lopecia, or hair loss, is a common and often distressingproblem. Physicians may find it difficult to make a spe-
ific diagnosis. However, a systematic approach to the patientith hair loss will enable the clinician to make an accurateiagnosis in the majority of cases. The correct diagnosis isased on a detailed history, physical examination, micro-copic analysis of the hair and, in some cases, scalp biopsynd pertinent laboratory tests (Fig. 1). With the appropriateiagnosis, proper patient counseling and treatment can be
nitiated.
valuating the Patientistory
he history is extremely important in developing a differen-ial diagnosis. A detailed history includes the chief complaint,ast medical history, medications, allergies, family history,nd diet. If the patient is a woman, a history of menses,regnancy, and menopause also should be assessed (Table). Pregnancy, crash diets, or a strict vegetarian diet can causerofuse telogen shedding.1
After a general review of systems, questions should beirected specifically toward hair loss. All too frequently, thehief complaint is “hair loss.” Thus, the physician needs toork with the patient to clarify and qualify the complaint toarrow the differential diagnosis. Specific questions that cane helpful are listed in Table 2.
ase Western School of Medicine, Department of Dermatology, Cleveland,OH.
ddress reprint requests to Paradi Mirmirani, MD, Kaiser PermanenteVallejo Medical Center, Department of Dermatology, 975 Sereno Drive,
urationhe duration and onset of alopecia should be determined.or example, if hair loss is of sudden onset, a generalizedhysical insult, illness, nutritional deprivation, toxicity fromrugs, or pregnancy may be the cause. However, chronic hair
oss could be secondary to a genetic syndrome or hormone-elated disorder.2
istributionocalized, diffuse, or patterned thinning can be the key to diag-osis. When a patient presents for evaluation of hair loss, theyay be referring to a single patch of alopecia or to extensive hair
reakage from use of hair care products. Patterned alopecia iseen most commonly in androgenetic alopecia.
allout or Breakage?his differentiation is important as it separates 2 entirelyifferent categories of hair disease. If the hair is coming outby the roots,” then the patient should be asked whetherncreased shedding or increased thinning is the main feature.or example, markedly increased hair shedding, usuallyithout increased thinning, occurs with telogen effluvium.
n androgenetic alopecia, increased thinning without in-reased shedding is the main finding.
air Care Routineair care practices and the use of hair cosmetics (eg, bleach-
ng, permanent waving) can be a key factor in determininghe cause of hair loss.
linical Examinationthorough examination of the hair typically involves an
ssessment of the patient’s global appearance as well as aetailed inspection of the hair and scalp (Table 3). The tex-ure, color, and length of the hair often modify or alter the
ppearance of hair thinning and should be documented as
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12 A. Han and P. Mirmirani
art of the examination. Hair distribution over the rest of theody is assessed to see whether there is too little or too muchair in other areas. Acne or other signs of virilization also areoted. After establishing a global picture of hair loss, a moreetailed examination is undertaken.
xtent and Distribution of Hair Losshe extent and distribution of hair loss may be readily appar-nt on visual inspection. In other cases, a close evaluation ofhe hair and scalp can be accomplished by serially parting the
able 1 General Medical History
All major medical problems (with special attention to thefollowing)
Thyroid abnormalitiesAnemiaAutoimmune diseases
Past and current medicationsPrescriptionOver the counterHerbals
Family historyMenstrual and pregnancy history
Figure 1 Basic approach
Diet history (crash diets, strict vegetarian, etc)
air starting at the center part. In this manner the density ofair at various areas can be compared while also making notef other findings. Various tools that can be used in docu-enting the extent and distribution of hair loss include draw-
ngs, description of hair loss by scalp section (frontal hairline,emporal, occipital, top, vertex), established grading scalessee the section “Androgenetic Alopecia”), or percent of scalpair loss (see section “Alopecia Areata”); photographs can bevery helpful adjunct.
carring or Nonscarring?oncicatricial alopecias demonstrate visible follicular open-
ngs, whereas cicatricial alopecias are devoid of follicular or-fices. Differentiation of these 2 types of hair loss can signif-cantly narrow the differential diagnosis.
able 2 Focused Alopecia History Questions
1. When did the hair loss start?2. Was the onset sudden or gradual?3. Where have you noticed the most hair loss?4. Is the hair coming out by the roots (shedding or
thinning), or is it breaking?
assessment of alopecia.
5. What is your normal hair care routine?
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Clinical approach to the patient with alopecia 13
ull Test Resultspull test is useful for determining ongoing or excessive hair
hedding or loosely anchored hair. Approximately 50 closelyrouped hairs are grasped between the thumb, index, andiddle fingers, and gentle traction is applied as the fingers
re pulled firmly and slowly away from the scalp (Fig. 3A). Inormal adults, 2 to 5 telogen hairs will be obtained in thisanner. If excessive shedding is present, as in telogen efflu-
ium or alopecia areata, 6 or more hairs are easily pulled out.false-negative pull test may result if the examination is
erformed within 24 hours of the hair being washed.
istal Hair Shaft Evaluationhe hair tips should be examined to see whether they are
apered, broken, or miniaturized. The tips can be held againstcontrasting white or black background, depending on the
olor of the hair, to view them more clearly (Fig. 2). Taperedair indicates new growth, whereas broken or cut hair islunt at the ends. Miniaturized hair is tapered at the end, butuch finer in caliber.
he Tug Testhis test is an additional procedure useful for determining
he presence of hair breakage. To perform the tug test, hairsre grasped at the base and center of the hair shaft and gentlyulled (Fig. 3B). If the hair shaft is fragile or damaged, theair will break off. Any hair breakage constitutes an abnor-ality and a cause should be investigated.
calp Evaluationhe scalp should be examined for signs of inflammation,rythema, drainage, or scaling.
icroscopic Examinationhe Hair Mounthe purpose of the hair mount is to microscopically examine
he hair shaft or bulb. The hairs obtained from the hair pullan be used for this examination. Supplies needed to performhair mount include a contrasting black or white velvet
ackground for hair placement and examination, glass slides,overslips, and a mounting medium (Fig. 4).
To examine the hair bulb or hair shaft, a mounting me-ium that does not dissolve keratin must be used. Four to five
able 3 The Physical Examination
Global appearanceIs the scalp readily visible?What is the texture, color, and length of the hair?Is the distribution of hair on the body normal?Are there signs of virilization (e.g. acne)?
Detailed examinationWhat is the extent and distribution of the hair loss?Is the hair loss scarring or nonscarring?Is the pull test normal?What is the appearance of the distal hair shaft?Is the tug test normal?Is the scalp affected?Are daily hair counts normal?
hort segments of hair are placed on a glass slide on which a m
rop of mounting medium (Balsam, Permount (Fisher Scien-ific, Pittsburgh, PA)), or Harleco synthetic resin (Matsunamilass, Osaka, Japan) has been placed. If a dermatophyte in-
ection is suspected, the hairs may be mounted in 20% po-assium hydroxide, which dissolves keratin and allows forasy visualization of fungal elements. The telogen bulb can beecognized by its distinctive club shape (Fig. 5A). An anagenulb can be recognized by its dark keratogenous zone, me-ulla, inner root sheath, and outer root sheath (Fig. 5B). Theair shafts can be examined for fractures, irregularities, twist-
ng and coiling, and any extraneous matter.
he Scalp Biopsycalp biopsies can be used to make or confirm a diagnosis oflopecia and can be essential to guiding therapy. Scalp biop-ies should be performed in all cases of cicatricial alopecia tostablish the underlying cause and to help select appropriatereatment. The biopsy should be taken from the active borderf hair loss where some hairs still remain. A four millimeterunch biopsy is adequate and must include subcutaneous fato ensure sampling of the entire follicular unit and any ana-en follicles. The biopsies may be sectioned horizontally orertically (Fig. 6). Vertical sections are useful for giving in-ormation about the epidermis. Horizontal sections are be-oming the method of choice as they offer the advantage ofvaluating large numbers of follicles simultaneously, deter-ining hair density, telogen/vellus ratio, anagen to telogen
atio and the location of any inflammatory infiltrate.4
aboratory Evaluationaboratory tests may be useful in establishing a diagnosis. Aareful history can help direct what laboratory tests to order.basic evaluation, including thyroid stimulating hormone,
erum iron, and ferritin, may be necessary to exclude thyroid
igure 2 Use of a contrasting color card to assess hair tips. Note the
iniaturized hairs.
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14 A. Han and P. Mirmirani
ysfunction and iron deficiency anemia. In women with an-rogenetic alopecia and virilizing signs such as acne, hirsut-
sm, and/or irregular menses, a basic endocrine panel to ruleut hyperandrogen states is advised (Table 4).5 In cases ofcarring alopecia secondary to discoid lupus erythematous,n antinuclear antibody (ANA) is warranted. If there is anylinical suspicion of syphilitic alopecia, an RPR is necessary.
theraily Hair Countshis test can be useful for quantifying how much hair aatient is losing. As many as 100 telogen hairs are shed eachay in normal individuals.3 Patients are asked to collect allairs shed in the shower, sink, pillow, brush, and anywherelse for 24 hours. This procedure is repeated 3 to 4 times.ecause shampooing and daily hair care practices affect hairhedding, it is important to collect the hair on a nonshampooay. If the patient is losing less than 100 hairs a day, they cane reassured that no active hair shedding is taking place.
igure 4 Hair mount supplies. F
pproach to Specificypes of Alopeciasing the systematic and methodical approach to hair lossescribed above and keeping in mind the differential di-gnoses of hair loss, the practicing clinician can make theorrect diagnosis in almost all patients with alopecia. Theesults of the evaluation can be summarized to the patients follows: “Based on a review of your medical history,etailed examination of your hair and scalp, and labora-ory test(s), the cause of hair loss is most likely X.” Confi-ent that the physician has undertaken a thorough evalu-tion, the patient is often more open and accepting ofounseling and treatment suggestions.
oncicatricial Alopecia Withair “Coming Out by The Roots”ndrogenetic Alopecia (AGA)GA is a common hereditary thinning of hair induced byndrogens in genetically susceptible men and women. Thisondition is also known as male-pattern hair loss or commonaldness in men and as female-pattern hair loss in women. Inusceptible hair follicles of the scalp, dihydrotestosterone,
Figure 3 A, Hair pull test. B,Tug test.
igure 5 A, Telogen hair bulbs. B, Anagen hair bulbs.
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Clinical approach to the patient with alopecia 15
he potent metabolite of testosterone, binds to the androgeneceptor. The hormone-receptor complex then activates theenes responsible for the gradual and progressive transfor-ation of large, terminal follicles to miniaturized follicles.he miniaturization process is accompanied by shortening of
he anagen phase.3
istory. Patients often report hair thinning without an in-rease in shedding1 with complaints including, “I’m losingy hair ” or “I can see my scalp.” The onset of AGA may occur
n either sex at any time after puberty. It is estimated that halff the population experiences this hereditary hair loss by age0.6 Affected individuals exhibit a pattern of polygenic inher-
tance and often have a positive family history of AGA.7,8
linical Findings and Diagnosis. In men, the patterns ofGA are well recognized. They vary widely in extent but
nvolve thinning in 3 scalp regions: frontal/parietal scalp,
igure 6 Vertical (A) and horizontal (B) sections of a scalp biopsy.
able 4 Useful Laboratory Tests in the Evaluation of Alopecias
Thyroid stimulating hormoneSerum iron and ferritinAntinuclear antibodyRPRWomen with signs of virilization
Free testosteroneProlactin17-hydroxyprogesterone
Cortisol
aPR, rapid plasma reagin
ertex, and bitemporal region9 (Figs. 7 and 8). Such pat-erned hair loss is characteristic of AGA and is not present inther causes of hair loss. Well-known diagrams for gradingnd documenting AGA in men have been established by Nor-ood and Hamilton (Fig. 9).Similar to men, AGA in women is also a patterned hair loss;
hinning typically occurs on top, whereas the frontal hairlineemains intact. Less-common patterns include hair loss of therontal and temporal scalp, or diffuse thinning. Women withong hair may have a “skimpy” appearance of the distal hair
igure 7 Schematic showing common areas of hair loss in men withndrogenetic alopecia.
igure 8 A, Decreased scalp coverage in a patterned distribution inndrogenetic alopecia involving the vertex, top of the scalp, anditemporal areas. Miniaturized hairs were noted on closer examina-ion. B, Common pattern of hair loss in all areas except the temporal
nd occipital fringe in a man with androgenetic alopecia.
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16 A. Han and P. Mirmirani
ecause of a shortening of the anagen phase.3 With advancedGA, the scalp may be visible (Fig. 10A) but generallyomen do not become bald. Increased spacing between hairsakes the central “part ” look wider over the frontal scalp
ompared with the occipital scalp (Fig. 10B). The presence of
igure 9 Norwood and Hamilton grading scales for androgeneticlopecia. From Hordinsky M: Alopecias, in Dermatology. Nework, Elsevier, 2003, 1, pp 1033-1050.
Figure 10 A, Diffuse thinning making the scalp more vis
the central part in a women with female-pattern hair loss.
ner caliber, miniaturized hairs with variations in diameternd length supports the diagnosis of AGA. The pull test isegative in AGA. Biopsy of the scalp is not needed routinelyut is helpful when the diagnosis is uncertain or if a dualiagnosis is suspected. Extensive hormonal evaluation is usu-lly not performed except when signs of virilization areresent.
elogen Effluviumelogen effluvium refers to the diffuse shedding of telogenair that occurs 2 to 3 months after a severe bodily stress. Thetressful event causes the premature and simultaneous shiftf a large number of follicles from the anagen to telogenhase.1 Telogen effluvium has been associated with high fe-er, childbirth, severe infections, major surgery, hyperthy-oidism, hypothyroidism, crash diets, and inadequate pro-ein intake; severe psychological stress also may be a factor.10
ategories of drugs that may cause telogen effluvium areisted in Table 5.11,12 Telogen effluvium is self-limited andeversible if the cause of the hair shedding is found andliminated. The shedding usually ceases within 6 months andreatment is unnecessary. Reassurance and an explanation ofhe process are generally sufficient.
istory. In telogen effluvium, acute and often dramatic haiross occurs. A thorough assessment includes a review of sys-
a woman with female-pattern hair loss. B, Widening of
able 5 Drugs Implicated in Causing Telogen Effluvium
ems, past medical history, exposure to medications, dietaryistory, recent illnesses, and a menstrual and reproductiveistory. In addition, a review of the family history for anyenetic predisposition to hair loss should be performed, asndrogenetic alopecia can often be unmasked by a telogenffluvium.
linical Findings and Diagnosis. Global examination mayeveal a “normal” hair density and good scalp coverage. Telo-en effluvium usually is not extensive enough to cause de-ectable thinning because loss of more than 50% of the scalpair must occur before alopecia is clinically apparent.1
arked shedding of hair is noted and a pull test during thective stage of the disease is positive. In cases of resolvingelogen effluvium, shorter, regrowing frontal hairs may bebserved. Examination of the central part widths, hair cali-er, and patterns of loss in other parts of the scalp is neededo rule out concomitant androgenetic alopecia or alopeciareata. Laboratory tests should be directed by the history andndertaken if a hormonal or nutritional deficiency cause isuspected. Thyroid disease and iron deficiency anemia arewo occult causes of hair loss in women and can be easilycreened for with serum ferritin and thyroid-stimulating hor-one tests.
lopecia areata (AA)/Totalis/UniversalisA is an unpredictable, usually patchy, nonscarring hair loss
hat affects 1.7% of the population.13 Any hair-bearing skinay be affected. AA occurs equally in men and women anday occur at any age, although there is an increased inci-ence in younger age groups.3 AA is hypothesized to be anrgan-specific autoimmune disease mediated by T-lympho-ytes directed against hair follicles.14 Genetic predispositionnd environmental factors may trigger the initiation of dis-ase.15 There is a high frequency of a family history of AA inffected persons, ranging from 10% to 42% of cases.16 AA haseen reported to be associated with classic autoimmune dis-rders (eg, thyroid diseases, vitiligo, diabetes, perniciousnemia, and atopy).15,17
Figure 11 A, Patchy alopecia areata with significant
Patients usually present with several episodes of hair loss F
nd hair regrowth during their lifetime. The course of theisease is irregular and unpredictable. Recovery from hair
oss may be complete, partial, or nonexistent. The incidencef the severe chronic form of AA is 7% to 10%.15 Indicators ofpoor prognosis are atopy, the presence of other immuneiseases, family history of AA, young age at onset, nail dys-rophy, extensive hair loss, and ophiasis.18
istory. Patients typically complain of acute onset hairhedding, or a newly recognized “bald spot” that may beecurrent. Patients usually are asymptomatic, although atimes a patient may have an odd sensation or discomfort in anrea of active or developing alopecia. A thorough historyetailing onset, duration, and location of hair loss, familyistory of alopecia, personal or family history of atopy orther autoimmune diseases, and general review of systemshould be performed.
linical Findings and Diagnosis. The physical examinationill reveal bare, round patches of hair loss with retained
ollicular markings; the underlying scalp may be normal in
th of hair. B, Ophiasis pattern of alopecia areata.
igure 12 Nail pitting of alopecia areata.
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18 A. Han and P. Mirmirani
ppearance or have a slight orange/salmon color. The pullest may be positive at the periphery of the alopecia, indicat-ng an active stage of disease. A frequent feature of AA patchesre “exclamation-mark” hairs that may be present at the mar-in. “Exclamation-mark ” hairs are broken, short hairs thataper proximally.
The clinical presentation of AA can be categorized accord-ng to the pattern or extent of hair loss. Investigational guide-ines published in 2004 describe 3 specific subcategories ofA: patchy alopecia areata; alopecia totalis, indicating total
oss of scalp hair; and alopecia universalis, referring to loss ofair over the entire scalp and body. The guidelines propose atandardized method for quantifying the amount of scalpair loss by calculating a Severity in Alopecia Tool (SALT)core. In addition, prognostic factors such as the duration ofair loss, loss of body hair, nail changes, and type of hair leftn the scalp also are assessed. Using all of the above factors,he clinician can better predict the efficacy of treatment.19,20
The most common presentation of AA is scattered roundr oval patches of hair loss (Fig. 11A). Hair loss also canresent in an ophiasis (band-like) pattern in the temporo-ccipital scalp (Fig. 11B) and in the frontoparietal scalp in asisaipho” pattern (opposite of ophiasis). Nail pitting, ob-erved in 10% to 66% of patients with AA, may be noted (Fig.2).21 A history suspicious for autoimmune disease shouldirect further laboratory testing. A scalp biopsy may be nec-ssary to distinguish questionable cases of AA from the otheroncicatricial forms of alopecia.
yphilitic Alopeciayphilis is a systemic disease caused by the spirochete Trepo-ema pallidum. If untreated, the disease progresses throughhree stages of infection. The alopecia of syphilis usually oc-urs in the secondary stage and can occur in as many as 48%f patients.22
istory. Individuals with syphilitic alopecia complain of audden onset, patchy, incomplete hair loss. As with the cu-aneous manifestations of lues, syphilitic alopecia may be aimic of the other nonscarring alopecias and should always
e considered in the differential.
linical Findings and Diagnosis. Syphilitic alopecia often isescribed as irregular, “moth-eaten” hair loss scatteredhroughout the scalp. It may resemble a diffuse and patchylopecia areata.23 The eyebrows, eyelashes, and beard maylso be lost. Diffuse hair shedding similar to telogen efflu-ium may also be present.24 The diagnosis is made by a highndex of suspicion confirmed by positive serology.
oose Anagen Hairoose anagen hairs can occur sporadically on normal scalps,s part of the loose anagen hair syndrome (with no associatedbnormalities), or in association with a syndrome with otherevelopmental defects (eg, Noonan’s syndrome, nail-patellayndrome, ectodermal dysplasias).25
Loose anagen hair syndrome is predominantly a disease ofhildhood and presents with anagen hairs on the scalp that
an be pulled out easily and painlessly. The disease can be c
poradic or familial.26 The condition is due to defective an-horing of the hair shaft to the follicle, which enables thenagen hairs to be separated from the inner root sheath andeleased from the follicle with minimal traction.27
Loose anagen hair syndrome typically is diagnosed inhildhood, usually in children younger than 2 years of age,ith the mean age of patients being 6 years.22 Adult casesave occasionally been described, mostly in parents of af-ected children.25 Although the hair density and hair lengthmprove with age, most patients with loose anagen hair syn-rome continue to show a small percentage of loose anagenairs on a pull test, indicating that the defect of hair shaftnchorage is still present, but to a lesser degree.
istory. The typical patient with loose anagen hair syn-rome is a child with slow-growing hair and diffuse or patchylopecia in areas of friction. Other observations include aecrease in the number of haircuts and sparse or fine hair.he history should also include a review of any developmen-
al abnormalities.
linical Findings and Diagnosis. The clinical manifesta-ions of the disorder are typically mild, and it is likely thatnly a small proportion of children with the conditioneek dermatological advice. Hairs in loose anagen syn-rome can be pulled easily and painlessly from the scalp.he diagnosis of loose anagen hair syndrome is based on
he microscopic evaluation of the hair, which shows aisshapen bulb and a ruffled cuticle on the proximal por-
ion of the hair (Fig. 13).
oncicatricial Alopecia With Hair Breakageinea capitisinea capitis is a fungal infection of the scalp hair follicles
igure 13 Loose anagen hair with loss of the inner root sheath, aisshapen bulb, and a ruffled cuticle.
aused by different species of the genera Microsporum and
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Clinical approach to the patient with alopecia 19
richophyton, with most cases in the United States beingaused by T. tonsurans. This dermatophyte disease is consid-red a public health problem, particularly in inner cities. Onetudy found a 13% prevalence of positive dermatophyte scalpultures in eight city schools.28 Tinea capitis is a disease ofhildhood, most often affecting children between ages 3 and.29 Surveys within the United States suggest that large familyize, crowded living conditions, and low socioeconomic sta-us may contribute to the increased incidence of tinea capi-is.30 Tinea capitis can be transmitted via infected persons,allen infected hairs, and select animal vectors. Spread ofinea capitis by fomites is also common. Humans may be-ome infected with zoophilic dermatophytes by direct con-act with family pets or with wild animals. Cats and dogs arehe major sources of M. canis.29
istory. Patients will often present with a complaint of acutenset hair breakage and loss in a localized area of the scalp. Aetailed history of exposure to anyone suspected of having aermatophyte infection is warranted. Additionally, question-
ng should focus on contacts with pets and the use of con-aminated hairbrushes, combs, or hats.
linical Findings and Diagnosis. The clinical appearance ofinea capitis varies with the species of dermatophyte involvednd with the degree of host resistance. The clinical presenta-ions may vary from a few patchy areas of broken hairs to ancute, severe, inflammatory process affecting a large area ofhe scalp.31 The key features are areas of patchy, partial haiross with broken hairs (appearing like “black dots” on thecalp) and scalp scaling. Diagnosis is made by (1) examina-ion of the hair with a Wood’s light, (2) microscopic exami-ation of a hair mount with 20% potassium hydroxide, and3) fungal culture of the scale and broken hairs. Prominentervical or occipital lymphadenopathy occurs in all types ofinea capitis and is an important clinical clue to the properiagnosis of the disease. Lymphadenopathy is seldom asso-
Figure 14 A, Trichotillomania. B, Trichotill
iated with other noninfectious causes of hair loss.29 Without e
denopathy, the diagnosis of tinea capitis should beuestioned.
tructural Hair Shaft Anomaliesertain structural hair shaft anomalies can present with anding of hair breakage. Conditions that exhibit increasedragility and lead to clinically apparent alopecia include tri-horrhexis nodosa, pili torti, monelithrix, trichothiodystro-hy, and bamboo hair. A detailed discussion of structuralair shaft anomalies leading to alopecia is present elsewhere
n this journal.
richotillomaniarichotillomania is a disorder in which a patient compul-ively pulls or breaks off his or her own hair. It is notedredominantly in girls and women and occurs more com-only in children than in adults.32 The prevalence of tricho-
illomania in the general population has not been studied.ne survey of 2500 college students reported the lifetimerevalence to be 0.6%.33
istory. Trichotillomania can present differently in chil-ren, adolescents, or adults. Patients may or may not ac-nowledge that they are pulling or picking at their hair.ther picking disorders (eg, skin picking, nail biting) often
ccompany the hair pulling behavior. A careful history eval-ating any underlying psychiatric abnormality or stress isarranted.
linical Findings and Diagnosis. Irregular patches of in-omplete hair loss are typical of this condition. The scalp ishe most frequent hair-pulling site, followed by the eye-rows, eyelashes, pubic area, trunk, and extremities. Thehapes of the alopecic patches are often bizarre and may bengulated (Fig. 14A). The hairs in the areas of hair loss areften short with a mixture of broken and tapered tips. Otherlues to the diagnosis of trichotillomania are changing pat-erns of hair loss from visit to visit, and the loss of the upper
a, loss of the upper eyelashes exclusively.
yelashes exclusively (as hair pulling from the lower eye-
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ashes can be very painful; Fig. 14B). Evidence of skin pickingr nail biting is often found. The evaluation is often difficult,nd a scalp biopsy may be helpful in reaching the correctiagnosis.
nagen Arrest/Anagen Effluviumhe diffuse hair breakage and loss that follow the use ofhemotherapeutic agents is termed anagen arrest or anagenffluvium. Chemotherapeutic medications cause a temporaryrrest of mitotic activity in the matrix region of anagen hair.he arrest results in constriction of the hair shaft and subse-uent hair breakage (Fig. 15).34 Approximately 80 to 90% ofair is affected. The alopecia occurs one to three weeks afterhe administration of a chemotherapeutic medication.1 Withubsequent treatments, all scalp hair typically is lost. Anagenrrest occurs with the use of many drugs including, but notimited to, those listed in Table 6.35 The hair follicle typicallyycles out of the anagen phase and remains in telogen phasentil a few months after the pharmacologic effects of theffending drug have ceased.
istory. Patients will complain of a large amount of hair lossccurring within a few weeks of receiving systemic chemo-herapy. A thorough drug history often makes the diagnosisbvious.
linical Findings and Diagnosis. Medications are capable ofroducing many patterns of alopecia; however, anagen arrestill affect almost the entire scalp. The hair loss is usually
onfined to the scalp, although other hair bearing areas maye involved. The scalp skin is usually unremarkable. If aistory of chemotherapeutic use is not found, a scalp biopsy
igure 15 Schematic of attenuation of the hair shaft due to chemo-herapeutic insult (anagen arrest).
nd screening for hormonal causes may be indicated.
icatricial Alopeciaicatricial alopecias represent a group of disorders character-
zed by the permanent and pathologic destruction of the hairollicle leading to irreversible hair loss. The hair follicle can beestroyed by a primary process aimed directly at the follicleprimary cicatricial alopecia) or due to a nonfollicular processsecondary cicatricial alopecia). The latter group may occurs a result of inflammatory/autoimmune diseases (ie, follicu-ar mucinosis, scleroderma/morphea), infection (bacterial,iral, or fungal), neoplastic processes (ie, primary and meta-tatic carcinoma; granulomas), and physical agents (ie, x-ays, burns).
The North American Hair Research Society (NAHRS) de-ised a preliminary working classification of the primary cic-tricial alopecias based on the predominant inflammatoryell present in the biopsy specimen. This classification wasevised to unify terminology and diagnostic categories.36 Theause and pathogenesis of many of these disorders is largelynknown. Although unique clinicopathologic features allowor accurate diagnosis in some cases, diagnostic certainty isften elusive and reflects the limits of present understand-ng.37
The epidemiology of primary cicatricial alopecias in theeneral population is unknown. The prevalence has beeneported to range from 3.2 to 7.3% in two retrospective stud-es.38,39 The most common causes of cicatricial alopecia in-lude chronic cutaneous lupus erythematosus, lichen plano-ilaris, and pseudopelade, but can vary depending oneographic location and referral pattern.40
istoryatients with cicatricial alopecia may present with acute on-et or ongoing hair loss and symptoms. Symptoms includeruritus, irritation, pain, erythema, and/or drainage from thecalp. A thorough history should be completed to evaluate forutoimmune disease, systemic illness, infections, neoplasms,ssociated inflammatory skin disease, and radiation treat-ent or burns.
linical Findings and Diagnosisn all forms of cicatricial alopecia, the diagnostic hallmark isisible loss of follicular ostia. Signs of scalp inflammationerythema, scaling, pustules, scalp bogginess and compoundollicles (polytrichia) are also commonly seen. Another char-cteristic finding in active areas of cicatricial alopecia is a
able 6 Common Antineoplastic Agents Causing Anagen Ar-est/Effluvium
ositive pull test with anagen bulbs seen on the hair mountFig. 5B).
hronic Cutaneous Lupus Erythematosus. Chronic cuta-eous lupus erythematosus is a common cause of scarringlopecia. Women are more commonly affected than mennd it is uncommon in children.41 Erythema, scale, andigmentary changes are more pronounced than in thether forms of scarring alopecia. Follicular plugging anddherent scale may be present. The “carpet tack” sign maye elicited with retraction of the scale, revealing keratoticpikes that correspond to follicular openings on thendersurface.42
ichen Planopilaris (LPP). LPP is more common in womennd presents with perifollicular erythema and acuminate ker-totic plugs at the margins of expanding areas of alopecia
Figure 16 A, Lichen planopilaris. Note the perifollicularprints in the snow.”
Figure 17 A, Frontal fibrosing alopecia. B, Ce
Fig. 16A).43 Fifty percent of patients with LPP lack evidencef lichen planus at sites other than the scalp.44
rontal Fibrosing Alopecia. Frontal fibrosing alopecia is aecently described variant of LPP that affects middle-agedo older women.46 This disease presents as a band-likeronto-temporal alopecia that progresses to involve theemporal-parietal scalp (Fig. 17A). None of the describedatients have had evidence of lichen planus elsewhere onheir body.47
seudopelade (as described by Brocq). Patients with pseu-opelade present with irregularly defined, white colored, co-lescing patches of alopecia with atrophy and loss of folliculararkings (Fig. 16B).45 Follicular hyperkeratosis and inflam-ation are usually not seen. This type of presentation has
een likened to “footprints in the snow.”
ma and scaling. B, Pseudopelade of Brocq with “foot-
erythe
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entral Centrifugal Cicatricial Alopecia. Central centrifu-al cicatricial alopecia is seen primarily in black women andas been referred to as “follicular degeneration syndrome” orhot comb alopecia.” This disorder starts at the crown anddvances to the parietal scalp without clinically evident scalpnflammation (Fig. 17B).
olliculitis Decalvans, Dissecting Cellulitis, and Tufted Fol-iculitis. These represent a group of scarring alopecias with auppurative phase. These diseases affect men and womenrom young adulthood to middle age. Clinically, any regionf the scalp may be involved. These disorders are character-zed by recurrent follicular pustules, patchy scarring alopeciaFig. 18A), tufted or compound follicles (Fig. 18B), and theresence of boggy plaques.48 A biopsy is warranted in allcarring alopecias to determine the predominant infiltrate, itsocation, and extent; this information can help guide thehysician’s choice of treatment.37
onclusionshe majority of common hair loss disorders can be readilyiagnosed in the outpatient setting. A systematic approachonsisting of a detailed history, meticulous physical exami-ation, and directed laboratory tests and scalp biopsy, willllow the clinician to make the correct diagnosis. Appropriateounseling and treatment can then be specifically directed athe etiology of hair loss.
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Figure 18 A, Dissecting c
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