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REVIEW
open access to scientific and medical research
Open Access Full Text Article
http://dx.doi.org/10.2147/CCID.S53985
Epidemiology and burden of alopecia areata:
a systematic review
Alexandra C Villasante Fricke
Mariya Miteva
Department of Dermatology and
Cutaneous Surgery, University of
Miami Miller School of Medicine,
Miami, FL, USA
Correspondence: Mariya Miteva
Department of Dermatology and
Cutaneous Surgery, University of Miami
Miller School of Medicine, 1600 NW
10th Avenue, Rosenstiel Medical
Science Building, Room 2023A,
33136 Miami, FL, USA
Email mmiteva@med.maimi.edu
Background: Alopecia areata (AA) is an autoimmune disorder characterized by patches of
non-scarring alopecia affecting scalp and body hair that can be psychologically devastating.
AA is clinically heterogenous, and its natural history is unpredictable. There is no preventative
therapy or cure.
Objective: The objective of this study is to provide an evidence-based systematic review on
the epidemiology and the burden of AA.
Methods and selection criteria: A search was conducted of the published, peer-reviewed
literature via PubMed, Embase, and Web of Science. Studies published in English within the last
51 years that measured AA’s incidence, prevalence, distribution, disability-adjusted life years
(DALYs), quality of life, and associated psychiatric and medical comorbidities were included.
Two authors assessed studies and extracted the data.
Results: The lifetime incidence of AA is approximately 2% worldwide. Both formal population
studies found no sex predominance. First onset is most common in the third and fourth decades
of life but may occur at any age. An earlier age of first onset corresponds with an increased
lifetime risk of extensive disease. Global DALYs for AA were calculated at 1,332,800 in 2010.
AA patients are at risk for depression and anxiety, atopy, vitiligo, thyroid disease, and other
autoimmune conditions.
Conclusion: AA is the most prevalent autoimmune disorder and the second most prevalent
hair loss disorder after androgenetic alopecia, and the lifetime risk in the global population is
approximately 2%. AA is associated with psychiatric and medical comorbidities including depres-
sion, anxiety, and several autoimmune disorders, and an increased global burden of disease.
Keywords: hair loss, hair, prevalence, incidence, burden of disease
Introduction
Alopecia areata (AA) is a common, clinically heterogenous, immune-mediated, non-
scarring hair loss disorder.
1–3
The disease may be limited to one or more discrete, well-
circumscribed round or oval patches of hair loss on the scalp or body, or it may affect
the entire scalp (alopecia totalis) or the entire body (alopecia universalis).
1,2
Moreover,
the course of disease is unpredictable, with spontaneous regrowth of hair occurring
in 80% of patients within the first year, and sudden relapse at any given time.
2,3
In
AA, CD4+ and CD8+ T-cells violate the immune privilege of the anagen hair follicle,
leading to loss of the growing hair shaft.
1,3,4
CD8+ T-cells are present in significantly
greater quantities than CD4+ cells, and a subset of them known as CD8+ NKG2D+
T-cells has been found both necessary and sufficient to induce AA in C3H/HeJ mice.
5,6
A predominant Th1 cytokine profile has been discovered at the site of AA lesions.
3,7
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Recently, a genome-wide association study demonstrated a
genetic predisposition to AA.
7
Environmental insults, such
as viral infections, trauma, or psychosocial stress, have also
been suspected to possibly contribute to the development of
the disease.
3
Treatment options for AA have limited success, no cure
has been found, and no therapy has been able to prevent
disease relapse.
1,2,8
Treatment options include topical, locally
injected, or systemic steroids; topical immunotherapy; topical
minoxidil; topical irritants such as anthralin; and systemic
immunosuppressants such as cyclosporine or methotrexate.
8,9
Success rates vary depending on the extent and duration of
disease. Psychosocial support and therapy is also an impor-
tant part of disease management, as this often disfiguring
disease can be psychosocially burdensome.
The objectives of this review are to 1) to assess the
epidemiology of alopecia areata, including its incidence,
prevalence, and distribution by sex and age – a brief descrip-
tion of the genome-wide association studies is also included;
and 2) to assess its burden of disease including its comorbid
psychiatric and medical conditions. Burden of disease is
measured by disability-adjusted life years (DALYs), which
combine years lost to disability (morbidity) and years lost
to death (mortality) so that one DALY represents 1 year of
healthy life lost.
9
Materials and methods
A search of the literature was performed in order to answer
the question: what is the epidemiology and burden of alopecia
areata? A search was performed first on PubMed with the
terms “alopecia areata epidemiology”, which yielded 208
results. All titles and abstracts were scanned to determine
whether each article answered the question. Further searches
were performed including: “alopecia areata prevalence”,
“alopecia areata incidence”, “alopecia areata distribution”,
“alopecia areata burden”, “alopecia areata DALY”, “alopecia
areata demographics”, “alopecia areata comorbidity”, and
“National Alopecia Areata Registry”. Similar searches were
also performed on Embase and Web of Science.
Articles chosen for inclusion were peer-reviewed with
available full-text or abstract in English, providing primary
data, and were published in the last 51 years. Additionally,
secondary data generated by the World Health Organization
(WHO) in the Global Burden of Disease Study were included.
For the purpose of defining the epidemiology of AA, we
selected articles with data on the prevalence, incidence, and
distribution by sex or age. For the burden of disease, we
selected articles with data on DALYs as well as associated
psychiatric or medical comorbidities.
Results
Epidemiology: prevalence and incidence
Two population studies have measured the incidence and
prevalence of AA, both based in Olmsted County, Minnesota,
USA.
10,11
Mirzoyev et al analyzed data from the Rochester
Epidemiology Project, assessing 530 newly diagnosed
patients with AA from 1990 to 2009.
10
Estimated incidence
was 20.9 per 100,000 person-years with a cumulative lifetime
incidence of 2.1%.
10
The cumulative AA incidence increased
almost linearly with age.
10
Almost 20 years prior, Safavi et al
estimated the overall incidence of AA at 20.2 per 100,000
person-years with a lifetime incidence of 1.7% using data
from 1975 through 1989.
11
Three years prior to that, using
data from a survey conducted between 1971 and 1974,
prevalence was estimated at 0.1% to 0.2%, with lifetime
risk of 1.7%.
12
Hospital-based studies from across the world have esti-
mated the incidence of AA to be between 0.57% and 3.8%,
as detailed in Table 1.
13–16
An estimated 2.4 million doctor
office visits in the USA are for AA, which accounts for 25%
of visits for all types of alopecia.
17
Prevalence in Japan was
calculated to be 2.45%.
18
Episodes of AA last less than 6
months in the majority of patients.
13,19
Epidemiology: family history of AA
Patients with AA reporting a family history of the disease have
been estimated between 0% and 8.6%.
13,16,20
In children, rates
of family history of AA have been reported to be between
Table 1 Incidence of alopecia areata globally
Incidence, % Number of persons in study Country Type of study Comments References
2.1 530 patients USA Population study Lifetime incidence 10
1.7 292 patients USA Population study Lifetime incidence 11
2 n/a USA and Britain Review and hospital-based study 14
0.7 808 patients, 572 controls India Hospital-based study 15
3.8 219 patients Singapore Hospital-based study 16
0.57 187 patients Mexico Hospital-based study 13
Abbreviation: n/a, not applicable.
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Epidemiology and burden of alopecia areata
10% and 51.6%.
19,21–23
One study found that males were more
likely to have a family history than females were.
24
Epidemiology: distribution by sex
No significant difference in the incidence of AA was found
between males and females in either of the two population
studies.
10,11
Ten different hospital-based studies from across the
world, however, have cited a female predominance, ranging from
a ratio of 2.6:1 to 1.2:1.
13,15,16,22,24–29
Contrarily, four studies have
shown a male predominance ranging from 2:1 to 1.1:1.
15,20,30,31
In
children, there was a male predominance at 1.4:1 in two studies,
with one citing boys as having more severe involvement; a third
study reported girls as having more severe disease.
16,19,23
Male patients were reported as receiving a diagnosis of
AA at an earlier age than female patients.
24
Females were
found to have a greater likelihood of extensive AA than
males.
19
Females were found to have higher rates of comorbid
nail involvement and concomitant autoimmune disease, par-
ticularly thyroid disease.
24
Some studies report no statistically
significant differences in the age of onset, duration, or type
of AA by sex or ethnicity.
32
Epidemiology: distribution by age and
body site
AA has historically been more prevalent in the younger
age groups.
33
The largest age group presenting for care was
21–40-years of age, followed by the 1–20-year age group, the
41–60-year age group, and finally the 61–80-year age group.
16
Similarly, peak in visits for AA has been reported in the
30–59-year age group and the 31–35-year age group.
17,18
Age of onset
AA sufferers experience their first onset of AA by age 40
years in 82.6%–88% of patients and by age 20 years in 40.2%
of patients.
15,16,20
The mean age of onset has been reported as
between 25.2 and 36.3 years, as depicted in Table 2.
10,16,20,32,34
Age of onset for females compared to males has been variously
reported as lower (24.2 vs 26.7 years),
16
the same,
20
and higher
(36.2 vs 31.5 years).
10
In children, the mean age of onset has
been reported as between ages 5 and 10 years.
21–23,35
Epidemiology: distribution by body site
The scalp is the most common site of involvement, with
or without involvement of other body sites (such as the
eyebrows, eyelashes, and beard).
13,16
Specifically, the most
common site was the occipital region, involved in 38.4% of
males and 33.4% of females.
36
Upon first presentation, 58%
of adult patients had patchy hair loss with less than half the
scalp involved.
16
On the other hand, in children, 80%–85%
had mild to moderate hair loss involving less than half the
scalp.
21–23,35
A later age of onset correlated with a less exten-
sive alopecia, or in other words, onset in the first 2 decades
was more often associated with severe alopecia.
15,16,20
Alopecia totalis and universalis occurred in 7.3% of AA cases
and always occurred before the age of 30 years.
16
Nail changes occur in 10.5%–38% of AA patients, with
common findings including pitting, trachyonychia, and
longitudinal ridging.
15,16,32
Nail changes correlated with
disease severity, as they were found in more severe AA.
15,16,32
Furthermore, nail dystrophy is a poor prognostic indictor
of AA.
16
Results: burden of disease
Burden of disease: DALYs
In the Global Burden of Disease Study, WHO measured
the global DALYs lost to AA in 2010 to be 1,332,800.
37
For
comparison, the DALYs of psoriasis are 1,050,660, and for
diabetes mellitus they are 46,857,100.
37
The DALYs for AA
have been increasing linearly since 1990, when the global
DALYs were under 1 million. No deaths have been reported
from AA between 1990 and 2010. The disability weight for
AA, which ranges from 0 to 1, was 0.035.
9
AA is thought to
account for 0.071% of total US DALYs.
9
Burden of disease: quality of life
Over half of patients with AA experience poor health-related
quality of life (QOL).
38
Though patients of all ages and both
sexes may experience decreased QOL with AA, risk fac-
tors for poor health-related QOL include age between 20
and 50 years, female sex, lightening of skin color, hair loss
greater than 25%, family stress, and job change.
38
Patients
with extensive AA experienced more adverse psychological
effects than those with limited AA.
16
Burden of disease: psychiatric
comorbidity
A 66%–74% lifetime prevalence of psychiatric disorders
has been reported in AA patients, with a 38%–39% lifetime
Table 2 Age of onset of alopecia areata globally
Age of onset, years Country Type of study Reference
25.2 Singapore Hospital-based 16
28.98 People’s Republic
of China
Hospital-based 20
36.3 USA Hospital-based 32
32.2 Taiwan Hospital-based 34
33.6 USA Population 10
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Villasante Fricke and Miteva
prevalence of depression and a 39%–62% prevalence of
generalized anxiety disorder.
39–42
Adjustment disorders
are also commonly found with AA.
40
Table 3 outlines the
rates of psychiatric disorders in AA patients compared to
the general population. Approximately 50% of psychiatric
disorders presented earlier than did AA, with the other half
presenting after the onset of AA.
42
Furthermore, stressful
events preceding hair loss were recalled in 9.8% of adults
and in 9.5%–80% of children.
16,21,35
The rate of psychiatric
comorbidity was influenced by the age of onset of AA, with
an increased risk of depression in patients aged ,20 years
and an increased risk of anxiety and obsessive-compulsive
disorder in those aged 40–59 years.
42
No patients were acutely suicidal in a study of 45 AA
patients, four with alopecia totalis and 28 with alopecia
universalis.
43
One patient in that study, however, answered yes
to “dying is the best solution for me.” Four patients affirmed
that they “wish [they] were dead,” and one denied that “life
is still worth living.”
43
A recent letter to the editor, however,
reports the death of four Australian males aged 14–17 years
who were affected by AA with no known pre-existing psy-
chological disorders, and with social withdrawal that began
after the onset of the alopecia.
44
Burden of disease: comorbid medical
conditions
The incidence of atopy in patients with AA has been reported
to be between 11% and 38.2%.
15,33,45,46
In children with AA,
atopy is seen in 26.6% of patients, though one study found
no significant personal history of atopy compared to con-
trols.
19,35
A personal or family history of atopy was reported in
60.7% of adults with AA and in 25% of children with AA.
16,21
Specifically, atopic dermatitis was reported in 15.6% of adults
with AA and in 39.5% of children with AA.
13,47
Five percent of patients in one study were discovered
to have subclinical hypothyroidism due to Hashimoto’s
thyroiditis.
35
Seventy-five percent of those discovered to
have Hashimoto’s thyroiditis had a family history of thyroid
disorder.
35
Thyroid function abnormalities were found in
8.9% of patients with AA.
29
Similarly, the prevalence of
thyroid peroxidase antibodies in AA patients was reported
to be 17.7%, about double that of the general population,
with a female-to-male predominance of 6.7:1.
48
In general,
AA patients were significantly more likely to have a family
history of thyroid disorder.
35
In addition to autoimmune thyroid disease, it has been
long suspected that there is an association between AA and
other autoimmune disorders such as vitiligo, systemic lupus
erythematosus, psoriasis, inflammatory bowel disease, and
rheumatoid arthritis.
34,46
Incidence of the aforementioned
disorders in AA can be seen in Table 4. Positive autoimmune
antibodies (ANA, SMA, Anti-Tg, or PCA) were reported
in 51.4% of patients with AA.
29
Patients with a family his-
tory of vitiligo were more likely to develop extensive AA.
15
Some studies, however, did not observe a correlation with
autoimmune conditions in the AA patients or in family his-
tory of autoimmune disorders, with the exception of thyroid
disorder.
17,35
Most recently, diabetes mellitus was found in 11.1% of
AA patients, as shown in Table 4.
46
Significant increases in
levels of insulin, c-peptide, and HOMA-IR were reported
in AA patients compared to controls, suggesting increased
insulin resistance in AA patients.
49
Approximately 36.6% of
AA patients in one study reported family history of diabetes
mellitus type 2.
13
Down syndrome was found in 1.4% of AA patients with
onset of disease before age 15 years and with extensive
involvement in all of these patients.
19
Summary of genome-wide
associations in AA
A review on AA would not be complete without a mention
of the current literature on genomic associations. Previously,
genes in the human leukocyte antigen (HLA) region were
implicated in AA as well as some genes outside of HLA
including PTPN22 and AIRE.
50
In 2010, Petukhova et al
published reports of a genome-wide association study that
Table 3 Psychiatric disorders in alopecia areata (AA) patients
compared to the general population
Disorder AA patients, % General
population, %
Major depression 8.8 1.3–1.5
Generalized anxiety disorder 18.2 2.5
Social phobias 3.5 0.9–2.2
Paranoid disorder 4.4
,1
Notes: Data from Koo et al.
55
Table 4 The incidence of autoimmune disorders in alopecia
areata (AA)
Autoimmune disorder Incidence in AA, % Reference
Vitiligo 1.8–7.0 15,16,33,46,47
Thyroid disorder 2.3–14.6 16,33,34,46
Irritable bowel syndrome 2.0 46
Psoriasis ± psoriatic arthritis
1.9–6.3 34,46
Systemic lupus erythematosus 1.5 34
Rheumatoid arthritis 0.9–3.9 19,34,46
Diabetes mellitus 0.4–11.1 15,46
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Epidemiology and burden of alopecia areata
discovered 139 single nucleotide polymorphisms (SNPs)
associated with AA, mostly genes related to inflammation
and immune-modulation, HLA, and cytokines.
7
Specifically,
those SNPs include: genes that control the activation and
proliferation of regulatory T-cells; cytotoxic T lymphocyte-
associated antigen 4; interleukins 2 and 21; interleukin-2
receptor A; Eos (or Ikaros family zinc finger 4); HLA;
genes expressed within the hair follicle, including PRDX5
and STX17; and the ULBP (cytomegalovirus UL16-binding
protein) gene cluster on chromosome 6q25.1, encoding acti-
vating ligands of the natural killer cell receptor NKG2D.
7,51
Using an Immunochip, Redler et al discovered that the
strongest associations were observed for variants of the major
histocompatibility complex class II DQ beta 1 (HLA-DQB1)
and class II DQ alpha 2 (HLA-DQA2).
51
Examples of SNPs
associated with AA in genes that regulate T-cell function
include the promoter regions of Foxp3 and ICOSLG, and
the CTLA4 CT60 polymorphism.
52,53
Most recently, Betz
et al discovered three novel loci: ACOXL/BCL2L11(BIM)
(2q13); GARP (LRRC32) (11q13.5); and SH2B3(LNK)/
ATXN2 (12q24.12).
54
Discussion and conclusion
Epidemiology
This systematic review provides a summary of the existing
data on the worldwide incidence and prevalence of AA and
its burden. Comparison between studies was attempted in
relation to geography, age, and sex. Generally, a concern with
the population studies is that their sample from a population
register may not be representative of the true population at
risk of AA. In fact, both population studies cited in the cur-
rent review were based in Minnesota.
10,11
However, there are
also concerns that hospital-based studies may fail to provide
an unbiased sample of the population at risk with respect to
exposure status. These concerns aside, our literature search
found that the estimated incidence of AA was approximately
2% in the population studies and close to 2% in hospital-
based studies globally (Table 1).
10,11,13–16
There is no clear conclusion about whether the disease
varies according to sex. There appears to be no significant
difference in the incidence of AA between males and
females as both formal population studies found none,
and hospital-based studies are mixed in citing a female vs
male predominance.
10,11,13,15,16,19,20,22–32
Again, hospital-based
studies depend on access to care, and in some cases, willing-
ness to participate in the study, which may bias the results.
Most patients experience their first onset of AA by
age 40 years, with a peak of incidences occurring in their
20s and 30s (Table 2).
10,15,16,20,32,34
The younger the age
of onset, the greater the lifetime likelihood of extensive
alopecia.
15,16,20
Access to care and delay in presentation
may also play a role in the age distribution seen. Family
history of AA is present in a minority of patients with AA,
and is seen more often in patients who present with AA as
children.
13,16,19–23,36
The scalp is involved with or without involvement of
other body sites in almost all cases of AA, with the occipital
scalp being the most commonly involved site.
13,16,36
Nail
involvement can be seen in severe AA and is a poor prog-
nostic factor.
15,16,32
Burden
The Global Burden of Disease Study, which estimates the
DALYs for AA to be 1,332,800, or a weighted 0.035, may
underestimate the true population-based prevalence and dis-
ease burden due to patients with AA who do not present for
care.
9
Furthermore, it considers the disability imposed by itch
and disfigurement, but does not take into account emotional
distress, interpersonal relationships, or financial impact.
9
AA leads to decreased QOL in half of its sufferers and is
associated with an approximately 70% lifetime prevalence of
psychiatric disorders, most commonly depression, anxiety,
and adjustment disorders.
38–42
It has even been implicated
in suicide.
44
In about half of patients, however, psychiatric
disorders presented earlier than AA, and in a portion of cases,
stressful events were recalled preceding hair loss.
16,21,35,42
AA appears to be associated with atopy and many
autoimmune diseases including vitiligo and thyroid
disorders.
13,15,16,21,29,33–35,45–47,49
Some studies did not find
association with autoimmune diseases.
17,35
Genome-wide
association studies, however, implicate genes in the HLA
region and genes involved in inflammation and immune
modulation in AA, many of which could plausibly affect
multiple autoimmune conditions.
7,51,54
Discrepancies in the
incidence of associated conditions seen in Table 4 may, in
part, be due to differences in the prevalence of atopy and
autoimmune diseases across the globe and over time.
Extensive AA leads to greater disfigurement and psycho-
social distress. Factors that increase the likelihood of exten-
sive AA such as alopecia totalis and/or universalis include:
younger age of onset; associated autoimmune or atopic
disease, particularly thyroid disease and atopic dermatitis;
nail changes; Down syndrome; positive family history of
vitiligo; and positive family history of AA.
15,16,32
In conclusion, studies on the occurrence of AA have
contributed to a greater appreciation of the disease burden.
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The estimated high prevalence of 2% globally underscores
the importance of disease awareness, of unveiling the role
of genomics in influencing the likelihood of developing AA,
and of discovering potential molecule-oriented treatments.
Yet, epidemiological studies on AA are limited, and no clear
conclusions can be drawn. Possible sources of heterogeneity
in research results arise from 1) the different methodologies
utilized to collect the data: hospital-based medical records,
insurance databases, registries, or primary care databases,
which may under-represent patients with no access to health
care; and/or 2) case definition: self-diagnosis, primary care
physician’s diagnosis or dermatologist’s diagnosis of AA.
There is a need for international research collaborations using
standardized methodology to address those knowledge gaps.
Disclosure
The authors report no conflicts of interest in this work.
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