nej mcp 072110

7/27/2019 Nej Mcp 072110

1/11

clinical practice

T h e n e w e n g l a n d j o u r n a l o f medicine

n engl j med 357;16 www.nejm.org october 18, 20071620

Hair Loss in Women

Jerry Shapiro, M.D.

From the Department of Dermatologyand Skin Science, University of BritishColumbia, and Vancouver Coastal HealthResearch Institute both in Vancouver,Canada; and the Department of Derma-tology, New York University, New York.Address reprint requests to Dr. Shapiroat the Department of Dermatology andSkin Science, University of British Co-lumbia, 835 W. 10th Ave., Vancouver, BCV5Z 4E8, Canada.

N Engl J Med 2007;357:1620-30.

Copyright 2007 Massachusetts Medical Society.

A 45-year-old white woman presents with a 1-year history of scalp-hair loss. She washospitalized with appendicitis 14 months ago. She has been a vegetarian for 20 years.She takes no medications. Her father was bald. On physical examination, she has dif-fuse, nonscarring hair thinning with a widened part over the central portion of thescalp. How should this problem be evaluated and treated?

The Clinical Problem

Hair loss, or alopecia, is a very common presenting symptom, and more than onethird of women have clinically significant hair loss during their lifetime. The effectof hair loss on patients emotions is often greatly underestimated by physicians.

After bone marrow, hair is the second fastest growing tissue of the body. As a re-sult, many metabolic derangements can be manifested with alopecia, and hair lossmay be the f irst clinical sign of systemic disease.

Hair Biology

The scalp contains, on average, 100,000 hairs. More than 90% of these hairs are ac-tively growing, and they are referred to as anagen hairs. Anagen hairs are anchoreddeeply into the subcutaneous fat and cannot be pulled out easily. Hair is constantlycycling and regenerating on the scalp. Each hair shaft may persist on the scalp for3 to 7 years before falling out and being replaced by a new hair. The anagen phase,which lasts for most of this period, is followed by a 2-week phase of catagen, duringwhich there is programmed apoptosis; the trigger factor for catagen is unknown. Aftercatagen, the hair goes into telogen, a resting phase that lasts 3 months. As comparedwith anagen hair, telogen hair is located higher in the skin and can be pulled out rela-tively easily. Normally, the scalp loses approximately 100 telogen hairs per day.

In addition to the ratio of anagen hair to telogen hair, the diameter of the hairfollicles determines scalp coverage. Vellus hairs have a hair-shaft diameter of less than0.03 mm, whereas terminal hairs have a diameter greater than 0.06 mm. The optimalhairs for scalp-hair growth and scalp coverage are anagen and terminal hairs.

Causes of Hair Loss

Hair loss is typically categorized as scarring (which occurs in discoid lupus, lichenplanopilaris, and folliculitis decalvans)1 or nonscarring. This review focuses on non-scarring alopecia.

The most common cause of such hair loss, female-pattern hair loss, is frequentlyreferred to as androgenetic alopecia; however, the role of androgens in this type ofhair loss remains uncertain.2,3 This condition is often familial.2 Female-pattern hairloss can develop any time after the onset of puberty3; by 70 years of age, 38% of

ThisJournal feature begins with a case vignette highlighting a common clinical problem.Evidence supporting various strategies is then presented, followed by a review of formal guidelines,

when they exist. The article ends with the authors clinical recommendations.

The New England Journal of Medicine

Downloaded from nejm.org on November 30, 2012. For personal use only. No other uses without permission.

Copyright 2007 Massachusetts Medical Society. All rights reserved.

7/27/2019 Nej Mcp 072110

2/11

clinical practice

n engl j med 357;16 www.nejm.org october 18, 2007 1621

women have female-pattern hair loss.4 It affectsthe central portion of the scalp, sparing the fron-tal hairline, and is characterized by a wider mid-line part on the crown than on the occipital scalp(Fig. 1). In some women, hair thinning over thelateral area of the scalp also occurs. The severityof hair loss is staged according to the Ludwig

classification,5 in which increasing stages (I toIII) correspond to increasing widths of the mid-line part. If hair thinning is more evident in thefrontal portion of the scalp, the part may resem-ble a fir tree in what is known as a Christmas treepattern behind the frontal hair line (Fig. 2). Thispattern is referred to as frontal accentuation.3

Other manifestations of hair loss include hairthinning on the lateral scalp and male patternsinvolving thinning on the frontotemporal and ver-tex areas of the scalp. Male patterns of hair lossmay be associated with hyperandrogenism, but the

majority of women with female-pattern hair losshave normal serum androgen levels.6-8 One study6

showed a prevalence of biochemical hyperandro-genemia of 38.5% among women with moderate-to-severe alopecia; approximately one quarter ofthese women had no other signs of hyperandro-genemia, such as hirsutism or menstrual distur-bances.

Another common cause of alopecia is telogen

effluvium. This condition results from an abruptshift of large numbers of anagen hairs to telogenhairs on the scalp, with a corresponding changein the ratio of anagen hair to telogen hair fromthe normal ratio of 90:10 to 70:30. It is not un-usual for women with telogen effluvium to losemore than 300 hairs per day. This form of alope-cia generally begins approximately 3 months aftera major illness or other stress (e.g., surgery, par-turition, rapid weight loss, nutritional deficiency,high fever, or hemorrhage) or hormonal derange-ment (e.g., thyroid dysfunction); it has also been

reported after the initiation of treatment with cer-tain medications (Table 1). This process is distinct

l

A B

DC

Figure 1. Marked Thinning of Hair on the Crown of the Scalp in a Woman with Female-Pattern Hair Loss and Fairly

Normal Occipital Density.

The centroparietal portion of the scalp, which shows decreased hair density (Panels A and B), would be classified

as Ludwig stage II (a moderately widened central part). In this patient, hair thinning also extends laterally (Panels Cand D).




7/27/2019 Nej Mcp 072110

3/11



from anagen eff luvium, the hair loss associatedwith chemotherapeutic agents that cause imme-diate destruction and release of anagen hair.

If the cause of telogen eff luvium is removed,hair loss lasts for up to 6 months after removal ofthe trigger. Chronic telogen effluvium refers tohair loss lasting more than 6 months. In somepatients, this type of hair loss lasts for years.10Prolonged telogen effluvium may be due to mul-tiple sequential triggers, although in some pa-tients, no trigger is identified.10 Telogen effluviummay evolve into or reveal female-pattern hair loss,but the frequency of such cases is unclear.

A less frequent cause of nonscarring alopecia isalopecia areata. The estimated lifetime incidenceof this condition is 1.7% (Fig. 3).11 It is usuallymanifested as round patches of alopecia that maybecome multifocal and may coalesce into largeareas affecting more than 50% of the scalp. Oc-casionally, there is diffuse generalized alopecia,requiring a scalp biopsy for confirmation. Alope-cia areata is frequently reversible, but it tends to be

recurrent, and it can progress to total loss of scalphair (alopecia totalis) in 5% of women and totalloss of body hair (alopecia universalis) in 1% ofwomen. The cause is unknown, but it is thoughtto be autoimmune. Other causes of nonscarringalopecia are certain hair-care practices (Table 2),compulsive hair pulling (trichotillomania), severe

bacterial infections, tinea capitis, and, in rarecases, abnormalities causing fragility or breakageof irregularly shaped hair.

In some cross-sectional studies, iron deficiencyand reduced iron levels have been associated withhair loss, including female-pattern hair loss andtelogen effluvium, but data are limited.12-14 Sucha relationship might be explained by the observa-tion that iron is required as a cofactor for the activ-ity of ribonucleotide reductase, a rate-limiting en-zyme controlling DNA synthesis and required byrapidly dividing hair matrix cells.

Str ategies and Evidence

Evaluation

The history taking should include an assessmentof the duration and pattern of hair loss, includingwhether hair is shedding (suggesting alopecia area-ta or telogen eff luvium) or is primarily thinning(suggesting female-pattern hair loss). It is impor-tant to establish whether the hair is falling outfrom the root (suggesting telogen eff luvium, fe-male-pattern hair loss, or alopecia areata) or break-ing off along the shafts (as occurs with certainhair-care practices, trichotillomania, or tinea ca-pitis) (Table 2).

Patients should be asked about hair-care prac-tices that may damage hair (e.g., braiding thatcauses traction alopecia), as well as about the lossof eyelashes, eyebrows, and axillary, pubic, or bodyhair, since any hair-bearing area can be affectedby alopecia areata or trichotillomania. A historyof illness, childbirth, surgery, psychosocial stress,or a new medication predating the onset of hair

loss by 1 to 3 months suggests telogen eff luvium.Acne, irregular menstrual cycles, or hirsutism mayindicate androgen excess contributing to female-pattern hair loss. Symptoms of hyperthyroidismor hypothyroidism should also be assessed, andcurrent and previous medications should be care-fully reviewed (Table 1). A history of following astrict vegetarian diet or heavy menses may suggestiron-deficiency anemia.

Figure 2. Frontal Accentuation of Hair Lossin Female-Pattern Hair Loss.




7/27/2019 Nej Mcp 072110

4/11

clinical practice


The clinical examination should be performedin four stages. First, the scalp should be inspectedfor inflammation, scale, and erythema (Fig. 4).Next, scarring associated with hair loss should beassessed. Nonscarring alopecia (Fig. 5A) is charac-terized by visible follicular openings (ostia), where-as scarring alopecias (Fig. 5B) are devoid of ostia.

The third step is to examine the pattern of distri-bution of hair loss and the density of hair, and thefourth step is to assess the quality of the hair shaftin terms of caliber, fragility, length, and shape. Ifthe hair tips are blunt, hair breakage may be im-plicated. Tapered tips are normal. To assess theongoing activity and severity of hair loss, a pull

Table 1. Medications Associated with Hair Loss.*

Type of Hair Loss

Interval betweenStart of Treatment

and Hair Loss MedicationsEstimated

Incidence (%)

Telogen effluvium 23 mo Acetretin, heparin, interferon alfa, isotretinoin, lithium,ramipril, terbinafine, timolol, valproic acid, warfarin

>5

Acyclovir, allopurinol, buspirone, captopril, carbamazepine,cetirizine, cyclosporine, gold, lamotrigine, leuprolide, lova-statin, nifedipine

15

Amiodarone, amitriptyline, azathioprine, dopamine,naproxen, omeprazole, paroxetine, prazosin, sertraline,venlafaxine, verapamil

10

* This list is not comprehensive. Data are from Litt.9

l

Figure 3. Alopecia Areata with Round, Random Patches of Hair Loss That Coalesce.




7/27/2019 Nej Mcp 072110

5/11



Table2.

CharacteristicsofNonscarringHairLoss.

Characteristic

Fe

male-PatternHairLoss

TelogenE

ffluvium

AlopeciaAreata

TineaCapitis

Hair-CarePractices,

TractionAlopecia,

orTrichotillomania

Distribu

tion

Usua

llyc

en

tra

lport

iono

fthesca

lp,

sparing

the

fron

talha

irline

(less

comm

on

ly,

ha

irthinn

ingon

the

latera

l,fron

totempora

l,orvertex

portionso

fthesca

lp)

Genera

lized

Usua

llypa

tchy,

bu

tmay

bemu

ltifoca

lan

d

pa

tchesmayco-

alesce;

totala

lopec

ia

in5

10%

ofpa

tien

ts

withthiscon

dition

Any

areao

fthesca

lp;may

b

efoca

lormu

ltifoca

l

Anyareao

fthesca

lp;may

bepa

tchy

withirregula

rangu

lar

borders;

trac-

tiona

lopecia

frequen

tlya

ffec

tsthe

fron

talan

dtempora

le

dgeso

fthe

sca

lp

Onse

t

Gra

dualw

ithprogress

ion

Abrup

tw

itha

trigger

fac

tor

(e.g.,

bloo

d

loss,

iron

de

fic

ien-

cy,

thyro

idimba

l-

ance,

orinitiation

ofdrugtrea

tmen

t)

Abrup

t,usua

llywaxes

an

dwanes

Gra

dua

lora

brup

t

Gra

dua

lora

bru

pt,depen

dingon

the

cause

Appearance

Ha

irthin

ningw

ithorw

ithou

tbare

pa

tch

es;w

idem

idlineparton

the

crown

Ha

irthinningw

ithno

barepatc

hes

Ha

irthinn

ingw

itha

brup

t

barepa

tches;

exc

la-

ma

tionpo

intha

irs

Infla

mma

tionorno

inflam-

m

ation;sca

lepresen

t

Bro

ken

ha

irswi

thblun

tra

ther

than

ta-

pere

dtips;d

egreeo

finflamma

tion

due

toha

ir-c

areprac

tices

depen

ds

on

theo

ffen

dingagen

t;no

inflam-

ma

tionw

ith

trac

tiona

lopec

iaor

tricho

tilloman

ia

Degreeo

fs

he

dding

Minima

l

Prom

inent

Prom

inen

t

Prom

inen

t

Bro

ken

ha

irscan

bes

he

d;variesw

ith

offen

ding

ha

ir-careagen

t;m

inima

l

withtrac

tion

alopec

iaan

dtricho

til-

loman

ia

Pa

tien

tsage

atonse

t

Pu

bertyoro

lder

Anyage,b

utno

t

common

in

childho

od

Anyage;mos

tpa

tien

ts

have

firs

tpa

tchbe-

fore

20yro

fage

An

yage;common

in

childhoo

d

Anyage

Resu

lto

fpu

lltes

t

Usually

nega

tive

Pos

itive

Pos

itive

Po

sitive

Usua

llynega

tive

Other

history

Oftenf

am

ily

historyo

fha

irloss

Prev

iousm

ajor

ill-

nessors

tress

May

bepersona

lor

fam

ily

historyo

f

otherau

toimmune

disease

Prev

iouscon

tac

tw

ithan

i-

ma

ls(e

.g.,

kittens

)as-

soc

iatedw

ithcerta

in

derma

top

hy

tes

Bac

kbrus

hing(

i.e.,

brus

hingorcom

b-

ing

ha

irina

direc

tion

differen

tfrom

tha

to

fha

irg

row

th);useo

fperma-

nen

twaves,

bleac

h,

orre

laxan

tsor

bra

iding;

tric

ho

tilloman

iamay

be

assoc

iatedw

itho

therpsyc

hiatric

con

ditions




7/27/2019 Nej Mcp 072110

6/11

clinical practice


test (Fig. 6) should be performed. Table 2 sum-

marizes characteristics that help in distinguishingamong common nonscarring hair-loss conditions.

Laboratory Testing

Clinicians often assess the ferritin level to rule outiron deficiency (particularly in menstruating wom-en, vegetarians, and women with a history of ane-mia13-15) and the thyrotropin level to rule out thy-roid dysfunction in women with diffuse hair loss,although the yield of such universal testing hasnot been proved. If the ferritin level is less than70 ng per milliliter, iron supplementation is rec-ommended.15 However, its effects on hair loss andregrowth have not been rigorously evaluated incontrolled trials; data suggestive of efficacy arelimited to case series indicating cessation of hairloss and new hair growth with iron supplementa-tion in women with low ferritin levels,16 and notall case series have shown a benefit of iron sup-plementation.12

In women with female-pattern hair loss andother conditions suggesting androgen excess (e.g.,hirsutism, acne, or irregular menses), assessment

of free testosterone is recommended; the yield oftesting is expected to be low in the absence ofother features suggesting androgen excess. A Ve-nereal Disease Research Laboratory test is recom-mended if the patient has any risk factors forsyphilis.

If tinea is suspected, scale from the area of alo-pecia should be examined by means of a potas-sium hydroxide scraping for hyphae and sent for

culture. Hair shafts should be plucked for cultureas well. Examination with a Woods lamp willshow a green fluorescence if a specific group ofdermatophytes (Microsporum canis) is present.

If the diagnosis remains in question, a 4-mmpunch biopsy of tissue from the scalp may be use-ful. This test is especially useful when evaluatingpatients suspected of having scarring alopecia.

Management

Therapies for female-pattern hair loss include top-ical minoxidil, antiandrogen medication, and hairtransplantation in selected patients. Baseline pho-tographs (typically of the midline part) should betaken and used on subsequent visits for compari-son. Six months to 1 year of treatment may be re-quired before there is considerable improvement.

Figure 4. Marked Scarring Hair Loss with a Central

Distribution, Follicular Hyperkeratosis, and Pustulesin a 44-Year-Old Woman.

A biopsy specimen revealed folliculitis decalvans, a rarepermanent scarring condition that occurs with folliculitis.

A

B

l

Figure 5. Nonscarring and Scarring Hair Loss.

Panel A shows a typical circular patch of nonscarring

hair loss in alopecia areata with distinct follicular open-ings, or ostia. Panel B shows a patch of scarring alope-

cia with no follicular ostia.




7/27/2019 Nej Mcp 072110

7/11

7/27/2019 Nej Mcp 072110

8/11

clinical practice


Antiandrogen Therapies

Antiandrogen agents (including the androgen-receptor blockers spironolactone, cyproterone ac-etate, and f lutamide and the 5-reductase inhib-itor finasteride) and oral contraceptives are notcommonly used to treat female-pattern hair lossin North America, but they are used more com-monly in Europe. None of these agents are FDA-approved for female-pattern hair loss. Cyproteroneacetate is not approved in the United States, andneither flutamide nor finasteride is approved for

any indication in women, although finasteride isapproved for the treatment of hair loss in men.In an open-label study of cyproterone acetate

(50 to 100 mg daily for 10 days of the menstrualcycle) or spironolactone (200 mg daily) in womenwith female-pattern hair loss,19 more than 80% ofwomen had either hair regrowth or stabilization ofhair loss, but this study was uncontrolled. In a

randomized trial comparing topical 2% minoxidilsolution plus an oral contraceptive with cyproter-one acetate (52 mg per day) plus an oral contracep-tive in women with female-pattern hair loss, thelatter combination resulted in greater hair densityin women with hyperandrogenism, whereas inwomen without hyperandrogenism, minoxidil hada greater effect.20 If antiandrogen agents are usedin women of reproductive age, an oral contracep-tive should be prescribed concomitantly, sincethese agents are known teratogens.

In two small, uncontrolled studies, finasteride(Propecia) at a minimum dose of 2.5 mg per dayappeared to have a benefit for women with female-pattern hair loss.21,22 However, in a double-blind,controlled trial23 involving postmenopausal womenwith female-pattern hair loss, treatment with fin-asteride at a dose of 1 mg per day was not signifi-cantly better than placebo. Like the antiandrogens,

l

A B

Figure 7. Female-Pattern Hair Loss with Frontal Accentuation before and after Treatment with Topical 5% MinoxidilSolution in a 58-Year-Old Woman.

Panel A shows hair loss before treatment, and Panel B shows regrowth after 6 months of treatment.




7/27/2019 Nej Mcp 072110

9/11


finasteride is a known teratogen, and its use is notrecommended in women of reproductive age.

Hair Transplantation

Hair surgery is increasingly used to treat manywomen with female-pattern hair loss.24 Clinical ex-perience indicates that when the newer technique

of follicular-unit transplantation is performed byan experienced surgeon, a natural result is possible(Fig. 8). However, data on long-term outcomes arelacking, and rates of graft failure, although con-sidered to be very low, remain uncertain. Costsvary, but they may range from $4,000 to $15,000per session, depending on the size of the area treat-ed and the surgeon. One or two sessions are usu-ally suff icient for a cosmetically acceptable result.Hair density in the donor (occipital) area must besufficient to yield the required number of grafts

with no visible scarring. Complications, whichare rare, include infection, permanent scalp dys-thesias, and arteriovenous malformations (whichoccur in less than 1% of patients). Many surgeonsuse minoxidil therapy in patients who have under-gone hair transplantation (Fig. 9), although thisstrategy has also not been rigorously studied.25

Treatment of Other Causes of Hair Loss

Tinea resulting in hair loss is treated with sys-temic antifungal agents. Adverse hair-care prac-tices should be discontinued. Detailed discus-sions of the treatments of trichotillomania andalopecia areata are beyond the scope of this ar-ticle. Briefly, trichotillomania may improve withcounseling, cognitive behavioral therapy, or phar-macotherapy (e.g., antidepressants).26,27 For alo-pecia areata, treatment depends on the extent ofscalp involvement. Limited patches affecting less

than 50% of the scalp are generally treated withintralesional corticosteroid injections, whereasfor more extensive scalp-hair loss, treatments in-clude topical minoxidil solution, anthralin, pso-ralen and ultraviolet A (PUVA) therapy, and topi-cal immunotherapy with a contact sensitizer orallergen; data on optimal therapy are limited.11,28

Area s of Uncertainty

There are limited data from randomized, double-blind, controlled trials to evaluate and comparevarious therapies for female-pattern hair loss. Theroles of iron deficiency in causing hair loss andiron supplementation in treatment remain uncer-tain. Critical evaluation of graft survival and otheroutcomes of hair transplantation is needed.

Guidelines

The American Academy of Dermatology pub-lished guidelines in 1996 for the management ofhair loss in women,29 but these guidelines ante-

dated many current treatment options. An up-dated review of the evaluation and treatment offemale-pattern hair loss was published in 2005.30Guidelines for the treatment of alopecia areatahave been issued by the British Association ofDermatologists.28

clinical practice

A

B

l

Figure 8. Female-Pattern Hair Loss before and afterHair Transplantation in a 45-Year-Old Woman.

Panel A shows hair loss before transplantation, andPanel B shows the results, at 9 months, of grafting

with 1575 follicular units.




7/27/2019 Nej Mcp 072110

10/11

clinical practice


Conclusions

and R ecommendations

Determining the cause or causes of hair loss inwomen can be diff icult and should be guided bythe patients history including the pattern ofhair loss, other medical conditions, the use of

hair treatments, and the family history of hairloss as well as by the physical examination.The history of the patient in the vignette sug-gests telogen eff luvium from appendicitis or irondeficiency related to her vegetarian diet; her fam-ily history suggests female-pattern hair loss. Herhair loss on the central portion of the scalp alsosuggests female-pattern hair loss, which may havebeen revealed by telogen effluvium. Although dataare lacking to provide support for routine testingand treatment for iron deficiency in the manage-ment of hair loss, I would check the patients

ferritin and thyrotropin levels.Although objective data are lacking to show

the superiority of 5% minoxidil solution over 2%minoxidil solution, on the basis of clinical expe-rience and reports of greater patient satisfactionwith the former, I would initiate treatment withtopical 5% minoxidil solution twice daily, withthe plan to continue this treatment indefinitelyif there is evidence of efficacy within 1 year. Ifthe results are unsatisfactory, hair transplanta-tion might be considered, if this procedure isavailable and affordable to the patient and if thehair in the donor area has sufficient density. Iwould carefully review the patients expectationsregarding therapy, with attention to the magni-tude of improvement that can be realistically an-ticipated. Results of treatment are usually seenin 6 months to 1 year.

Dr. Shapiro reports receiving consulting fees from Pfizer. Noother potential conflict of interest relevant to this article wasreported.

The North American Hair Research Society Web site (www.nahrs.org) is a resource for patients with hair loss.

814 mm

Elliptical strip

12002000follicular units

Follicularunit

Needle

B

C

D

F G

E

A

812 cm

Forceps

l ll

I

Figure 9. Hair Transplantation with Grafts Obtained from an Elliptical Strip

from the Back of the Scalp.

An elliptical strip averaging in size from 8 to 14 mm wide and 8 to 12 cm

long is excised from the occipital portion of the scalp (Panels A and B).This strip is subdivided into 1200 to 2000 follicular units of two to threehairs each (Panel C). Slits are made with a tiny spear or needle (Panel D).

The needle is then removed, and follicular units are planted in these slits(Panel E). With appropriate placement and orientation of follicular units,

it is possible to increase hair density from Ludwig stage II (Panel F) to Lud-wig stage I (Panel G) in a patient with female-pattern hair loss.




7/27/2019 Nej Mcp 072110

11/11


clinical practice

References

Ross EK, Tan E, Shapiro J. Update onprimary cicatricial alopecias. J Am AcadDermatol 2005;53:1-37. [Erratum, J AmAcad Dermatol 2005;53:496.]

Birch MP, Lalla SC, Messenger AG. Fe-male pattern hair loss. Clin Exp Dermatol2002;27:383-8.

Olsen EA. Female pattern hair loss.

J Am Acad Dermatol 2001;45:Suppl 3:S70-S80.

Birch MP, Messenger JF, MessengerAG. Hair density, hair diameter and theprevalence of female pattern hair loss. BrJ Dermatol 2001;144:297-304.

Ludwig E. Androgenetic alopecia. ArchDermatol 1977;113:109.

Futterweit W, Dunaif A, Yeh HC, Kings-ley P. The prevalence of hyperandrogen-ism in 109 consecutive female patientswith dif fuse alopecia. J Am Acad Derma-tol 1988;19:831-6.

Kasick JM, Bergfeld WF, Steck WD,Gupta MK. Adrenal androgenic female-pattern alopecia: sex hormones and thebalding woman. Cleve Clin Q 1983;50:111-22.

Miller JA, Darley CR, Karkavitsas K,Kirby JD, Munro DD. Low sex-hormonebinding globulin levels in young womenwith diffuse hair loss. Br J Dermatol 1982;106:331-6.

Litt JZ. Litts drug eruption referencemanual. 12th ed. Abdingdon, United King-dom: Taylor & Francis, 2006.

Whiting DA. Chronic telogen effluvi-um: increased scalp hair shedding in mid-dle-aged women. J Am Acad Dermatol 1996;35:899-906.

Madani S, Shapiro J. Alopecia areata

update. J Am Acad Dermatol 2000;42:549-66.

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

Sinclair R. There is no clear associationbetween low serum ferritin and chronicdiffuse telogen hair loss. Br J Dermatol2002;147:982-4.

Rushton DH, Ramsay ID, James KC,Norris MJ, Gilkes JJ. Biochemical and tri-chological characterization of diffuse alo-pecia in women. Br J Dermatol 1990;123:

187-97.Kantor J, Kessler LJ, Brooks DG, Cot-

sarelis G. Decreased serum ferritin is as-sociated with alopecia in women. J InvestDermatol 2003;121:985-8.

Trost LB, Bergfeld WF, Calogeras E.The diagnosis and treatment of iron defi-ciency and its potential relationship to hairloss. J Am Acad Dermatol 2006;54:824-44.

Hard S. Non-anemic iron deficiency asan etiologic factor in diffuse loss of hairof the scalp in women. Acta Derm Vene-reol 1963;43:562-9.

DeVillez RL, Jacobs JP, Szpunar CA,Warner ML. Androgenetic alopecia in thefemale: treatment with 2% topical min-oxidil solution. Arch Dermatol 1994;130:303-7.

Lucky AW, Piacquadio DJ, Ditre CM, etal. A randomized, placebo-controlled trialof 5% and 2% topical minoxidil solutionsin the treatment of female pattern hairloss. J Am Acad Dermatol 2004;50:541-53.

Sinclair R, Wewerinke M, Jolley D.Treatment of female pattern hair loss withoral antiandrogens. Br J Dermatol 2005;152:466-73.

Vexiau P, Chaspoux C, Boudou P, et al.Effects of minoxidil 2% vs. cyproteroneacetate treatment on female androgeneticalopecia: a control led, 12-month random-

ized trial. Br J Dermatol 2002;146:992-9.Iorizzo M, Vincenzi C, Voudouris S,

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

Piraccini BM, Tosti A. Finasteride treat-ment of female pattern hair loss. ArchDermatol 2006;142:298-302.

Treb RM. Finasteride treatment of pat-terned hair loss in normoandrogenic post-menopausal women. Dermatology 2004;209:202-7.

Price VH, Roberts JL, Hordinsky M, et

al. Lack of efficacy of finasteride in post-menopausal women with androgenetic alo-pecia. J Am Acad Dermatol 2000;43:768-76.

Unger WP, Unger RH. Hair trans-planting: an important but often forgot-ten treatment for female pattern hair loss.J Am Acad Dermatol 2003;49:853-60.

Avram MR, Cole JP, Gandelman M, etal. The potential role of minoxidil in thehair transplantation setting. Dermatol Surg2002;28:894-900.

Dougherty DD, Loh R, Jenike MA,Keuthen NJ. Single modality versus dualmodality treatment for trichotillomania:sertraline, behavioral therapy, or both?J Clin Psychiatry 2006;67:1086-92.

Swedo SE, Lenane MC, Leonard HL.Long-term treatment of trichotillomania(hair pulling). N Engl J Med 1993;329:141-2.

MacDonald Hull SP, Wood ML,Hutchinson PE, Sladden M, Messenger AG.Guidelines for the management of alope-cia areata. Br J Dermatol 2003;149:692-9.

Drake LA, Dinehart SM, Farmer ER, etal. Guidelines of care for androgenetic al-opecia: American Academy of Dermatolo-gy. J Am Acad Dermatol 1996;35:465-9.

Olsen EA, Messenger AG, Shapiro J, etal. Evaluation and treatment of male andfemale pattern hair loss. J Am Acad Der-

matol 2005;52:301-11.Copyright 2007 Massachusetts Medical Society.

22.

23.

24.

25.

26.

27.

28.

29.

30.

viewcurrentjobpostingsatthenejmcareercenter

Visit our online CareerCenter for physicians

atwww.nejmjobs.orgto see the expanded features andservices available. Physicians can conduct a quick searchof the public database by specialty and view hundreds

of current openings that are updated daily onlineat the CareerCenter.


Downloaded from nejm org on November 30 2012 For personal use only No other uses without permission

nej mcp 072110

Documents