 years of age.
• 37% of postmenopausal females show some evidence of hair loss.
RISK FACTORS
• Positive family history of baldness
• Physical or psychologic stress
• Pregnancy
• Poor nutrition
Genetics
• In whites, androgenic alopecia follows a dominant trait with incomplete penetrance.
• Hereditary incidence notable in men and women with a strong family history of baldness
PATHOPHYSIOLOGY
See "Description"
ETIOLOGY
• Telogen effluvium
- Postpartum
- Drugs (oral contraceptives, anticoagulants, retinoids, -blockers, chemotherapeutic agents, interferon)
- Stress (physical illness, fever, or psychologic)
- Hormonal (hypo- or hyperthyroidism, hypopituitarism)
- Nutritional (malnutrition, iron deficiency, zinc deficiency)
- Diffuse alopecia areata
• Anagen effluvium
- Mycosis fungoides
- X-ray treatment
- Drugs (chemotherapeutic agents, allopurinol, levodopa, bromocriptine)
- Poisoning (bismuth, arsenic, gold, boric acid, thallium)
• Cicatricial alopecia
- Congenital and developmental defects
- Infection (leprosy, syphilis, varicella zoster, cutaneous leishmaniasis)
- Basal cell carcinoma
- Epidermal nevi
- Physical agents (acids and alkali, burns, freezing, radiodermatitis)
- Cicatricial pemphigoid
- Lichen planus
- Discoid lupus erythematosus
- Sarcoidosis
• Androgenic alopecia
- Adrenal hyperplasia
- Polycystic ovaries
- Ovarian hyperplasia
- Carcinoid
- Pituitary hyperplasia
- Drugs (testosterone, danazol, adrenocorticotropic hormone, anabolic steroids, progesterones)
• Alopecia areata
- Unknown, but possibly autoimmune
• Traction alopecia
- Trichotillomania (direct self-pulling of the hair)
- Tight rollers or braids
• Tinea capitis
- Microsporum sp.
- Trichophyton sp.
ASSOCIATED CONDITIONS
Alopecia areata
• Down syndrome
• Vitiligo
• Diabetes


DIAGNOSIS
SIGNS AND SYMPTOMS
History
• Hair loss
• Pruritus (in tinea capitis)
Physical Exam
• Scaling of the scalp (in tinea capitis)
• Broken hairs (in tinea capitis and traction alopecia)
• Tapered hair at the borders of the patch of alopecia (in alopecia areata)
• Easily removable hairs at the periphery of the patch of alopecia (in alopecia areata)
• Inflammation (in tinea capitis)
• Hair-pull test: 3 cm above ear, pinch 20-40 hairs and exert slow, gentle traction while sliding fingersup hair shaft. Telogen(aka "club") hair bulbs are unpigmented and ovoid. Anagen hairs have elongated and possibly pigmented bulb with gelatinous root sheath.
• Light hair-pull test (positive if anagen hairs come loose easily; seen in alopecia areata)
• Hair pull test with >6 club hairs consistent with telogen effluvium
TESTS
Lab
Consider
• TSH
• CBC (may reflect an underlying immunologic disorder or anemia)
• Free testosterone and dehydroepiandrosterone sulfate in women with androgenic alopecia
• Serum ferritin
• VDRL or RPR for syphilis
• Lymphocyte T- and B-cell number (sometimes low in patients with alopecia areata)
• Drugs that may alter lab results:Thyroid drugs and iodine preparations (including topicals) will alter thyroid tests.
Diagnostic Procedures/Surgery
• Direct microscopic examination of the hair shaft
• Potassium hydroxide examination of the scale, if present (positive in tinea capitis)
• Fungal culture of the scale, if present
• Scalp biopsy (sometimes)
• Drugs that may alter lab results:Antifungal drugs may make potassium hydroxide examination falsely negative.
Pathological Findings
Scalp biopsy with routine microscopy and direct immunofluorescence will aid in the diagnosis of tinea capitis, diffuse alopecia areata, and the scarring alopecias due to lupus erythematosus, lichen planus, and sarcoidosis
DIFFERENTIAL DIAGNOSIS
Search for type of alopecia and then for possible reversible causes.
TREATMENT
STABILIZATION
Outpatient treatment
GENERAL MEASURES
• Traction alopecia
- Only with discontinuation of the hair pulling will the disorder resolve.
- Psychologic or psychiatric intervention may be necessary.
- Successful therapeutic approaches have included medications, behavior modification, and hypnosis.
• Tinea capitis
- 6-8 weeks of oral therapy are often necessary. Topical medications are ineffective.
- Careful hand washing and laundering of head wear and towels
Diet
No special diet
MEDICATION (DRUGS)
• Androgenic alopecia: Topical minoxidil (Rogaine) 2%; finasteride (Propecia), 1 mg PO daily
• Alopecia areata: High-potency topical steroids, topical anthralin, intralesional steroids, psoralen with long-wave UV radiation, cyclosporine
• Tinea capitis: Griseofulvin (ultramicrosize) 250-375 mg/d PO in adults, 5.5-7.3 mg/kg/d in children. Alternatively, ketoconazole 200 mg/d PO. Treatment for 6-8 weeks.
• Contraindications
- Griseofulvin: Pregnancy, porphyria, hepatocellular failure
- Ketoconazole and cisapride (Propulsid) should not be used together.
- Itraconazole and cisapride should not be used together.
• Precautions
- Topical minoxidil
 Burning and irritation of the eyes
 Salt and water retention
 Tachycardia
 Angina (rare)
- Topical steroids
 Local burning and stinging
 Pruritus
 Skin atrophy
 Telangiectasias
 Hypothalamic-pituitary-adrenal (HPA) suppression if high-potency steroids used for prolonged duration
- Griseofulvin
 Photosensitivity reaction
 Lupuslike syndrome
 Oral thrush
 Granulocytopenia
- Ketoconazole
 Anaphylaxis
 Hepatotoxicity
 Oligospermia
 Neuropsychiatric disturbances
 Gynecomastia
- Itraconazole
 Hepatotoxicity
 Nausea, vomiting
- Finasteride
 Not indicated for use in women
 Caution when there is liver disease
• Significant possible interactions
- Griseofulvin and warfarin: Decreased activity of warfarin
- Griseofulvin and barbiturates: Depressed activity of griseofulvin
- Ketoconazole and warfarin: May enhance activity of warfarin
- Ketoconazole and isoniazid, rifampin: Decreased activity of ketoconazole
- Ketoconazole and phenytoin: May alter metabolism of either drug
- Itraconazole and terfenadine: Prolonged QT and ventricular arrhythmias
- Itraconazole and astemizole: Prolonged QT and ventricular arrhythmias
- Itraconazole and cisapride: Contraindicated
- Itraconazole and digoxin: May result in elevated levels of digoxin
- H2 blockers or antacids and ketoconazole: Decreased absorption of ketoconazole. If necessary, give H2 blocker or antacids at least 2 hours after ketoconazole dose. Avoid using the proton pump inhibitor omeprazole for the same reason.
SURGERY
• Androgenic alopecia: Hair transplantation, scalp reduction, transposition flap, and soft-tissue expansion.
• Cicatricial alopecia: Only effective treatment is surgical (graft transplantation, flap transplantation, or excision of the scarred area).
FOLLOW-UP
PROGNOSIS
• Telogen effluvium
- Maximum shedding 3 months after the inciting event (medication, stress, nutritional deficiency) and recovery following correction of the cause
- Rarely permanent baldness
- Chronic effluvium uncommon
• Anagen effluvium
- Shedding begins days to a few weeks after the inciting event, with recovery following correction of the cause.
- Rarely permanent baldness
• Cicatricial alopecia
- Hair follicles permanently damaged
• Androgenic alopecia
- After 12 months of using topical minoxidil, 39% of subjects reported moderate to marked hair growth.
- Prognosis depends on treatment response.
• Alopecia areata
- Usually resolves within 3 years without treatment
- Recurrence common
• Traction alopecia
- Depends on behavior modification
• Tinea capitis
- Usually complete recovery
PATIENT MONITORING
With ketoconazole, monitor liver enzymes
REFERENCES
1. Ross EK. Management of hair loss. Dermatol Clin. 2005;23(2):227-243.
2. University of Texas at Austin School of Nursing, Family Nurse Practitioner Program. Recommendations to diagnose and treat adult hair loss disorders or alopecia in primary care settings (non pregnant female and male adults). 2004 May. 21 pages. NGC:003722 at www.guidelines.gov
3. Fiedler VC, Alaiti S. Treatment of alopecia areata. Dermatol Clin. 1996;14:733-738.
4. Habif TP. Hair Diseases: Clinical Dermatology, 4th ed. 2004.
5. Jackson EA. Hair disorders. Prim Care. 2000;27:319-332.
6. Rietschel RL. A simplified approach to the diagnosis of alopecia. Dermatol Clin. 1996;14:691-695.
7. Sperling LC. Hair and systemic disease. Dermatol Clin. 2001;19:711-726.
8. Whiting DA. Chronic telogen effluvium. Dermatol Clin. 1996;14:723-731.

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