DOI: 10.1111/jdv.

15489 JEADV

REVIEW ARTICLE

JAK inhibitors for alopecia areata: a systematic review and

meta-analysis
K. Phan,1,2 D.F. Sebaratnam1,2,3,*
1
Department of Dermatology, Liverpool Hospital, Sydney, NSW, Australia
2
Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia
3
Departments of Dermatology, Sydney Children’s Hospitals’ Network, Sydney, NSW, Australia
*Correspondence: D.F. Sebaratnam. E-mail: deshan.sebaratnam@health.nsw.gov.au

Abstract
There have been a number of case reports and small clinical trials reporting promising outcomes of Janus Kinase (JAK)
inhibitors tofacitinib, ruxolitinib and baricitinib for alopecia areata (AA). The majority of the literature to date is based on
small volume data, with a lack of definitive evidence or guidelines. To determine the expected response of AA to JAK
inhibitor therapy and factors which influence response and recurrence rates. A systematic review and meta-analysis was
performed according to PRISMA guidelines. From 30 studies and 289 cases, there were 72.4% responders, good
responders 45.7% and partial responders 21.4%. Mean time to initial hair growth was 2.2  6.7 months, and time to
complete hair regrowth was 6.7  2.2 months. All 37 recurrences occurred when treatment was ceased after
2.7 months. Oral route was significantly associated with response to treatment compared to topical therapy. No differ-
ence was found between paediatric and adult cases in proportion of responses. There is promising low-quality evidence
regarding the effectiveness of JAK inhibitors in AA. Future large-sized randomized studies are required to confirm findings.
Received: 3 October 2018; Accepted: 18 January 2019

Conflicts of Interest
None to declare.

Funding sources
None.

Introduction JAK1/3 signalling to amplify the inflammatory response around

Alopecia areata (AA) is one of the most common autoimmune
diseases with a lifetime risk of 2% in the United States.1,2 From
cases which do not spontaneously remit, these patients often fol-
low a protracted clinical course with the worst cases eventuating
in alopecia totalis (AT) or alopecia universalis (AU). Persistent
AA and its variants can lead to significant disfigurement exerting
a detrimental impact on patient wellbeing, which may be inde-
pendent of objective severity.3 Currently employed management
strategies include camouflage, topical, intralesional and systemic
corticosteroids, minoxidil, diphenylcyclopropenone and system-
atic agents such as methotrexate.4
Recently, laboratory studies have focussed on understanding
the autoimmune mechanisms underlying the pathophysiology of
AA. There is evidence from comparative genomic studies and
transcriptional profile analysis of model mice with AA as well as
human tissue that cytotoxic CD8(+) NKG2D(+) T cells are inte-
gral to the development of AA.5–8 This subset of T cells was
shown in mice to release IFN gamma, which promoted IL-15
production in hair follicles via Janus Kinase (JAK)1/2 signalling.
IL-15 also stimulated IFN gamma production by T cells via
hair follicles. Given that these pathways are mediated by JAK
receptors, this understanding provides the rationale for the
development and testing of JAK receptor inhibitors.
There have been a number of case reports and small clinical
trials reporting promising outcomes of JAK inhibitors tofaci-
tinib, ruxolitinib and baricitinib for AA in paediatric and adult
patients. However, the majority of the literature to date is based
on small volume data with a lack of information addressing the
following questions: (i) what is the expected response of AA to
JAK inhibitor therapy? (ii) does route of administration oral ver-
sus topical affect outcome? (iii) what patient factors are associ-
ated with positive response to therapy? (iv) does the drug choice
(tofacitinib vs. ruxolitinib vs. baricitinib) influence therapeutic
outcome? (v) in what time period are patients expected to show
a response to therapy? (vi) how durable are results after cessation
of JAK inhibitor therapy? and (vii) how do outcomes compare
between paediatric cases versus adult cases? To address these
current gaps in knowledge, we performed a systematic review
and meta-analysis of available individual patient data from case
reports/series/clinical trials, as well as cohort studies.

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JAK inhibitors for alopecia areata 851

Methods

20 after drug cessation,

12 after drug cessation,

5 after drug cessation,
2.125 months median
Search strategy
The present study was performed according to PRISMA guide-

2 months off

4 months off
Recurrence
lines. Electronic searches were performed using Ovid Medline,
PubMed, EMBASE, Cochrane Central Register of Controlled

–
Trials (CCTR), Cochrane Database of Systematic Reviews
(CDSR), ACP Journal Club and Database of Abstracts of

60.5% (17.2–100%)
32.9% (1.2–87.4%)
Review of Effectiveness (DARE) from their dates of inception

47.14  35.97%
64.7% (10–88%)
Median change:

Median change

56.3% reached
Mean change:

Mean change:
to July 2018. To achieve the maximum sensitivity of the search

SALT score
Change in
strategy, we combined the terms: ‘alopecia areata’ AND ‘JAK

SALT50
inhibitor’ OR ‘ruxolitinib OR tofacitinib OR baricitinib’ as
either key words or MeSH terms. The reference lists of all
retrieved articles were reviewed for further identification of

11.74  13.81
potentially relevant studies, assessed using the inclusion and

Duration of
treatment

7.5 (4–17)
9.5  3.5
(months)

12 (4–18)
exclusion criteria.

–
Selection criteria
Eligible studies for the present systematic review and meta-ana-

Oral and topical

JAK inhibitors
PO tofacitinib

PO tofacitinib

PO tofacitinib

PO tofacitinib
lysis included those in which patient from case reports, case ser-
Table 1 Characteristics and outcomes of included studies in the present systematic review and meta-analysis

Treatment

AA, alopecia areata; AT, alopecia totalis; AU, alopecia universalis; BD, twice a day; PO, oral; SALT, Severity of Alopecia Tool.
5 mg BD

5 mg BD

5 mg BD

5 mg BD
ies, cohort studies or clinical trials with AA/AU/AT were treated
with JAK inhibitor therapy. Studies that did not report response
or complications as endpoints were excluded. All publications
were limited to those involving human subjects. Language was

10.54  10.66
Duration of

not an exclusion factor. Abstracts, conference presentations, edi-

10.8  8.9
5 (0.5–43)

18 (2–54)
Alopecia

8 (1–35)
torials, reviews and expert opinions were excluded. The search
(years)

strategy is included in Table S1.

35/66 (53.0%)

16/33 (48.5%)

40/90 (44.4%)

23/32 (71.9%)

25/92 (27.2%)
Data extraction
All data were extracted from article texts, tables and figures. Two
investigators independently reviewed each retrieved article (K.P.,
Men

D.F.S). Discrepancies between the two reviewers were resolved by

discussion and consensus. Individual patient level data extracted
30.51  16.25

from case reports/case series/clinical trials were pooled together as

34.5 (18–70)
age (years)

31.2  9.3
37 (19–65)

30 (18–54)

‘individual cases’ group. Clinical trials and cohort studies report-

Mean

ing descriptive statistics of cohort-level data were also included.

Main treatment outcomes included the following: any response to
treatment (defined as 5–100% hair regrowth), partial response
66

33

90

32

92
N

(defined as 5–50% hair regrowth) and good response (defined as

50–100% hair regrowth). Other data collected included the fol-
AA/AU/AT
AA type

lowing: AA subtype, prior failed treatments, duration of alopecia

AA

AA

AA

AA

prior to therapy, JAK inhibitor used and route of administration,

time to initial regrowth, duration of treatment, recurrence rates,
Pooled
Cohort

Cohort

Cohort

Cohort
Study

as well as time between drug cessation and recurrence.

cases
study

study

study

study
type

Statistical analysis
2015–2018

From extracted summary data from cohort studies, clinical trials,

as well as pooled cases data, a meta-analysis of proportions was
2016

2018

2017

2017
Year

conducted for response outcomes. To incorporate heterogeneity

(anticipated among the included studies), transformed propor-
Author

Pooled
Crispin

cases

tions were combined using DerSimonian–Laird random-effects

Park
Lee

Liu

models. Heterogeneity was evaluated using Cochran Q and I2 test.

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852 Phan and Sebaratnam

Meta-analysis was performed using the meta for package for R
version 3.3.
For individual patient level data, the data were analysed using
descriptive statistics. Univariate analysis was performed according to
factors: responders vs. non-responders, good versus partial respon-
ders and paediatric versus adult cases. Correlation analysis was per-
formed using Spearman correlation. Time to event (hair regrowth)
was analysed using Kaplan–Meier analysis. All analyses were per-
formed using the meta for package for R version 3.4 or SPSS version
24. P values < 0.05 were considered statistically significant.
Results
A total of 196 studies were identified through six electronic data-
base searches and from other sources such as reference lists (Fig-
ure S1). After exclusion of duplicate or irrelevant references, 85
potentially relevant articles were retrieved. There were some
studies with overlapping populations that were removed.5,9,10
After detailed evaluation of these articles, a total of 30 arti-
cles6,7,11–38 were included in the present study, comprising four
cohort studies (comprising 221 patients) and 26 case reports/
case series/trials with individual patient level data (comprising
92 patients).
Summary characteristics of included cohort studies are found in
Table 1, and of the pooled individual cases from case reports/series
in Table 1 and Table S2. Mean age ranged from 30 to 37 years,
proportion of men ranged from 27.2% to 71.9%. The duration of
alopecia ranged from 5 to 18 months. Treatment duration ranged
from 7.5 to 12 months. From the pooled individual case data, 14
cases (26.9%) had prior failed systemic therapy, for example with
methotrexate. Nine cases (9.8%) had a major autoimmune comor-
bidity including psoriasis, psoriatic arthritis and thyroid disease.
From pooled case data, the most common treatments were oral
tofacitinib (45 cases, 48.9%), followed by topical tofacitinib (25
cases, 27.2%) and oral ruxolitinib (17 cases, 18.5%).

(a)
Studies

Crispin 2016
Lee 2018
Liu 2017
Park 2017
Pooled cases 2015−2018

Overall (I^2=45.14 % , P = 0.121)

0.51 0.62 0.73 0.84 0.95

Logit Proportion

(b)
Studies

Crispin 2016
Park 2017
Pooled cases 2015−2018

Overall (I^2=73.51 % , P = 0.023)

0.22 0.34 0.46 0.58 0.7

Logit Proportion

(c)
Studies

Crispin 2016
Park 2017
Pooled cases 2015−2018

Overall (I^2=68.35 % , P = 0.042)

0.08 0.17 0.26 0.35 0.44

Logit Proportion

Figure 1 Pooled meta-analysis of proportion of patients with (a) any positive response (5–100%), (b) good response (50–100%) and
(c) partial response (5–50%) hair growth to JAK inhibitor therapy for alopecia areata.

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JAK inhibitors for alopecia areata 853

Efficacy of JAK inhibitors for alopecia areata recurrences occurred when JAK inhibitor therapy was ceased, on
Pooled meta-analysis based on data from cohort studies and case average, after 2.7 months. Characteristics of recurrent cases are
reports of responders to JAK inhibitor therapy is shown in Fig. 1. summarized in Table S3.
Based on a total of 289 patients, the proportion of patients with
any response was 72.4% (95% CI 64.5–79.2%). The proportion of Predictors of response to JAK inhibitor therapy
patients with good response was 45.7% (95% CI 31.7–60.3%) and We performed univariate analysis to determine predictors of
the proportion of patients with partial responses was 21.4% (95% responders to JAK inhibitor therapy for alopecia areata. Oral
CI 12.4–34.4%). From the pooled case data, the mean time to ini- JAK inhibitors were significantly associated with response to
tial hair growth was 2.2  6.7 months, and time to complete hair treatment compared to topical therapy (77.8% vs. 46.4%,
regrowth in those cases that did was 6.7  2.2 months (Table S1). P = 0.003), with odds ratio 4.0 (95% CI 1.56–10.45) as reported
There were 12 cases of recurrence of alopecia areata from the in Table 2. There was no difference between responders and
pooled cases, and 25 recurrences from the cohort studies. All 37 non-responders in terms of age, sex, duration of AA, AA sub-
type, JAK inhibitor, nor the duration of treatment.
Table 2 Comparing characteristics and outcomes of Responders We performed univariate analysis to determine predictors of
versus Non-responders to JAK inhibitors for alopecia areata,
good responders versus partial responders, summarized in
based on pooled case reports/case series
Table 3. Again, only oral treatment route was significantly asso-
Parameter Responder Non-responder P-value ciated with good response (85.4% vs. 42.9%, P = 0.001) with an
N 63 28 – odds ratio of 7.8 (95% CI 2.07–29.41). There was no difference
Men 18 (28.6%) 7 (25%) 0.223 between responders and non-responders in terms of age, sex,
Women 33 (52.4%) 11 (39.3%) —
duration of AA, AA subtype, JAK inhibitor, nor the duration of
Age (years) 31.54  15.48 26.89  18.21 0.304
treatment. Time to initial hair regrowth was also similar between
Duration of 10.66  10.50 9.63  11.47 0.741
alopecia (years)
these two groups.
AA 41 (65.1%) 19 (67.9%) 0.449
We compared demographics and outcomes of men versus
AU 19 (30.2%) 6 (21.4%) — women (Table S4). Although there was a significant difference in
AT 3 (4.8%) 3 (10.7%) — the proportion of AA, AU and AT cases, we found no differences
Failed systemic 10 (26.3%) 4 (28.6%) 0.871 in the route of therapy used, nor the proportion of responders,
therapy good or partial responses. The % change in SALT score was also
Major autoimmune 8 (12.7%) 1 (3.6%) 0.178 similar between men and women.
comorbidity
Correlation analysis found that age, duration of AA, duration
Treatment route
of treatment, initial SALT score, nor time to initial hair growth
Topical 14 (22.2%) 15 (53.6%) 0.003
were not significant predictors of change in SALT score with
Oral 49 (77.8%) 13 (46.4%) —
JAK inhibitor therapy (Table S7).
Topical (n = 29)
Topical tofacitinib 12 (85.7%) 13 (86.7%) 0.941
Comparison of JAK inhibitors for alopecia in paediatric
Topical ruxolitinib 2 (14.3%) 2 (13.3%) —
Oral (n = 62)
versus adult populations
Oral tofacitinib 34 (69.4%) 10 (76.9%) 0.794
The duration of AA was shorter in paediatric cases compared
Oral ruxolitinib 14 (28.6%) 3 (23.1%) — with adults (4.03 vs. 13.7 years, P = 0.001; Table S5). Paediatric
Oral baricitinib 1 (1.6%) 0 (0%) — cases were also associated with higher proportion of AU and AT
Mean duration of 13.19  15.56 8.47  8.01 0.134 (P < 0.001). Topical JAK inhibitors were used in 89.5% of pae-
treatment (months) diatric cases compared to 4.1% of adult cases (P < 0.001). The
Outcome average duration of treatment was also significantly longer for
Good response 48 (78.7%) – – paediatric cases (23.7 vs. 9.0 months, P < 0.001). However, the
Partial response 13 (21.3%) – – proportion of responders, good and partial responders, as well
Recurrences 12 (19.0%) – – as recurrence and changes in SALT scores were comparable and
Time to initial 2.16  1.92 – – not significantly different between the two groups (Table S5).
regrowth (months)
Time to complete 6.67  2.19 – –
regrowth (months)
Comparison of JAK inhibitors for alopecia areata variants
Change in SALT (%) 47.14  35.97% – –
Demographics and outcomes with JAK inhibitors in AA were
compared with the more severe AT and AU (Table S6). We
AA, alopecia areata; AT, alopecia totalis; AU, alopecia universalis; N, num-
ber of cases; SALT, Severity of Alopecia Tool; Data expressed as n(%) or
found that higher proportion patients with AA received oral
mean  standard deviation. One case (n = 1) was excluded due to inade- agents compared to patients with AT/AU. Despite this, compa-
quate assessment of response due to drop-out from follow-up. rable proportions of patients achieved any response in AA and

JEADV 2019, 33, 850–856 © 2019 European Academy of Dermatology and Venereology
854 Phan and Sebaratnam

Table 3 Comparing characteristics of Good versus Partial Discussion

responders to JAK inhibitors for alopecia areata, based on pooled To our knowledge, this is the first systematic review and meta-
case reports/case series
analysis of studies of JAK inhibitor therapy for AA and its vari-
Parameter Good Partial P-value ants. By pooling individual patient level data from case reports,
responder responder case series and clinical trials, we were able to perform univariate
N 48 14 – analysis to assess factors which contribute to response to JAK
Men 12 (25%) 5 (35.7%) 0.546 inhibitor therapy, as well as an assessment of the likely clinical
Women 26 (54.2%) 7 (50%) —
trajectory of patients based on available literature data. Overall,
Age (years) 33.47  15.52 23.55  15.95 0.072
our analysis supports the effectiveness of JAK inhibitors for AA,
Duration of 11.16  11.41 8.11  6.77 0.448
alopecia (years)
AU and AT.
AA 34 (70.8%) 6 (42.9%) 0.224
Specifically, we found that use of oral JAK inhibitor, regard-
AU 12 (25%) 7 (50%) — less of the specific agent, was associated with four times higher
AT 2 (4.2%) 1 (7.1%) — odds of achieving response, compared to patients who used topi-
Failed systemic 8 (27.6%) 2 (22.2%) 0.939 cal JAK inhibitors. Oral JAK inhibitor treatment was also associ-
therapy ated with seven times higher odds of achieving a good response
Major autoimmune 6 (12.5%) 2 (14.3%) 0.344 (50–100% regrowth) than a partial response (5–50% regrowth)
comorbidity
compared to topical treatment, with no difference between
Treatment route
tofacitinib, ruxolitinib or baricitinib. As such, the major deter-
Topical 7 (14.6%) 8 (57.1%) 0.001
mining factor in determining response appears to be the method
Oral 41 (85.4%) 6 (42.9%) —
of drug delivery, with oral agents associated with the best outcomes.
Topical (n = 15)
Interestingly, demographic factors including age, sex, previous
Topical tofacitinib 6 (85.7%) 7 (87.5%) 0.992
failure of systemic therapy, duration of AA and the actual JAK
Topical ruxolitinib 1 (14.3%) 1 (12.5%) —
Oral (n = 47)
inhibitor agent did not appear to influence response to therapy.
Oral tofacitinib 28 (68.3%) 5 (83.3%) 0.897
Further, no significant difference in responders or SALT score
Oral ruxolitinib 12 (29.3%) 1 (16.7%) — percentage changes was found between AA patients compared to
Oral baricitinib 1 (2.4%) 0 (0%) — AT/AU, suggesting that JAK inhibitors may still demonstrate
Mean duration of 11.96  11.86 15.07  19.82 0.466 effectiveness independent of objective severity a previously
treatment (months) refractory clinical course. These findings differ from those of Liu
Outcome and colleagues,28 who found a negative correlation between
Recurrences 11 (22.9%) 1 (7.1%) 0.189 duration of current disease episode with SALT score change, as
Time to initial 1.69  0.73 2.1  1.14 0.345 well as higher SALT score change with AA versus AT/AU sub-
regrowth (months) types. However, it is interesting to note that even though their
Time to complete 6.91 + 2.12 – –
correlation was statistically significant, the correlation coefficient
regrowth (months)
was small (rho 0.28) suggesting a weak correlation. Overall,
Change in SALT (%) 77.66  16.58 25.21  12.03 <0.001
our results suggest that demographic characteristics, disease
AA, alopecia areata; AT, alopecia totalis; AU, alopecia universalis; N, num-
severity and duration of AA may not be useful as predictors of
ber of cases; SALT, Severity of Alopecia Tool; Data expressed as n(%) or
mean  standard deviation. response in this setting. Jabbari and colleagues24 have notably
demonstrated considerable correlation between gene expression
AT/AU. Furthermore, the percentage change in SALT score was profile as well as Alopecia Areata Disease Activity Index scores
also not significantly different between AA and AU/AT with clinical response. Future research should target molecular-
(P = 0.578). level indexes and transcriptional profiling as better means of pre-
dicting patient response to JAK inhibitor treatment.
Safety of JAK inhibitors for alopecia Our time course analysis showed that time to initial hair
Pooled complication rates are summarized in Table S8. The growth was 2.2 months, and time to complete hair regrowth was
most common complication observed was low-grade infection. 6.7 months. All cases of relapse in this systematic review were
These included from 313 total cases: 57 (18.2%) upper respira- associated with cessation of therapy, on average after 2.7 months.
tory tract infections, 7 (2.2%) urinary tract infections and 77 As such, the optimal time to assess for initial response to JAK inhi-
(24.6%) total infections. Lipid abnormalities were observed in bitor therapy would be at approximately 3 months. Our results
37 (11.8%) of patients, 3 (1%) developed leucopenia and 5 also suggest that the therapeutic response may only be maintained
(1.6%) transaminitis. There were no cases of new malignancies whilst the patient is on JAK inhibitor treatment, and that once
or tuberculosis reactivation. No patients required hospitalization ceased, relapse of AA may be expected within 3 months.
for JAK inhibitor-related adverse events.

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JAK inhibitors for alopecia areata
In our analysis, we did not find significant difference in
response rates, changes in SALT score, or time profile of
response in men compared with women. Similarly, we also
found similar response rates, good response or partial response
in paediatric cases compared with adult cases. This is in spite of
the paediatric group having a lower proportion of cases with oral
JAK inhibitor treatment. These findings are supportive of the
efficacy of topical treatment in young patients. In adult cases,
topical treatment may be first line for those with mild-to-mod-
erate AA disease, or as an adjunct or second-line therapy.
In our systematic review, we found an overall low complica-
tion rate. The most common side-effect was infections in the
form of upper respiratory tract infections and urinary tract infec-
tions. There were no cases of new malignancies or reactivation of
tuberculosis. Laboratory changes were minimal, and most com-
mon were mild transaminitis, mild lipid abnormalities and
cytopenias, although the prevalence was low. As complication
rates were low, we did not find any significant difference in com-
plication profiles between oral versus topical JAK inhibitors,
although intuitively topical agents would be of lower risk. Topical
agents may be the more appealing treatment option in paediatric
population, with lower theoretical risk of complications compared
to oral agents, but the ability to achieve similar outcomes com-
pared to adult AA/AU/AT on oral JAK inhibitor treatment.
Although there is limited safety data of JAK inhibitors in the
context of AA, there is increasing evidence of its safety profile in
rheumatology and rheumatoid arthritis. In a study of over 5000
patients and over 12 000 person-years of exposure to tofacitinib,
there were 107 reported cases of malignancy, which are similar
to rates reported for the use of biologic agents.39,40 More unique
to tofacitinib compared to biologic therapy, there appears to be
an increased risk of viral reactivation particularly with herpes
zoster infections, with twofold higher risk compared to use of
biologic agents in rheumatoid arthritis patients.41,42 This risk
appears to be dose dependent, with significantly higher risk
when used as doses 10 mg twice daily.41 Tuberculosis reactiva-
tion has also been reported with tofacitinib43 and baricitinib.44
Gastrointestinal perforation is another serious complication that
has been reported with incidence of 1.29 cases per 1000 patient-
years in rheumatoid arthritis patients treated with tofacitinib.45
As such, it is important to emphasis for clinicians using JAK
inhibitors that the possibility of serious and lethal adverse effects
is very plausible, and that safety profile data for this class of
agents in AA are still in its infancy.
The present findings are limited by several constraints. This
meta-analysis was based on available low-quality evidence, pre-
dominantly in the form of case reports. These findings require
confirmation in large cohort or database studies, with prospec-
tive follow-up and evaluation. Findings are also susceptible to
observer bias as a result of clinician and study participants being
unblinded during treatment and outcomes assessment. Case
reports and small case series have a high risk of bias, and the
JEADV 2019, 33, 850–856
855
simple combination of their results does not ameliorate this.
There is also significant selection bias and publication bias, given
that it is likely that only positive results are published. A small
sample size of patients also limits statistical power of analysis.
We acknowledge that a meta-analysis of clinical cases does not
replace the degree of evidence provided by randomized clinical
trials; however, it does serve as a hypothesis generator to explore
some clinical questions regarding the use of JAK inhibitors in
AA that have not been investigated thus far in case series and trials.
In summary, the current evidence to date is low-quality in
nature but is promising regarding the efficacy and safety of JAK
inhibitors in the treatment of AA. Patients need to maintain JAK
inhibitor treatment in order for hair regrowth to be sustained.
Further studies are required to better understand factors influ-
encing JAK inhibitor treatment outcomes in patients with AA
and its subtypes.
Ethics approval
Not required as this is a systematic review.
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Supporting information
Additional Supporting Information may be found in the online
version of this article:
Figure S1. PRISMA search strategy for the present systematic
review and meta-analysis
Table S1. Search strategy employed in Ovid Medline.
Table S2. Summary demographics and outcomes from individ-
ual patient data from pooled cases.
Table S3. Demographics and treatment characteristics of recur-
rent cases following JAK inhibitor therapy for alopecia areata,
based on pooled case reports/case series.
Table S4. Demographics and treatment outcomes of male versus
female cases, based on pooled case reports/case series.
Table S5. Demographics and treatment outcomes of pediatric
(age <18 years) versus adult (age ≥18 years) cases, based on
pooled case reports/case series.
Table S6. Demographics and treatment characteristics of alope-
cia areata versus alopecia totalis/alopecia universalis cases on
JAK inhibitor therapy.
Table S7. Correlation analysis of patient characteristics versus %
change in SALT score following JAK inhibitor treatment for
alopecia areata, based on pooled case reports/case series.
Table S8. Adverse effects and complications of JAK inhibitor
therapy for alopecia areata.
© 2019 European Academy of Dermatology and Venereology