Review Alopecia areata: emerging concepts 
Alnpecia areata: emergjng concepts 
A.J. Papadopoulos, R.A. Schwartz and C. Krysicka Janniger 
ABSTRACT 
Alopecia areata is a common, unpredictable, non-scarring form of hair loss. This disorder affects ali age 
groups, with a higher prevalence in children and adolescents. Limited scalp involvement is the most 
common presentation but more severe forms of the disorder, involving the entire scalp or body, also 
exist. Research has linked alopecia areata with certain HLA-Class II alleles, implicating an autoimmune 
etiology. Various therapeutic modalities have been employed to gain clinically acceptable hair regrowth. 
Alopecia areata is a common clisorcler, hypothesizecl 
to be autoimnrnne in etiology, ancl estimatecl to affect 
almost 2% of the US population (1). This 11011-scarring 
alopecia affects both sexes equally and is seen in ali 
age groups. A higher incidence is founcl in chilclren ancl 
young aclults, with common presentation before the age 
of five years (2-4). The unpreclictable severity and course 
of the clisorcler exacts a high emotional cost from the 
affected patient ancl may result in psychiatric comor-
biclity (5). 
Etiology 
The etiology of alopecia areata is as of yet unclear, 
but is presumed to be clue to an autoimmune reaction. 
Consistent evidence of autoantiboclies directed against 
anagen stage hair follicle structures are found in both 
affected humans ancl in mouse models (6,7). Though 
autoantiboclies are postulatecl to play an integral role in 
the clisease process, current research implicates a cell-
mecliatecl autoimmune mechanism as the tmderlying 
pathogenic etiology (S). Supporting this theo1y is that 
activatecl CD4 ancl CDS T lymphocytes have been founcl 
in a characteristic peri- ancl intrafollicular inflammat01y 
infiltrate of anagen hair follicles of affected inclivicluals 
(9-11). The transfer of alopecia areata by T lymphocytes 
cultivatecl from affectecl scalp ancl transferrecl to human 
scalp explants on a severe combinecl immunocleficiency 
mouse model has been demonstratecl (12). Recent 
investigations on mouse models reported that trans-
plantecJ alopecia areata tissue to normal mice woulcl 
not induce alopecia areata if a specific monoclonal anti-
body, anti-CD44v10, was injected into the mice shortly 
after transplant surge1y (8). CD44v10 is believed to be 
involvecl in the activation mechanism of CD4 ancl CDS 
lymphocyte migration into tissue and the initiation of 
the subsequent defense response against antigenic 
stimuli (8). Similar research has demonstrated that in-
Acta Dermatoven APA Vol 9, 2000, No 3 83 
Alopecia areata: emerging concepts 
vivo depletion of CD4+ cells using CD4+ cell-clepleting 
OX-35/OX-38 monoclonal antibocly (MoAb) partially 
restores hair growth in rats affected with alopecia areata 
(11). Cmrent investigative efforts strongly implicate CD4 
and CD8 T-cell lymphocytes in the pathogenic auto-
immune etiology of this clisorcler. 
Alopecia areata, similar to many other autoimnmne 
cliseases, is linkecl with certain HLA-Class II alleles. The 
I-ILA antigen DQ3 (DQB1 *03) has been identifiecl as a 
general susceptibility marker for alopecia areata (13-
15). Patients with the more severe forms of the disorcler, 
alopecia totalis and alopecia universalis, were found to 
express the HLA alleles DQB1 *0301, DRB1 *0401 and 
DRB1 *1104 in a significantly higher frequency (8). Mil-
cler, patchy forms of alopecia areata were also founcl to 
be associatecl with a significantly higher frequency of 
DRB1*1104, but no association was reported with the 
other two aforementionecl alleles (8). 
Clinical description 
Alopecia areata usually appears abruptly asa patch 
of clearing on the scalp with no evidence of scarring. 
Scalp involvement is the most clinically distinguishing 
characteristic, but axillae, eyebrows ancl eyelashes may 
also be involvecl (16). Milcl, limitecl involvement of the 
scalp is the most common presentation; multiple patches 
may become confluent over tirne. Regression may occur, 
with new hair growth taking place; recurrences in diffe-
rent locations occur unpredictably. Severe involvement 
may produce a loss of all scalp hair (alopecia totalis) or 
ali hair on the body (alopecia universalis). Patients with 
alopecia areata that have a hist01y of atopy may have a 
less favorable prognosis (17). 
Clinical variants of alopecia areata exist (16). Ophi-
asis alopecia areata describes band-like hair loss 
affecting the tempo ral and occipital regions of the scalp. 
Reticular alopecia areata describes a type that clinically 
shows patches of hair loss in various stages of clisease 
activity. Diffuse alopecia areata has been attributecl to a 
short anagen phase ancl subsequent inability of hair to 
grow. Alopecia areata has also been linked with a 
number of autoimmune cliseases (18). 
Alopecia areata produces nail changes in 3-30% of 
affectecl patients (3, 18-20). In one stucly of 201 affectecl 
chilclren uncler 16 years nail changes were clinically 
eviclent in 60 (3). Of these 60 children, nail changes 
were more common in severely affected children (18 
out of 34) than in chilclren with localizecl clisease (42 
out of 167). In another stucly, 21 patients hacl clinical 
evidence of nail changes out of a total of 136 patients 
(103 adults, 33 chilclren) affectecl with alopecia areata. 
Nail changes were founcl to be more common in chil-
84 
dren, especially in chilclren with severe , long-standing 
disease (19). The nail changes associatecl w ith alopecia 
areata usually accompany hair loss , but may occa-
sionally precede or follow the onset of hair loss by 
months oryears (16). The main patterns of nail changes 
are: diffuse fine pitting (most common), thin and brittle 
fingernails ancl toenails, longitudinal ridging and rough 
smface trachyonychia (3,20-22). 
Systemic associations 
Atopy, vitiligo ancl autoimnmne thyroid clisease, 
namely Hashimoto's thyroiclitis ancJ Graves' clisease, are 
more prevalent in patients with alopecia areata (23)' 
Serum thyrotropin measurement has been recommen-
ded for ali children with this clisorcler. (23) Although 
cbildren are frequently screenec\ for thyroicl disease, the 
presence of clisease in these patients is only 10% (3). A 
recent stucly on the evaluation of thyroid function in 
northern Indian patients with alopecia areata revealed 
that thyroicJ disease was clinically evicJent in only 16 
(0.85%) ofthe 1700 affectecl patients evaluated over the 
interval of 1983-1997 (24). The incidence of thyroicl 
structmal and functional abnormalities is much higher 
in affectecl patients (78 percent) than in controls (33 
percent) (21). One study of45 affected children, 16 years 
of age ancl younger, reportecl thyroicl function abnorma-
lities in 24 percent of these children (25). Thyroicl 
function abnormalities include abnormal thyroid hor-
mone (T3,T4) and thyroicl stimulating hormone (TSH) 
values and the presence of antithyroicl ancl antimicro-
somal antiboclies (25). Celiac clisease, systemic lupus 
e1ythematosus and diabetes mellitus may also possibly 
be increasecl in incidence in patients with alopecia areata 
(2,3,26-29). 
Differential diagnosis 
Mik! forms of alopecia areata are seen as solita1y 
areas of non-scarring hair loss on the scalp ancl should 
be clistinguishecl from trichotillomania ancl tinea capitis. 
Other forms of non-scarring alopecia, including trau-
matic alopecia and congenital hair loss synclrornes such 
as congenital triangular alopecia, must also be consi-
derecJ in the differential diagnosis (30-33). Alopecia 
neoplastica, a rare form of alopecia, is associated most 
commonly with breast cancer; it may resemble localized 
alopecia areata (34,35). Systemic lupus e1ythematosus, 
syphilis ancl post-febrile alopecia may also at times 
resemble alopecia areata (16). 
Alopecia areata may be first eviclent in young pati-
ents as the sudclen onset of c!ifti.1se alopecia (16,17). 
Telogen efl1uvium, believed to be associated with high 
Review 
Acta Dermatoven APA Vol 9, 2000, No 3 
Review 
i'ever, severe ernotional stress, sudden starvation ancl 
certain rnedications, rnust also be considerec.l in the cliffe-
rential diagnosis of cliffuse alopecia. Other conclitions 
associated with diffuse alopecia inclucle acroclerrnatitis 
enteropathica, arsenicisrn and thallium p oisoning, 
though these conclitions usually have systemic symp-
torns (16). Recent research has identified the human 
hairless gene, equivalent to a gene stuclied in mouse 
rnodels (hairless IRS/3 mouse), ancl has confirmed its 
association with a disease called atrichia or atrichia with 
papules (8,36). This conclition was previously named 
alopecia universalis congenita. These patients are bom 
with hair, but the hair matri:x cells progressively undergo 
apoptosis by the third month, culrninating in permanent 
hair loss (8,36). 
A skin biopsy specimen is c.liagnostic of alopecia 
areata, and is sometimes necessa1y to make a cliagnosis 
(37,38). On histological examination a peribulbar 
lymphocytic infiltrate resembles a "swann ofbees." (39). 
Scarring is characteristically absent. 
Treatment 
Treatment of alopecia areata rnay be clivicled into 
four clifferent categories of widely acceptecl therapeutic 
modalities (9,18,23,40-55): immune inhibitors such as 
s teroids or psoralen and UV-A light (PUVA); topical 
sensitizers such as squaric acicl dibutylester (SADBE) 
ancl cliphenylcyclopropenone (DPCP); non-specific 
irritants (anthralin) ancl the vasodilator minoxidil. Treat-
ment goals are hair regrowth that is cosmetica lly 
acceptable to the patient; hair loss is not preventecl with 
these treatments (23,53,56) . 
Miki forms of alopecia areata are mostly treatecl by 
intralesional injection of a glucocorticoid, usually 
triamcinolone, eve1y four to si:x w eeks (16,23). Steroid 
injection may procluce minimal transient atrophy or, less 
commonly, severe atrophy of the targetecl skin; the most 
common side effect of steroid injection is pain, which 
is a complicating factor in treatment of chilclren (53). 
Topical steroid application to areas of hair loss, usually 
appliecl twice daily, has also been found to be effica-
cious clinically, although combination treatment w ith 
minoxiclil, anthralin or injectec\ steroids is probably more 
tberapeutic (23,53,57). Systemic steroicls are reservecl 
for use in rapiclly progressive or extensive alopecia 
areata (53). 
Anthralin, the only non-specific irritant wiclely used 
for hair growth in alopecia areata, is applied topically 
as a O .5 or 1 o/o cream to affectecl areas once per da y for 
20-45 rninutes ; overnight application can also be used 
in certain patients who can tolerate the side effects 
(23,53). Application oftopical anthralin may cause pru-
Acta Dermatoven APA Vol 9, 2000, No 3 
Alopecia areata: emerging concepts 
ritus, e1ythema, scaling and folliculitis, necessitating the 
short application tirne (53). The combination therapy 
of anthralin and minoxidil has also shown favorable 
results in a group oftreatrnent-resistant patients (58,59). 
Minoxidil (5% topica l solution) is applied twice daily 
to areas ofhair loss. Side effects are limited to miki local 
irritation and, less frequently, allergic contact dermatitis 
(60-62). Topical sensitizers incluce an allergic contact 
dermatitis in appliecl areas of hair loss; weekly re-
stimulation with the patent allergen is neecled. Topical 
sensitizers have proven efficacy in patients with long-
standing alopecia areata involving more than 50 percent 
of the scalp (23,57,63) . Squaric acicl dibutyles ter 
(SADBE) has shown good tolerability and miki side 
effects. In one stucly of 144 patients with va1y ing degrees 
of alopecia areata, an 80% rate of regrowth was demon-
strated in patients with mile! alopecia areata ancl a 49% 
rate of regrowth was clemonstratecl in more severely 
affectecl p atients (52). A study of squaric acid clibutyl-
ester in a pediatric population of twenty-eight chilclren 
under the age of 13 w ith severe, long-standing, refra-
cto1y alopecia areata reported nine patients achieving 
cosmetically acceptable or complete regrow th, ancl si:x 
patients achieving significant regrowth (64). Diphenyl-
cyclopropenone (DPCP) is also an accepted modality 
for treatment of severe alopecia areata. One study 
demonstrated a 70% response rate in DPCP-treated 
patients with severe alopecia areata affecting more than 
40% of the scalp (65). Of these patients, 30.9% clemon-
strated complete remission, w hile 39. 7% unde1went par-
tial remission (65). Pruritus , dermatitis, urticaria, face 
and scalp edema and the clevelopment of vitiligo are 
known side effects of DPCP use (66). 
Cyclosporine is a potent immunomuclulatory agent 
whose mechanism involves inhibition ofT4 lymphocyte 
activation (67). A known side effect of cyclosporine is 
hypertrichosis, which bas been attributecl to p rolon-
gation of the anagen phase of hair grow th (68). In one 
stucly of 15 alopecia areata pati en t..'> treatecl with systemic 
cyclosporine, seven patients obtainecl cosmetica lly 
acceptable hair regrowth (67). Teshima et al describe a 
24 week regimen containing cyclosporine (2.5 mg/kg 
daily) and prednisolone (5mg/day) which p roduced a 
100% response rate in six patients with persistence of 
hair regrowth si:x months after cyclosporine was c.liscon-
tinued (69,70). A similar study combining cyclosporine 
w ith preclnisone reportecl two out of eight patients 
developing cosmetically acceptable hair regrowth (71). 
Gupta et al report cosmetically acceptable hair regrowth 
in three of si:x patients treated w ith 6 mg/kg cyclosporine 
daily for 12 weeks; hair loss occurred in ali patients 
within 3 months of discontinuation of cyclosporine (72). 
Larger stuclies need to be performed to determine the 
efficacy of systemcic cyclosporine in the treatment of 
alopecia areata . The significant sicle-effect profile of 
8J 
Alopecia areara: emerging concepls 
cyclosporine deters long-term treatment(73). Acknowledgment: 
C1yotherapy bas also been employed to stimulate 
hair growth in alopecia areata (49,50). One study, 
utilizing both children and adults, revealed hair re-
growth in greater than 60% of affected areas in 70 of 72 
patients (49). 
\'v'e c\ec\icate this work to Professor Jonas Lelis, 
Professor and Head Emeritus, Dermatology, Vilnius 
University School of Medicine, on the occasion of his 
85th birthclay, anc\ to his two c\istinguishec\ colleagues , 
Professor Geromanta Baleviciene, his successor, anc\ 
Genovaite Lapinskaite MD, his form er stuc\ent, President 
of the Association of Dermatovenereologists ofLithuania 
and Director of the Republican Hospital for Skin ancl 
Venereal Diseases in Vilnius. 
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89 
Alopecia areata: emerging concepts Review 
AUTHORS' 
ADDRESSES 
90 
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Anthony J. Papadopoulos MD, Dermatology, New Jersey Medical School, 
Newark, New Jersey. 185 South OrangeAvenue, Newark, 
New Jersey 07103-2 714 
RobertA. SchwartzMD, MPH, same address 
C amila Krysicka Janniger MD, same address 
Acta Dermatoven APA Vol 9, 2000, No 3