Alopecia in Children: The Most Common Causes

Andrew V. Atton and Walter W. Tunnessen, Jr

Pediatrics in Review 1990;12;25
DOI: 10.1542/pir.12-1-25

The online version of this article, along with updated information and services, is located on
the World Wide Web at:
http://pedsinreview.aappublications.org/content/12/1/25

Pediatrics in Review is the official journal of the American Academy of Pediatrics. A monthly
publication, it has been published continuously since 1979. Pediatrics in Review is owned, published, and
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Alopecia in Children: The Most
Common Causes
Andrew V. Afton, MD,* and Walter W. Tunnessen, Jr, MDt

hair follicle unit, problems related to

The questions below should help hair loss can often be traced to
EDUCATIONAL OBJECTIVE
focus the reading of this article. changes within the follicle. Normal
1. What are the four most common
hair growth is cyclical. The phase of E. The pediatrician should be able
disorders causing alopecia in chil- active hair growth, termed anagen, to differentiate traumatic alopecla
dren? may last for several years. Approxi- from other causes of hair loss in
2. What are the clinical features of
mately 85% to 90% of scalp hair is in childhood (Recent Advances, 90/
telogen effluvium? the anagen phase. On completion of 91).
the anagen phase, the follicle enters
3. How should kenons be treated?
a transitional phase, termed catagen,
4. What tests are helpful in the di- which lasts from several days to
agnosis of tinea capitis? weeks. The catagen phase is fol-
5. What are characteristic findings lowed by the final resting phase,
in the loose anagen syndrome? termed telogen. Typically, the telogen
phase lasts between 2 and 3 months. cle, is caused by pathogenic fungi
Anagen and telogen hair can be dis-
known as dermatophytes. It is esti-
Hair loss (alopecia) in children often tinguished by examining the hair shaft mated that this infection is responsi-
provokes anxiety not only for the root. Anagen hairs have long in-
ble for up to one half of the hair loss
child and his or her parents but also dented roots covered by an intact
seen .in the pediatric population. Chil-
for the pediatrician, who must distin- inner and outer sheath, while telogen
dren between the ages of 5 and 15
guish the etiologic possibilities. The hairs have club-shaped roots without years seem to be most commonly
list of causes of alopecia in dermatol- a sheath (Fig 1). At any one time,
affected.
ogy texts is usually long and the dis- 10% to 1 5% of the scalp hair is in the
The key clinical features of tinea
cussions tedious, both of which may telogen phase. It is estimated that the
capitis are scaling of the scalp, patchy
compound the diagnostic dilemma. normal scalp contains approximately
loss of hair, and broken hairs. The
The pediatrician does not need to 100 000 hairs. If 10% of the hair is in
variety of clinical manifestations of
memorize the great majority of a resting phase, which lasts about this infection and the frequency of
causes of hair loss, most of which 1 00 days, one can expect to lose
“missed” diagnoses has prompted
are uncommon and esoteric. If the normally up to 100 hairs per day. It
the admonition: “Always think of tinea
cause of the hair loss is not evident should be noted that clinically appar- whenever there are changes in the
after careful examination and a pe- ent hair loss is recognized only when
scalp or the hair.”
rusal of the common causes outlined a person has lost 25% to 50% of his Two genera of fungi are responsi-
in this review, referral to a dermatol- or her hair, either locally or generally.
ble for most tinea infections: Micros-
ogist is indicated.
ponum (M!cnosporum audouinll and
Fortunately, in 90% to 95% of chil- TINEA CAPITIS
Micnosponum canis), and Tnichophy-
dren with alopecia, one of the follow-
Tinea capitis, an infection involving ton (Tnichophyton tonsunans and Tn!-
ing is the cause: tinea capitis, trauma The M!cnos-
the scalp, the hair, and the hair folli- chophyton v!olaceum).
(including trichotillomania and trac-
tion), alopecia areata, or telogen efflu-
vium. As is true for any medical prob-
lem, a careful history and physical TABLE 1. Clues to Differentiate Alopecia in Children
examination, supported by selected Diagnosis Hair Loss Scalp Special Features
laboratory tests, usually directs the
Alopecia Complete in at- Smooth, no scale Exclamation pnt
clinician to the correct diagnosis
areata fected areas hairs; easy
(Table 1). epllation at
A basic understanding of the hair margins
growth cycle is helpful in evaluating Telogen efflu- Diffuse thinning No scale Hair pluck shows
hair loss. Because hair actually rep- vium increased telo-
resents the nonliving product of the gen count
Tinea capitis Patchy; rarely Various changes: Positive KOH or
complete scale; indura- fungal culture
“Resident Department of Dermatology, The tion; broken
Johns Hopkins Univensity, School of Medicine, hairs
Baltimore, MD. Trichotillo- Incomplete No scale Hair of various
tAssociate Pnofesson of Pediatrics and Den- mania lengths in area
matology, The Johns Hopkins University,
of alopecia
School of Medicine, Baltimore, MD.

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Alopecia

and deposit a metabolic product,

pteridine, which imparts a yellow-
green fluorescence to infected hairs
upon examination under ultraviolet
(Wood) light.
During the past two decades, T
tonisunans infections have become
the leading cause of tinea capitis, ac-
counting for 90% to 95% of all cases.
Since T tonsunans is an endothrix
(within the hair shaft) infection, no
fluorescence is produced upon Wood
lamp examination, eliminating a use-
ful, rapid diagnostic clue to tinea in-
fections. Tnichophyton infections are
notable for the variety of their clinical Fig 4. This boggy mass is studded with
appearance. A diffuse scaling of the pustules and represents a kenion, a hypersen-
scalp without hair loss may suggest sitivity reaction to fungi.
seborrheic dermatitis. At times
patches of scaling may be more lo-
calized and may be associated with lesions should not be incised, but
hair loss. One of the more confusing they should be treated with oral gris-
forms is an irregular area of hair loss eofulvin and a tapering dose of pred-
Fig 1. Anagen (left) and telogen (night) hair with little to no scalp scale, which is nisone if the lesion is large.
roots. Note the long sheath covering the root
characterized by tiny black dots on The widespread prevalence of ti-
of the anagen hair. The telogen hair has a club-
shaped root without a sheath. the scalp surface (Fig 3). The dots nea capitis directs us to consider this
are actually remnants of broken hairs diagnosis in any child with hair loss
and suggest the name “black dot” or scaling of the scalp. A KOH ex-
tinea capitis. This manifestation may amination of affected hair and scale
be mistaken for alopecia areata. as well as a fungal culture should be
Occasionally, tinea capitis (primar- performed. A useful, inexpensive,
ily caused by T tonsunans and M and easily interpreted fungal culture
can!s) may engender an intense hy- media, Dermatophyte Test Media
persensitivity response known as a (DTM, Baker Cumrnins Pharmaceuti-
kerion. One or more boggy, inflarn- cals, Miami, FL) allows the practi-
matory masses are present on the tioner to perform cultures and to in-
scalp surface, usually accompanied terpret them in the office (Fig 5). Epi-
by hair loss. The surface of the lesion lated hair and scale are placed on the
may be studded with pustules, sug- media slant which contains a phenol
gesting an abscess (Fig 4). Cervical red indicator. In the presence of
lymphadenopathy is almost always pathogenic fungi, a distinctive color
present, and fever and leukocytosis change of the media from yellow to
may occur. Although superinfection red is noted within 2 weeks. The bet-
with bacteria may occur, the primary tIes can be kept at room temperature,
cause of a kerion is a hypersensitivity eliminating the need for an expensive
Fig 2. Tinea capitis caused by microsponum response to a dermatophyte. These incubator. Although the organism re-
species. Hair loss, scale, and lusterless hair sponsible for the infection is not iden-
are typical. tified, if questions arise the slant can
be sent to a mycology laboratory for
fungal identification.
ponum species were responsible for The treatment of tinea capitis re-
the widespread school epidemics of quires the use of oral griseofulvin,
tinea capitis in the 1940s. Boys ap- because topical antifungal agents are
pear to be more prone to develop this not effective on the scalp. Griseoful-
infection than girls. Hair is lost in ir- yin is a safe medication for all age
regular patches with a fine gray-white groups and does not require labora-
scale noted on the scalp (thus the tory testing for hematologic or liver
term “gray-patch ringworm”), and the toxicity before or during its use. Ke-
infected hair is usually lusterless (Fig Fig 3. ‘Black dot” tinea caused by Tnicho- toconazole, another antifungal agent,
2). Microsponum species infect the phyton tonsunans. The dots are remnants of offers no advantage over griseofulvin.
outside of the hair shaft (ectothrix) broken hairs. Little scale is found. For tinea capitis, at least 1 5 mg/k/d

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 DERMATOLOGY

with gentle traction, another clue to sociation with other autoimmune dis-
the diagnosis. eases, supports this hypothesis.
The child with alopecia areata is The course of alopecia areata is
asymptomatic. The hair-bearing skin unpredictable. A chronic, relapsing
is smooth and generally shows no pattern is common, with regrowth of
signs of irritation or inflammation. hair in one area and loss in another.
Scaling is absent, and hair loss within About one third of affected children
the area of alopecia is usually corn- regrow their hair in 6 months. Another
plete. Other patterns of alopecia third regrow their hair in 5 years, and
areata include a diffuse type in which the remainder never have complete
hair loss of greater than 20% occurs hair regrowth. Less than 5% of chil-
more evenly over the scalp, without dren with the discoid (patchy) variety
the formation of well-defined patches. progress to alopecia universalis.
This pattern may sometimes be diffi- When regrowth occurs, it often takes
cult to distinguish from telogen efflu- the form of fine, poorly pigmented
Fig 5. Dermatophyte Test Media, a conven- vium or trichotillomania. Ophiasis re- vellus hair. If improvement continues,
ient office culture media for dermatophytes. fers to a pattern with a peculiar pre- the fine hair is eventually replaced by
The positive cultures have turned from gold to normal terminal hair.
dilection for the occipital and
red.
temporal-parietal regions of the Thiers has enumerated the follow-
scalp. It is important because of its ing conclusions about alopecia areata
of microsize griseofulvin must be poor prognosis for hair regrowth. Fi- based on a large number of reports
nally, the most severe expression of in the literature2: 1 ) the frequency of
given (usually as a single dose) with
food to enhance absorption. Six to the disorder is seen in the totalis and alopecia totalis is higher in children
universalis variants. These forms are than in adults; 2) there is an associ-
eight weeks of therapy should be pre-
characterized by total loss of hair on ation between severe alopecia areata
scribed, and family members should
be checked to make sure no one else the scalp or the entire body. and atopy; 3) extensive alopecia
is harboring the fungal infection. Re- A number of nail changes may aid areata of early onset carries a poor
in the diagnosis of alopecia areata. prognosis; 4) complete regrowth is
cent evidence suggests that concom-
itant use of selenium sulfide 2.5% About 25% of affected individuals unlikely in patients who develop alo-
lotion used as a shampoo two to have nail pitting or ridging. Alopecia pecia totalis or alopecia universalis
three times per week will decrease areata has been noted to occur in before puberty; 5) occurrence of re-
spore viability. The use of this adjunct association with other disorders such growth is inversely proportional to the
to therapy will reduce the period of as diabetes mellitus, Hashimoto thy- duration of disease; 6) girls have a
contagion, allowing the child to return
roiditis, vitiligo, Addison disease, per- better prognosis than boys; and 7)
early to school. After starting griseo- nicious anemia, and inflammatory limited, nonprogressive alopecia has
fulvin, we generally keep children out bowel disease. These associations a good prognosis.
of school for 2 to 3 days, during which have led to the suggestion to obtain The treatment of alopecia areata
two selenium sulfide shampoos are autoimmune antibodies, particularly should begin with an open discussion
to the thyroid gland, and thyroid func- with the child and his parents of what
given.
tion studies on all patients with this is known and unknown about this
disorder. Almost 25% of patients with disorder. The findings that point to a
alopecia areata in one study had ab- favorable or an unfavorable prog-
ALOPECIA AREATA
normal thyroid function tests.1 How- nosis need to be noted. A long list of
Alopecia areata represents the ever, a careful history, physical ex- therapeutic interventions has been
second most common cause of hair amination, and attention to growth used in the treatment of this disorder.
loss seen in children. Although chil- usually makes the added expense of Unfortunately, the presence of a long
dren of any age may be affected, theses examinations unnecessary. list means that there is no single ideal
onset at less than 2 years of age is Even if autoimmune antibodies are
unusual. Several patterns of hair loss found, they rarely are of clinical sig-
are seen. Onset may be insidious nificance.
with round or oval, sharply defined The causes of alopecia areata are
patches of alopecia that gradually co- unknown. Years ago, stress and psy-
alesce and enlarge by peripheral ex- chiatric disorders were felt to be the
tension (Fig 6). At the borders of the operative factors. Today, an autoim-
patch, hairs with a thin waist just mune phenomenon is thought to be
above the scalp may be found. Their primarily responsible for this condi-
tapered shape has led to the term tion. On histologic examination of a
“exclamation point” hairs that are felt scalp biopsy, the hair follicle bulbs in
to be characteristic of this disorder. areas of alopecia are found to be Fig 6. Patches of alopecia areata are almost
Hair at the periphery of the patches surrounded by an intense lympho- completely devoid of hair with a smooth scalp
of alopecia often can be removed cytic infiltrate. This finding, plus as- surface.

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Alopecia

or efficacious treatment. Indeed, der- the self-induced nature of the alope-

matologists vary in their recommen- cia.
dations from no therapy to extensive The precipitating events which trig-
and invasive ones. Although cortico- ger tnichotillomania are varied and in-
steroids offer the best chance for hair dude difficulties at home such as ill-
regrowth, the use of systemic ste- ness or moves, school-related prob-
roids should be discouraged because lems, and sometimes hospitalization
of the systemic side effects and the or other medical intervention. True
prompt loss of hair when they are psychiatric illness as a cause of tn-
discontinued. Intralesional cortico- chotillomania is rare. The classifica-
steroids often stimulate hair regrowth tion of tnichotillomania as a disturb-
in areas injected, but the hair re- ance of impulse control has come
growth is often not permanent. The under recent scrutiny based on the
use of injections in young children has significant improvement in symptoms
important psychological implications in patients treated with clomipramine.
and may not be worth the temporary This serotoninergic medication has
beneficial effect. Topical, high-po- unique and specific effects on nitualis-
tency corticosteroids are worth a Fig 7. An unusual patterned hair loss in tn-
tic behavior seen in obsessive-corn-
trial; however, one must be cautious chotillomania. pulsive disorders independent of its
not to continue therapy indefinitely antidepressant effect.
because local and systemic side ef- It is insufficient to assume that the
fects may result. acteristic and diagnostic clue is the disorder will resolve on its own, al-
More specialized treatments, such presence of hairs of different lengths though this may happen. Often, a
as contact sensitization with chemi- in the area of loss, reflecting regrowth frank and sincere discussion of the
cals, tars, and phototherapy, are best of hair pulled out or broken off at problem with both the parents and
left to a dermatologist. Localized various times. Primary lesions of tn- the child will help to hasten resolution
areas of alopecia areata of short du- chotillomania tend to involve fronto- of the symptoms. In severe cases,
ration often resolve spontaneously; temporal or panietotemporal regions psychologic or psychiatric consulta-
thus, not every case demands treat- of the scalp, particularly those oppo- tion may be indicated. Successful
ment. Children with extensive hair site the child’s handedness. Occipital therapeutic approaches have in-
loss may suffer embarrassment at areas are more likely to be involved cluded medications, behavioral mod-
school and may benefit from a well- in younger patients. It is notable that ification, and hypnosis. It is important
fitting wig. All families should be given the periphery of the scalp is usually to explain to the child and the parents
the name and address of the National spared. that, following discontinuation of the
Alopecia Areata Foundation (71 4 C In addition to the suggestive pres- pulling, negnowth of hair may be de-
Street, San Rafael, CA 94901) and of ence of hair of varying length in the layed and the loss may actually in-
local groups if available. Such orga- areas of alopecia, evidence support- crease due to a telogen effluvium ef-
nizations can aid significantly in cop- ing the diagnosis may be found by fect.
ing with this distressing disorder. examining the hair shaft bulbs of hair
found in the home, if available. In the TELOGEN EFFLUVIUM
case of tnichotillomania, many anagen
hairs will be found, rather than the This form of hair loss results from
TRICHOTILLOMANIA
expected telogen hair of physiologic the abrupt premature cessation of the
Trichotillomania, a term originally hair loss. Broken hair shafts may also normal growth, or anagen, phase in
coined by the French dermatologist be noted. If parental doubt persists, certain normal hair bulbs. The hair
Hallopeau, refers to a compulsion to a scalp biopsy may help to persuade follicle converts to the catagen phase
pull out one’s hair. Epidemiologic the parents. Although the changes on and, after a few weeks, enters the
studies of the incidence and preva- biopsy are not pathognomonic, find- telogen phase. Two to three months
lence of this disorder are lacking. It ings such as empty and disfigured later, the affected hair is shed as the
appears to be more frequent in fe- hair follicles on hemorrhage can new anagen phase begins.
male adolescents, although all age strongly support the clinical suspi- This type of hair loss is usually
groups and both sexes may be af- cion. noted initially by the patient or parent,
fected. The scalp hair is the principal Tnichotillomania is often seen in the because 25% to 50% of scalp hair
site involved in pulling, although eye- context of other compulsive disor- must be lost before alopecia is noted
brow, eyelash (25% to 30%), and ders such as thumb-sucking, nail-bit- clinically. The hair shed is undamaged
pubic (5%) hair may be involved. ing, and nose-picking. Acceptance of and demonstrates normal telogen
The hair loss may occur in ill-de- this diagnosis by the family and child hair bulbs. If a hair pluck is done,
fined and patchy or unnatural, pat- can be particularly difficult and is pulling 10 to 15 hairs forcibly from
terned, and sharply defined areas (Fig made more problematic by the ada- one area with a hemostat, the normal
7). The scalp is not scarred, and the mant denial and rationalization of the telogen to anagen ratio of hairs is
hair loss is never complete. A char- parents. The child rarely admits to increased greatly.

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 DERMATOLOGY

fined to wheelchairs with head sup-

TABLE 2. Events Associated ports rub their hair off in the contact
With Telogen Effluvium areas. Frictional hair loss does not
usually result in complete areas of
Childbirth
alopecia. Areas of trauma to the scalp
Convulsions
resulting in scars and destruction of
Crash diets (rapid weight loss)
Drugs: valproic acid; hypervita- hair follicles will also result in hair loss.
minosis A; heparin; coumadin; Androgen!c Alopecia. Male pattern
propranolol baldness is the most common cause
General anesthesia of hair loss in the general population,
High fever but it is an uncommon primary corn-
Hyperthyroidism plaint made to pediatricians. The on-
Hypothyroidism set is gradual, with thinning noted in
Oral contraceptives the frontal or vertex areas of the
Severe emotional stress scalp. There is usually a family history
Fig 8. Sebonrheic dermatitis. This infant dem-
Surgery onstrates significant hair loss and hypopigmen-
of early hair loss. Occasionally, tation.
women face a similar androgen sen-
sitivity of the hair follicles, but usually
Events precipitating the conversion not until the third or fourth decades. Psoniasis of the scalp is characterized
of anagen to telogen hair are shown Minoxidil topical therapy has been of
in Table 2. The number of hair follicles
by plaques of scale with distinct bor-
some help in selected cases of andro- dens set on an erythematous base.
affected and the resulting diffuse al- genic alopecia. Psoriatic plaques are almost always
opecia is dependent upon the sever- Anagen Effluvium. This disorder re- present on the body, and nail
ity and duration of the inciting stress. suIts from a toxic disruption to normal
The shedding actually marks the end changes (especially pitting) are fre-
hair growth, leading to diffuse hair
of this disorder rather than the begin- quently present.
loss in a few weeks. The most corn-
ning. The child and his parents can mon cause today is iatrogenic, the
be reassured that complete hair re- result of chemotherapeutic agents
growth is the rule, generally occurring Congenital Localized Alopecia
such as vincnistine, cyclophospha-
within 6 months. mide, and similar drugs. Thallium, A few congenital disorders associ-
lead, and arsenic may also interrupt ated with localized alopecia are wor-
LESS COMMON CAUSES OF HAIR hair growth, as can hypothyroidism. thy of mention because of their rela-
LOSS Severe malnutrition as a cause is tively frequent occurrence.
The four disorders discussed rarely seen in this country. Cutis Aplasia. The typical lesion is
a small punched-out area, one to a
above comprise 90% to 95% of the
few centimeters in width, on the yen-
cases of alopecia seen by the practic- Skin Disorders Which May Be
ing pediatrician. There is an assort- tex of the scalp, which is present at
Associated With Alopecia
birth. The lesion heals with scar tis-
ment of less common causes, some
of which deserve mention.
Sebonnheic Dermatitis. Seborrheic sue and never develops hair. It may
dermatitis is unusual in children be- also appear at birth as an atrophic
Acquired Causes
tween 1 year of age and puberty. patch of skin devoid of hair. Although
Infants frequently develop seborrheic this lesion is a common tnisomy 13
Tnaumatic. In addition to tnichotil- dermatitis, or cradle cap, partially as chnomosomal abnormality, it is asso-
lomania, other causes of trauma-in- a result of the stimulation of the se- ciated rarely with underlying difficul-
duced hair loss include traction and baceous glands by maternal andro- ties in the great majority of children.
frictional forms of alopecia. Traction gens. The scalp has a greasy scali- Nevus Sebaceus. This lesion is
alopecia most commonly results from ness to it, frequently with thinning of characterized by the presence, at
tension placed on hair shafts by re- the hair (Fig 8). The eyebrows and birth, of a well-circumscribed, fiat or
petitive hair styling, such as braiding postaunicular areas are usually in- slightly elevated, hairless, yellow to
and pony tails. The loss is usually volved as well. orange plaque with a leathery feel to
insidious and occurs along the part Atopic Denmatitis. Eczema is a the surface. The lesion is static until
lines or involves the hair under most common cause of itchy, scaly scalp. puberty when the surface becomes
stress. The scalp is unaffected. The hair loss associated with atopic verrucous. Approximately 5% to 10%
Frictional alopecia may be volun- dermatitis is usually traumatic, result- of these lesions develop cutaneous
tary or involuntary. The most easily ing from scratching. The scale is fine malignancies later in life. It is recom-
recognizable form occurs in infants and dry, although secondary pyod- mended that they be removed at or
who lay for long periods of time on ermas are common. shortly after puberty.
their backs and rub the hair off of Psoniasis. The hair loss associated Other Nevi. Occasionally, hair may
their occiput. This finding may indi- with psoniasis is usually the result of fail to grow oven other nevi, including
cate a lack of stimulation by care traumatic removal of hair because of hemangiomas, lymphangiomas, and
givers. Occasionally, children con- the thick, adherent, silvery scale. epidenmal and rnelanocytic nevi. In-

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Alopecia

spection of the surface of the scalp mania. Careful examination of the D. Trichotillomania.
or palpation of it may give the nec- scalp, hair, and historical pattern of E. Telogen effluvium.
essary clues to the correct diagnosis. the loss will usually be rewarded by 10. A 7-year-old epileptic boy on valproic
the correct diagnosis. acid develops diffuse thinning of his hair.
His scalp appears normal, but plucked hairs
LOOSE ANAGEN SYNDROME show an increased telogen count. The most
likely diagnosis is:
This syndrome is included in the REFERENCES A. Telogen effluvium.
discussion of disorders with alopecia B. Alopecia areata.
for two reasons: (1 ) it was only de- 1. Milgraum SS, Mitchell AJ, Bacon GE, et C. Tinea capitis.
al. Alopecia areata, endocrine function,
scribed recently, and (2) it may be and autoantibodies in patients 1 6 years of
D. Trichotillomania.
much more common than recognized E. Loose anagen syndrome.
age or younger. J Am Acad Dermatol.
previously. Prominent areas of alo- 1987;l 7:57-61 1 1. Each of the following is a true statement
pecia do not seem to be a character- 2. Thiers BH. In: Esterly NB, ed. Alopecia
about kerions except:
Areata Symposium. Pediatn Dermatol.
istic feature, although areas of A. They are caused by a hypersensitivity
1987:4:137-158
marked scalp hair loss may be pres- reaction to a dermatophyte.
ent. The primary complaint concerns B. They form a boggy, inflammatory mass
easy pulling out of hair without pain. on the scalp.
The disorder is most commonly de- C. They are associated with cervical lymph-
SUGGESTED READING
adenopathy.
scnibed in children, particularly blonde
Datloff J, Esterly NB. A system for sorting out 0. Their presence indicates a need for mci-
girls. On inspection of the hair that is
pediatric alopecia. Contemp Pediatr. sion and drainage.
easily epilated, the bulbs appear to 1986;3:53-72 E. The recommended therapy is oral gnse-
be anagen in nature, although they Guzzo C, Rabinowitz LG, Honig PJ. A head- ofulvin.
are commonly misshapened and lack to-toe guide to common fungal infections.
an outer root sheath. Parents may Contemp Pediatr. 1 986;3:53-78 12. An 11-year-old girl has scaling of her
Oranji AP, Peereboom-Wynia JDR, De Raey- scalp, patchy hair loss, and broken hairs. A
note that their children’s hair does maecker DMJ. Trichotillomania in childhood. fungal infection is suggested by a KOH
not grow or grows very slowly, and J Am Acad Dermatol. 1986;15:614-619 mount, but examination with Wood light
almost never requires cutting. The Price VH, Gunmer CL. Loose anagen syn-
shows no fluorescence. The most likely di-
cause of this disorder is not known. drome. J Am Acad Dermatol. 1 989;20:249-
agnosis is:
256
Although no treatment is available, A. Tinea capitis.
Rasmussen JE. Hair loss in children. Pediatn
the parents can be comforted to Rev. 1981 3:85-90 B. Trichotillomania.
know that the appearance of the hair Stroud JD. Hair loss in children. Pediatr Clin N C. Traumatic alopecia.
improves with time. Am. 1983;30:641 -658 D. Telogen effluvium.
E. Alopecia areata.

13. Typical findings in the loose anagen

SUMMARY syndrome include each of the following ex-
Self-Evaluation Quiz
cept:
The differential diagnosis of alope-
9. The four disorders responsible for 90% A. Hair pulls out easily.
cia in the pediatric age group is sim-
to 95% of alopecia in children include each B. Epilation is not painful.
plified by the fact that 90% to 95% of the following except: C. No prominent areas of alopecia are found.
of the cases are caused by four major A. Tinea capitis. 0. Hair does not grow or grows slowly.
entities: alopecia areata, telogen ef- B. Alopecia areata. E. The appearance of the hair worsens with
fluvium, tinea capitis, and trichotillo- C. Seborrheic dermatitis. time without treatment.

DEPARTMENT OF CORRECTIONS

In the article
on “Hemangiomas and Spitz Nevi” published in the March
1990 issue of Ped!atn!cs !n Rev!ew, the authors’ titles were reversed. Dr
Rasmussen is a Professor of Dermatology and Pediatrics in the Department
of Dermatology at The University of Michigan-Ann Arbor, and Dr Hartley is a
private practitioner.

PIR 30 pediatrics in review #{149} vol. 12 no. 1 july 1990

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 Alopecia in Children: The Most Common Causes
Andrew V. Atton and Walter W. Tunnessen, Jr
Pediatrics in Review 1990;12;25
DOI: 10.1542/pir.12-1-25

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