alopecia

MARCH 1, 2003 / VOLUME 67, NUMBER 5 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 1007

the hair is broken or shed at the roots, andwhether shedding or thinning has increased.The patients diet, medications, present andpast medical conditions, and family history ofalopecia are other important factors.

The physical examination has three parts.First, the scalp is examined for evidence oferythema, scaling, or inflammation. Follicu-lar units are apparent in nonscarring alope-cias but absent in scarring types. Second, thedensity and distribution of hair are assessed.Third, the hair shaft is examined for caliber,length, shape, and fragility.4

The pull test is an easy technique forassessing hair loss. Approximately 60 hairs aregrasped between the thumb and the index andmiddle fingers. The hairs are then gently butfirmly pulled. A negative test (six or fewerhairs obtained) indicates normal shedding,whereas a positive test (more than six hairsobtained) indicates a process of active hairshedding. Patients should not shampoo theirhair 24 hours before the test is performed.4

If the diagnosis is not clear based on the his-tory and physical examination, selected labo-ratory tests and, occasionally, punch biopsymay be indicated. A stepwise approach to thediagnosis of hair loss is provided in Figure 1.5,6

Androgenetic AlopeciaAndrogenetic alopecia, or hair loss medi-

ated by the presence of the androgen dihydro-testosterone, is the most common form of

Although alopecia can occuranywhere on the body, it ismost distressing when it af-fects the scalp. Hair loss canrange from a small bare patch

that is easily masked by hairstyling to a morediffuse and obvious pattern. Alopecia inwomen has been found to have significantlydeleterious effects on self-esteem, psychologicwell-being, and body image.1,2

PathophysiologyEvery hair follicle continually goes through

three phases: anagen (growth), catagen (invo-lution, or a brief transition between growthand resting), and telogen (resting).3 Disordersof alopecia can be divided into those in whichthe hair follicle is normal but the cycling ofhair growth is abnormal (e.g., telogen efflu-vium) and those in which the hair follicle isdamaged (e.g., cicatricial alopecia).

DiagnosisA careful history often suggests the underly-

ing cause of alopecia. Crucial factors includethe duration and pattern of hair loss, whether

Alopecia can be divided into disorders in which the hair follicle is normal but thecycling of hair growth is abnormal and disorders in which the hair follicle is damaged.Androgenetic alopecia is the most common cause of hair loss in women. Other disor-ders include alopecia areata, telogen effluvium, cicatricial alopecia, and traumaticalopecias. The diagnosis is usually based on a thorough history and a focused physicalexamination. In some patients, selected laboratory tests or punch biopsy may be nec-essary. Topically administered minoxidil is labeled for the treatment of androgeneticalopecia in women. Corticosteroids and other agents are typically used in women withalopecia areata. Telogen effluvium is often a self-limited disorder. Because alopecia canbe devastating to women, management should include an assessment for psychologiceffects. (Am Fam Physician 2003;67:1007-14,1017-8. Copyright 2003 American Acad-emy of Family Physicians.)

Disorders of alopecia can be divided into those in which the hair follicle is normal but the cycling of hair growth isabnormal and those in which the hair follicle is damaged.

Alopecia in WomenC. CAROLYN THIEDKE, M.D., Medical University of South Carolina, Charleston, South Carolina

PROBLEM-ORIENTED DIAGNOSIS

O A patient informa-tion handout on hairloss in women, writ-ten by the author ofthis article, is providedon page 1017.

Members of variousfamily practice depart-ments develop articlesfor Problem-OrientedDiagnosis. This articleis one in a series coor-dinated by the Depart-ment of Family Medi-cine at the MedicalUniversity of SouthCarolina, Charleston.Guest editor of theseries is William J.Hueston, M.D.

See page 907 for defi-nitions of strength-of-evidence levels.

alopecia in men and women. Almost all per-sons have some degree of androgenetic alope-cia.7 The hair loss usually begins between theages of 12 and 40 years and is frequently insuf-ficient to be noticed. However, visible hair lossoccurs in approximately one half of all per-sons by the age of 50 years8 (Figure 2). Inwomen, hairstyling may mask early hair loss.

Hair follicles contain androgen receptors.In the presence of androgens, genes that

shorten the anagen phase are activated, andhair follicles shrink or become miniaturized.With successive anagen cycles, the folliclesbecome smaller (leading to shorter, finerhair), and nonpigmented vellus hairs replacepigmented terminal hairs. In women, thethinning is diffuse, but more marked in thefrontal and parietal regions. Even personswith severe androgenetic alopecia almostalways have a thin fringe of hair frontally. The

1008 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 67, NUMBER 5 / MARCH 1, 2003

Evaluation of Alopecia in Women

Total testosterone, free testosterone,DHEA-S, prolactinlevels

Clinical evidence of androgen excess*

Hereditarydisorders

Trauma/injury:Mechanical

traumaBurnsCaustic agentsRadiation

Systemic disease:Discoid lupus

erythematosusSarcoidosisLichen planus

follicularisNecrobiosis

lipoidica diabeticorum

Others

Thyroid functiontests to rule outthyroid disease

VDRL test to rule outsyphilis

Ferritin level to ruleout iron deficiency

ANA test to rule outsystemic lupus erythematosus

*Clinical signs and symptoms of androgen excessinclude menstrual irregularities, infertility, hirsutism,severe cystic acne, virilization, and galactorrhea.

Neoplasm:Basal cell

carcinoma (morpheaform)

Squamous cellcarcinoma

Metastatic carcinoma (alopecia neoplastica)

LymphomaAdnexal tumors

Laboratory results normal; consider:Other nutritional deficiency

(malnutrition, sprue, zinc deficiency)Telogen effluviumTrauma (trichotillomania, traction

alopecia)Hereditary syndromesAlopecia areataAndrogenetic alopecia

Infection (fungal, bacterial,protozoan)

Female patient with alopecia

History and physical examination

Scarring present

Punch biopsy

Scarring absent

Biopsy not diagnostic Biopsy diagnostic

FIGURE 1. Suggested approach to the evaluation of alopecia in women. (DHEA-S = dehydroepiandrosterone sulfate; ANA= antinuclear antibody)

Adapted with permission from Healey PM, Jacobson EJ. Common medical diagnoses: an algorithmic approach. 3d ed. Philadelphia: Saun-ders, 2000:208-11, with additional information from Drake LA, Dinehart SM, Farmer ER, Goltz RW, Graham GF, Hordinsky MK, et al.Guidelines of care for androgenetic alopecia. American Academy of Dermatology. J Am Acad Dermatol 1996;35(3 pt 1):465-9.

remaining hair configuration may resemble amonks haircut.

Women with androgenetic alopecia do nothave higher levels of circulating androgens.However, they have been found to havehigher levels of 5-reductase (which convertstestosterone to dihydrotestosterone), moreandrogen receptors, and lower levels ofcytochrome P450 (which converts testos-terone to estrogen).6

Most women with androgenetic alopeciahave normal menses, normal fertility, andnormal endocrine function, including gen-der-appropriate levels of circulating andro-gens. Therefore, an extensive hormonal work-up is unnecessary. If a woman has irregularmenses, abrupt hair loss, hirsutism, or acnerecurrence, an endocrine evaluation is appro-priate. In this situation, total testosterone, freetestosterone, dehydroepiandrosterone sulfate,and prolactin levels should be obtained.6

Because the hair loss in androgenetic alope-cia is an aberration of the normal hair cycle, itis theoretically reversible. Advanced andro-genetic alopecia, however, may not respond totreatment, because the inflammation that sur-rounds the bulge area of the follicle mayirreparably damage the follicular stem cell.

TREATMENT

Minoxidil (Rogaine). The currently pre-ferred treatment for androgenetic alopecia istopically administered 2 percent minoxidil.6,8,9

Minoxidil appears to affect the hair follicle inthree ways: it increases the length of time fol-licles spend in anagen, it wakes up folliclesthat are in catagen, and it enlarges the actualfollicles. The mechanism by which minoxidileffects these changes is not known.Vellus hairsenlarge and are converted to terminal hairs. Inaddition, shedding is reduced.

In a randomized, controlled, double-blindclinical trial involving 550 women 18 to 45 years of age, treatment with 2 percentminoxidil solution resulted in a higher haircount compared with placebo.10 [Evidencelabel A, randomized controlled trial] Inanother study,11 50 percent of women treatedwith 2 percent minoxidil had at least mini-mal hair regrowth, and 13 percent had mod-erate regrowth. No significantly increasedbenefit has been shown for the 5 percentminoxidil solution compared with the 2 per-cent solution.8

The U.S. Food and Drug Administration(FDA) has labeled topically administeredminoxidil for the treatment of androgeneticalopecia. A dropper is used to apply minoxi-dil solution directly onto dry scalp twice daily.After each use, hands should be washed thor-oughly to avoid inadvertent application toother parts of the body. Minoxidil is listed asa pregnancy category C drug. It is not recom-mended for use in persons younger than 18 years.

The primary side effect of topical minoxidiltherapy is hypertrichosis (excessive hairgrowth). The hair growth is most often notedabove the eyebrows, in the malar region, andon the lateral cheeks. It occasionally occursabove the upper lip and on the chin. Facialhypertrichosis has been reported to affect 3 to5 percent of women treated with the 2 per-

Alopecia


An extensive hormonal work-up is not needed in womenwith androgenetic alopecia who have normal menses, fertility, and endocrine function.

FIGURE 2. Androgenetic alopecia.

cent solution and more than 5 percent ofwomen treated with the 5 percent solution.8

Hypertrichosis disappears after a year,even with continued use of minoxidil, andremits within one to six months if treatmentis stopped.8 Bleaching of longer, darker hairis helpful cosmetically. Hair removal proce-dures are seldom necessary. Explanations forthe occurrence of this side effect include localintravascular spread of minoxidil, inadver-tent manual transfer of the drug to the face,and transmission of residual minoxidil frompillows.8

Commercial preparations contain minoxi-dil in a propylene glycol base. Allergic reac-tions to this base limit the usefulness ofminoxidil therapy in some women. A com-pounding pharmacist can prepare an alterna-tive preparation in which minoxidil is sus-pended in a less sensitizing agent such aspolyethylene glycol.12

Exogenous Estrogen. In the past, exogenousestrogen was used to treat androgenetic alope-cia. This treatment is used less often now,because minoxidil is more effective. In fertilewomen with androgenetic alopecia whorequest oral contraception, it is important toselect a pill containing the least androgenicprogestin, such as norgestimate (in Ortho-Cyclen, Ortho Tri-Cyclen), norethindrone (inOvcon 35), desogestrel (in Mircette), orethynodiol diacetate (in Demulen, Zovia).8

Spironolactone (Aldactone). This drug is aweak competitive inhibitor of androgen bind-ing to androgen receptors. It also decreases thesynthesis of testosterone. For these reasons,orally administered spironolactone has been

tried in the treatment of androgenetic alope-cia, although questions remain about its use-fulness. Spironolactone can be beneficial inwomen who also have hirsuitism.13 However,the FDA has not labeled this drug for thetreatment of androgenetic alopecia.

Finasteride (Proscar). This agent has beenshown to be effective in men with alopecia.However, finasteride should not be used inwomen of childbearing age, because 5-reduc-tase inhibitors may cause abnormalities of theexternal genitalia in the male fetus. Moreover,finasteride has not been shown to be useful inpostmenopausal women with androgeneticalopecia.8

Tretinoin (Retin-A). Topical tretinoin ther-apy as an adjunct to minoxidil has shownsome promise.6,14

Other Treatments and Hair-Care Practices.When hair loss is extensive, wigs may beworn. The use of minigrafts, rather thanlarger plugs, in hair transplantation providesa more cosmetically pleasing outcome.15

Hairstyling, teasing, coloring, permanents,and the use of hair spray are supported,rather than prohibited, as means of dealingwith the cosmetic effects of androgeneticalopecia. Women may shampoo their hair asfrequently as they wish without fear of wor-sening hair loss.8

Alopecia AreataAlopecia areata is patchy hair loss of autoim-

mune origin7 (Figure 3). It usually presents as asingle oval patch or multiple confluent patchesof asymptomatic, well-circumscribed, non-scarring alopecia. Severity varies from a smallbare patch to loss of hair on the entire scalp.So-called exclamation point hairs are a hall-mark of the disorder. These hairs are usuallylocated at the periphery of the patch andextend several millimeters above the scalp.16

Alopecia areata occurs in 2 percent of thegeneral population, with men and womenequally affected. The condition may be pres-ent in persons of any age, but is more com-mon in children and young adults.16,17


The Author

C. CAROLYN THIEDKE, M.D., is assistant professor in the Department of Family Med-icine at the Medical University of South Carolina, Charleston, where she attendedmedical school and completed a family practice residency. Before entering academicmedicine, Dr. Thiedke was in private practice for 10 years.

Address correspondence to C. Carolyn Thiedke, M.D., Medical University of South Car-olina, Department of Family Medicine, 295 Calhoun St., P.O. Box 250192, Charleston,SC 29425 (e-mail: [email protected]). Reprints are not available from the author.

The course of alopecia areata is one ofspontaneous remissions and recurrences.Although patients with this disorder are usu-ally otherwise healthy, some have comorbidconditions such as atopy, thyroid disease, orvitiligo. Alopecia areata has been stronglyassociated with certain human leukocyteantigen class II alleles.17

TREATMENT

Immunomodulating agents used in thetreatment of alopecia areata include cortico-steroids, 5 percent minoxidil, and anthralincream (Psoriatec). Topical immunotherapeu-tic agents (e.g., dinitrochlorobenzene, squaricacid dibutyl ester, and diphenylcyclopro-penone) are also used, although managementregimens for these potent agents are challeng-ing. Dermatology consultation or referralmay be necessary. All of these agents stimu-late hair growth but do not prevent hair loss.Moreover, they probably do not influence thecourse of the disease.

Unless alopecia areata is mild and easilymasked, psychologic distress can be extreme.Therefore, most physicians feel obliged tooffer some form of treatment to affectedpatients.

Corticosteroids. The most common treat-ment for alopecia areata is intralesionalinjection of a corticosteroid, preferably tri-amcinolone acetonide (Kenalog). The rec-ommended dose is up to 3 mL of a 5 mg permL solution injected into the mid-dermis in

multiple sites 1 cm apart.17 A 0.5-inch-long30-gauge needle is used, and 0.1 mL isinjected into each site. Hair growth usuallybecomes apparent in four weeks. Treatmentcan be repeated every four to six weeks. Localskin atrophy, the predominant side effect, canbe minimized by taking care to inject into themid-dermis, rather than into the more super-ficial epidermis or the subdermal fat.

Topical corticosteroid therapy can be used,although it is not as effective as intralesionalinjections. Twice-daily application of 1 mL ofan intermediate-potency corticosteroid solu-tion or lotion to the entire scalp is routinelyused to supplement corticosteroid injections.16

Regimens that combine topical corticosteroidtherapy with anthralin or minoxidil also canbe beneficial.

Although oral corticosteroid therapy iseffective in the treatment of alopecia areata, itis seldom used because of potential adverseeffects. Systemic treatment may be indicated inwomen with progressive alopecia areata. Foractive, extensive, or rapidly spreading alopeciaareata, the recommended treatment in adultsweighing more than 60 kg (132 lb) is pred-nisone in a dosage of 40 mg per day for sevendays; the corticosteroid is then tapered slowlyby 5 mg every few days for six weeks.8 For lessextensive alopecia areata, prednisone is givenin a dosage of 20 mg per day or every otherday, followed by slow tapering in increments of1 mg once the condition is stable. Oral pred-nisone therapy can be used in combinationwith topical or injected corticosteroid therapy,as well as with topical minoxidil therapy.

Minoxidil. Topical administration of min-oxidil, particularly the 5 percent solution, hasbeen found to be somewhat effective in thetreatment of alopecia areata. In one study,8

Alopecia


FIGURE 3. Alopecia areata.

The most common treatment for alopecia areata is intra-dermal injection of triamcinolone acetonide at multiple sitesevery four to six weeks.

this treatment produced acceptable resultsin 40 percent of patients who had lost 25 to99 percent of their scalp hair.The FDA has notlabeled topically administered minoxidil forthe treatment of alopecia areata.

Anthralin. Treatment with anthralin, anonspecific immunomodulator, is safe andeffective, particularly in patients with wide-spread alopecia areata. Anthralin is availablein 0.1, 0.25, 0.5, and 1.0 percent creams,which can be applied once daily at home forprogressively longer periods, starting withfive minutes at a time and working up to aslong as one hour. After each applicationperiod, the scalp is rinsed thoroughly withcool to lukewarm water and then cleaned

with soap. New hair growth becomes appar-ent in two to three months. Approximately 25percent of patients have cosmetically accept-able results within six months.18

Selection of the optimal treatment ap-proach depends on the extent of the hair loss(Table 1). If less than 50 percent of the scalp isaffected, intralesional corticosteroid injectionsalone or with topical corticosteroid therapycan be tried. If more than 50 percent of thescalp is involved, a multiple-agent regimen isappropriate. Treatment should be continueduntil remission of the condition or until resid-ual bare patches can be covered with newlygrown hair. Hence, treatment may need to becontinued for months to years.

Telogen EffluviumTelogen effluvium is diffuse hair loss

caused by any condition or situation thatshifts the normal distribution of follicles inanagen to a telogen-predominant distribu-tion.3 Women with this disorder usually notean increased number of loose hairs on theirhairbrush or shower floor. Daily loss mayrange from 100 to 300 hairs. If hair loss is atthe lower end of the range, it may be inappar-ent. Telogen effluvium may unmask previ-ously unrecognized androgenetic alopecia.

A number of conditions are associated with


TABLE 1

Treatment Options for Alopecia Areata in Adult Women

Less than 50% scalp involvementIntralesional corticosteroid injections once a month (triamcinolone acetonide

[Kenalog] preferred)Intralesional corticosteroid injections once a month, plus topical application

of intermediate-potency corticosteroid solution or lotion twice dailyIntralesional corticosteroid injections once a month, plus topical application of

5% minoxidil solution (Rogaine) twice dailyPrednisone, 20 mg taken orally every day or every other day

Greater than 50% involvementTopical application of anthralin cream (Psoriatec), plus 5% minoxidil solution

once dailyTopical application of corticosteroid solution or lotion, plus 5% minoxidil

solution twice dailyPrednisone, 40 mg per day orally for 7 days, then tapered by 5 mg every few

days for six weeksReferral to dermatologist for topical immunotherapyScalp prosthesis (wig)

TABLE 2

Causes of Telogen Effluvium

Physiologic conditionsEarly stages of

androgenetic alopeciaPhysiologic effluvium of

the newbornPostpartum effluvium

Adapted with permission from Sperling LC, Mezebish DS. Hair diseases. Med Clin North Am 1998;82:1160.

Drugs and other substancesAnticoagulants (especially

heparin)AnticonvulsantsAntikeratinizing agents

(e.g., etretinate [Tegison])Antithyroid agentsHeavy metalsHormones

Injury or stressCrash or liquid protein dietsHigh fever (e.g., malaria)Hypothyroidism and other

endocrinopathies Major surgerySevere chronic illnessSevere infectionSevere psychologic stress

(e.g., life-threatening situations)

telogen effluvium (Table 2).19 Although stressis the most common underlying cause, the dis-order also can develop because of normalphysiologic events (e.g., lengthening of telogenin the postpartum state), some medications,20

and several endocrinopathies (thyroid, pitu-itary, and parathyroid disease). Telogen efflu-vium usually begins two to four months afterthe causative event and lasts for severalmonths. If telogen effluvium is suspected, athorough history should be obtained.

Treatment is based on identifying and treat-ing or correcting the underlying cause of telo-gen effluvium. It can be reassuring for womento understand the relationship of their hairloss to a specific event or agent, and to knowthat hair regrowth is probable (Figure 4).

Alopecia from Damage to Hair FolliclesCicatricial alopecia is hair loss resulting

from a condition that damages the scalp andhair follicle7 (Figure 5). In addition to a baldspot, the scalp usually has an abnormalappearance. Plaques of erythema with orwithout scaling or pustules may be present.Conditions that can be associated with cicatri-cial alopecia include infections (e.g., syphilis,tuberculosis, acquired immunodeficiencysyndrome, herpes zoster), autoimmune dis-ease (discoid lupus erythematosus), sarcoido-sis, scalp trauma (e.g., injuries, burns), andradiation therapy.7

If the cause of the disorder is not readilyapparent, a 4-mm punch biopsy of the scalpcan be helpful. Frequent findings on biopsyinclude lymphocytic proliferation around thefollicle, destroyed follicles, a thin and atrophicepidermis, and a densely sclerotic dermis.

Traumatic alopecia can be caused by cos-metic practices that damage hair follicles overtime.7 Cosmetic alopecia has been linked to theuse of brush rollers, curling irons, hair brusheswith square or angular tips, and tight braidingof the hair (Figure 6). Chemicals used repeti-tively on the hair also can damage follicles.Examination of the scalp shows short brokenhairs, folliculitis and, frequently, scarring.

Alopecia


FIGURE 4. Short hairs frontally, reflecting newgrowth after telogen effluvium.

FIGURE 5. Cicatricial alopecia with damage tothe underlying scalp.

FIGURE 6. Traumatic alopecia caused by tightbraiding.

Alopecia

Trichotillomania, another cause of trau-matic alopecia, is a compulsive behaviorinvolving the repeated plucking of oneshair.21 The behavior is frequently a responseto a stressful situation. Women display thisbehavior more often than men, and childrenmore often than adults. Children are oftenaware that they are plucking their hair andmay be amenable to behavioral interventions.When the behavior persists into adulthood,patients may not acknowledge the behavior.

Trichotillomania is often difficult to treat. Avariety of pharmacologic agents, mostly anti-depressants, have been tried with some suc-cess.22 A combination of pharmacologic andbehavioral therapies also has been attempted.23

The author indicates that she does not have any con-flicts of interest. Sources of funding: none reported.

REFERENCES

1. Girman CJ, Hartmaier S, Roberts J, Bergfeld W, Wald-streicher J. Patient-perceived importance of negativeeffects of androgenetic alopecia in women. J Wom-ens Health Gend Based Med 1999;8:1091-5.

2. Cash TF, Price VH, Savin RC. Psychological effectsof androgenetic alopecia on women: comparisonswith balding men and with female control sub-jects. J Am Acad Dermatol 1993;29:568-75.

3. Paus R, Cotsarelis G. The biology of hair follicles. N Engl J Med 1999;341:491-7.

4. Shapiro J, Wiseman M, Liu H. Practical manage-ment of hair loss. Can Fam Physician 2000;46:1469-77.

5. Healey PM, Jacobson EJ. Common medical diag-noses: an algorithmic approach. 3d ed. Philadel-phia: Saunders, 2000:208-11.

6. Drake LA, Dinehart SM, Farmer ER, Goltz RW, Gra-ham GF, Hordinsky MK, et al. Guidelines of care for

androgenetic alopecia. American Academy of Der-matology. J Am Acad Dermatol 1996;35(3 pt 1):465-9.

7. Dawber RP, Van Neste D. Alopecia areata. In: Daw-ber RP. Hair and scalp disorders: common present-ing signs, differential diagnosis, and treatment.Philadelphia: Lippincott, 1995:41-138.

8. Price VH. Treatment of hair loss. N Engl J Med1999;341:964-73.

9. Tosti A, Piraccini BM. Androgenetic alopecia. Int JDermatol 1999;38(suppl 1):1-7.

10. Jacobs JP, Szpunar CA, Warner ML. Use of topicalminoxidil therapy for androgenetic alopecia inwomen. Int J Dermatol 1993;32:758-62.

11. DeVillez RL, Jacobs JP, Szpunar CA, Warner ML.Androgenetic alopecia in the female. Treatmentwith 2% topical minoxidil solution. Arch Dermatol1994;130:303-7.

12. Scheman AJ, West DP, Hordinsky MK, Osburn AH,West LE. Alternative formulation for patients withcontact reactions to topical 2% and 5% minoxidilvehicle ingredients. Contact Dermatitis 2000;42:241.

13. Bergfeld WF. Retinoids and hair growth. J Am AcadDermatol 1998;39(2 pt 3):S86-9.

14. Sommer M, Wilson C. Therapeutic approaches tothe management of common baldness. Int J ClinPract 1999;53:381-5.

15. Avram MR. Hair transplantation in women. SeminCutan Med Surg 1999;18:172-6.

16. Bertolino AP. Alopecia areata. A clinical overview.Postgrad Med 2000;107(7):81-5,89-90.

17. Madani S, Shapiro J. Alopecia areata update. J AmAcad Dermatol 2000;42:549-66.

18. Fiedler-Weiss VC, Buys CM. Evaluation of anthralinin the treatment of alopecia areata. Arch Dermatol1987;123:1491-3.

19. Sperling LC, Mezebish DS. Hair diseases. Med ClinNorth Am 1998;82:1155-69.

20. Tosti A, Misciali C, Piraccini BM, Peluso AM, Bar-dazzi F. Drug-induced hair loss and hair growth.Incidence, management and avoidance. Drug Saf1994;10:310-7.

21. American Psychiatric Association. Diagnostic andstatistical manual of mental disorders. 4th ed.Washington, D.C.: American Psychiatric Associa-tion, 1994:618-21.

22. Keuthen NJ, OSullivan RL, Goodchild P, RodriguezD, Jenike MA, Baer L. Retrospective review of treat-ment outcome for 63 patients with trichotilloma-nia. Am J Psychiatry 1998;155:560-1.

23. Ninan PT, Rothbaum BO, Marsteller FA, Knight BT,Eccard MB. A placebo-controlled trial of cognitive-behavioral therapy and clomipramine in trichotillo-mania. J Clin Psychiatry 2000;61:47-50.


Telogen effluvium is diffuse hair loss that usually begins twoto four months after a causative event (e.g., stress, medica-tion use, endocrinopathy).

alopecia

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