REVIEWS

Axial psoriatic arthritis: An update

for dermatologists
Alice B. Gottlieb, MD, PhD,a and Joseph F. Merola, MD, MMScb
New York, New York and Boston, Massachusetts

Psoriasis is a chronic, immune-mediated, systemic, inflammatory disorder characterized by skin plaques

and, often, nail disease and arthritis that contribute to reduced quality of life. Psoriatic arthritisda
heterogeneous, inflammatory, musculoskeletal disease that can cause permanent damage to both
peripheral and axial jointsdis the most common comorbidity of psoriasis. Axial disease occurs in 25%
to 70% of patients with PsA, with some patients exclusively experiencing axial joint involvement. Early
therapeutic intervention is important for preventing permanent joint and spine damage and loss of
functionality in these patients. Because skin symptoms associated with psoriasis often precede psoriatic
arthritis, dermatologists are uniquely positioned to play an important role in identifying and treating
patients with psoriatic arthritis. Proactive screening of patients with all severities of psoriasis for the signs
and symptoms of psoriatic arthritis is key to early diagnosis and intervention. In this review, we discuss the
clinical presentation, risk factors, and treatment options for psoriatic arthritis with axial involvement, with
the aim of helping dermatologists understand the disease and identify patients who might benefit from
further assessment, treatment, and/or referral to a rheumatology practice. ( J Am Acad Dermatol 2021;84:92-
101.)

Key words: axial disease; inflammatory arthritis; inflammatory back pain; psoriasis; psoriatic arthritis.

P soriasis is a chronic, inflammatory, immune-
mediated skin disorder associated with sig-
nificant morbidity, reduced quality of life
(QOL), and mortality1-3 that affects approximately
7.4 million adults in the United States.3 Comorbidities
are common in patients with psoriasis, and psoriatic
arthritis (PsA) is one of the most frequently
observed.4 Approximately 25% to 30% of patients
with psoriasis develop PsA,5,6 an inflammatory,
seronegative, musculoskeletal disease that
can involve the joints, entheses, or spine.7
Characteristics of PsA are heterogeneous and include
nail and skin changes, peripheral arthritis, enthesitis,
dactylitis, and axial spondyloarthritis (SpA)8,9; the
symptoms can present alone or in combination with
one another.10 PsA affects men and women equally,
and it commonly develops when patients are 30 to
50 years old.11 Like psoriasis, PsA is associated with
multiple comorbidities, including cardiovascular dis-
ease, metabolic syndrome, obesity, diabetes, depres-
sion, uveitis, and anxiety.12
PsA is a potentially erosive disease, and approx-
imately 50% of patients exhibit structural damage
and functional impairment within 2 years of initial
assessment13; many patients experience irreversible
joint damage and disability with disease progres-
sion.14,15 Axial involvement occurs in 25% to 70% of
patients with PsA,11,16 with exclusive axial involve-
ment in 5% of patients.11 Common symptoms
include inflammatory back pain (eg, pain that
improves with activity but worsens with rest, morn-
ing stiffness lasting [30 minutes).11,17 The diagnosis

From the Icahn School of Medicine at Mt Sinai, New Yorka; and
Brigham and Women’s Hospital, Harvard Medical School,
Boston.b
Funding sources: Supported by Novartis Pharmaceuticals Corpo-
ration, East Hanover, NJ.
Disclosure: Dr Gottlieb has served as a consultant and/or as an
advisory board member for Avotres Therapeutics, Beiersdorf,
Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Incyte,
Leo Pharmaceutical Industries, Lilly, Novartis, Sun Pharma, UCB,
and XBiotech; has received research or educational grants from
Boehringer Ingelheim, Incyte, Janssen, Novartis, UCB, and
XBiotech; and holds stock options with XBiotech. Dr Merola
has served as a consultant for AbbVie, Biogen Idec, Celgene,
GlaxoSmithKline, Janssen, Lilly, Merck, Novartis, Pfizer, Sa-
mumed, Sanofi Regeneron, Science 37, and UCB; as an
investigator for Biogen Idec, Incyte, Novartis, Pfizer, and Sanofi
Regeneron; and as a speaker for AbbVie.
IRB approval status: Not applicable.
Accepted for publication May 11, 2020.
Reprints not available from the authors.
Correspondence to: Alice B. Gottlieb, MD, PhD, Icahn School of
Medicine at Mount Sinai, 10 Union Square East, New York, NY
10003. E-mail: alice.gottlieb@mountsinai.org.
Published online July 31, 2020.
0190-9622
Ó 2020 by the American Academy of Dermatology, Inc. Published
by Elsevier Inc. This is an open access article under the CC
BY-NC-ND license (http://creativecommons.org/licenses/by-nc-
nd/4.0/).
https://doi.org/10.1016/j.jaad.2020.05.089

92
J AM ACAD DERMATOL Gottlieb and Merola 93
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is confirmed by physical examination and imaging defining features of inflammatory neck/back pain
(eg, sacroiliitis, spinal ossifications).11,17 Among (Fig 1),27,28 as well as limited mobility.17 However,
patients with axial PsA, cervical spinal mobility and 20% of patients show no symptoms of axial involve-
lateral flexion significantly decrease within 5 years if ment18,29; these patients are usually diagnosed with
18
untreated. Additionally, sacroiliitis worsens with PsA because they present with other PsA-related
time; 37% and 52% of patients develop grade 2 symptoms, such as dactylitis or arthritis.29,30
or higher sacroiliitis within 5 and 10 years, respec- Sacroiliitis is a common feature of axial PsA (25%-
tively.18 Therefore, early 50% of patients)31-33 and is
identification and treatment frequently asymmetric (73%
of patients with axial PsA is CAPSULE SUMMARY of patients).32 Patients may
critical. present with alternating pain
Cutaneous manifestations d
Psoriasis is an inflammatory immune over the sacroiliac joint/
of psoriasis can precede the disease associated with psoriatic arthritis, buttock, with the pain typi-
onset of PsA by approxi- a disease that can involve peripheral and cally lasting longer than
mately 3 to 8 years,19 and axial joints and cause permanent joint 20 minutes and being worse
1% to 3% of patients with damage and loss of function if untreated. during the second half of
psoriasis develop PsA annu- d Dermatologists play an important role in the night (Fig 1).27,33,34
5,20
ally. Therefore, dermatol- the early diagnosis and treatment of Sacroiliitis can be assessed
ogists play a critical role in psoriatic arthritis by proactively clinically by asking simple
early detection for patients screening patients with psoriasis. questions (eg, ‘‘Is your pain
with PsA.11 However, PsA is worse at night?’’ or ‘‘How
frequently underdiagnosed, long does your pain typically
with up to 41% of patients with psoriasis treated at last?’’) to determine if a patient’s symptoms are
dermatology centers having undiagnosed PsA.6,21 To characteristic of inflammatory sacroiliac joint pain
address this problem, the new American Academy of (Fig 1).
Dermatology/National Psoriasis Foundation guide- Comorbidities are common, with psoriasis being
lines emphasize the role of dermatologists in recog- the most frequent (80% of patients).9 Other comor-
nizing PsA and recommend proactive screening of bidities of axial PsA include uveitis and inflammatory
patients.4 Therefore, it is important that dermatolo- bowel disease (IBD). Uveitis occurs in 6% to 7% of
gists be familiar with the signs of PsA, including those patients with PsA but is more common (up to 33%) in
associated with axial involvement. Here, we review those with axial involvement.35 Uveitis in axial PsA is
axial PsA and describe its clinical presentation, risk more common in men, in younger patients (aged
factors, pathology, and treatment options. \34 years), and in those positive for human leuko-
cyte antigen (HLA)-B27.35 IBD occurs in 11% of
CLINICAL FEATURES OF AXIAL PsA patients with axial PsA and is significantly more
Axial involvement in PsA usually occurs in young common in patients with axial involvement than in
patients (\40 years old).22 Although axial PsA had those with peripheral-only PsA (2%).22
been thought to be more prevalent in men, an
analysis of the US Corrona PsA/Spondyloarthritis
Registrydwhich compared patients with PsA with IMPACT ON QOL
and without axial involvementdfound no significant Axial PsA has a significant impact on QOL and is
differences in the proportion of men and women associated with worse disease than that seen in
with axial involvement.23 patients without axial involvement.23 In an analysis
Most patients with PsA have preceding psoriasis, of the US Corrona Registry, patients with axial
but a small percentage (approximately 15%) have no involvement had more severe skin manifestations,
psoriasis at diagnosis.24 That proportion may be higher tender joint counts, more enthesitis, and
lower if one includes inverse/intertriginous psoria- worse disease activity.23 Similarly, patients with axial
sis, which occurs in less frequently examined areas PsA had worse pain than patients without axial
of body folds.25 Patients with PsA can also present involvement and had significantly impaired physical
with enthesitis, dactylitis (sausage digit), nail function and QOL (P \ .001).23 Patients with axial
11,22,23,26
changes, and peripheral arthritis. Typical involvement also had decreased work productivity,
symptoms of axial PsA include morning back/neck with significantly higher proportions of missed work
stiffness that lasts longer than 30 minutes and neck or time (10.0% vs 3.3%), overall work impairment
back pain that improves with activity and worsens (32.3% vs 16.8%) and overall activity impairment
after prolonged inactivity,11,17,18,23 which are (37.0% vs 18.1%; P \ .001 for all). Problems with
94 Gottlieb and Merola
Abbreviations used:
AS: ankylosing spondylitis
axSpA: axial spondyloarthritis
DMARD: disease-modifying antirheumatic drug
HLA: human leukocyte antigen
IBD: inflammatory bowel disease
IL: interleukin
NSAID: nonsteroidal anti-inflammatory drug
PASI75: 75% improvement in the Psoriasis Area
and Severity Index
PsA: psoriatic arthritis
QOL: quality of life
SpA: spondyloarthritis/
spondyloarthropathies
TNF: tumor necrosis factor
TNFi: tumor necrosis factor inhibitor
walking and self-care and feelings of anxiety and
depression were also common.23
RISK FACTORS
Clinical factors associated with axial PsA include
more-severe skin psoriasis, a young age at PsA onset,
and severe peripheral arthritis. In 1 study, severe skin
psoriasis (P = .041) and younger age at PsA onset
(P \ .001) correlated with developing sacroiliitis.32
Additionally, peripheral joint erosions were more
common in patients with asymmetric sacroiliitis,
suggesting a possible association between periph-
eral arthritis and axial involvement in patients with
PsA.32 This association was further suggested by
another study in which radiographic damage to
peripheral joints increased the risk of developing
axial PsA.36 IBD, a known comorbidity of psoriasis,4
is also a risk factor for PsA and other SpAs, with both
being more common in patients with Crohn’s dis-
ease.37,38 Sacroiliitis is estimated to occur in 12% to
46% of patients with IBD,37 and clinically silent
macroscopic and microscopic colitis occur in
approximately 60% of patients with axial SpA
(axSpA),37 emphasizing the gut-axial axis. Uveitis
has been identified as a risk factor for PsA, but its role
as a risk factor for axial involvement remains
unclear.39
A notable risk factor for axial PsA is the presence of
HLA-B27.36,40 HLA-B27 is a known key genetic
marker of ankylosing spondylitis (AS), is present in
more than 80% of patients with AS, and is the only
known genetic marker common to AS and axial
PsA.41 Although its prevalence is lower in patients
with PsA (20%),41 patients with axial PsA are signif-
icantly more likely to be HLA-B27 positive than
patients without axial involvement (P \ .001).22,23
Patients with axial PsA and uveitis were also more
likely to be HLA-B27 positive.35,42 Given these
observations, whether HLA-B27epositive patients
J AM ACAD DERMATOL
JANUARY 2021
with psoriasis have AS or axial PsA remains a matter
of debate. Interestingly, some studies have suggested
that HLA-B0801 is the predominant genetic marker
associated with axial PsA.32,43 Additional studies are
needed, but testing for HLA-B27 and/or HLA-B0801
may identify patients with axial PsA. However, HLA-
B27 testing is not indicated for all patients with
suspected PsA.
DIAGNOSIS OF AXIAL DISEASE IN PsA
To aid nonrheumatologist clinicians in identifying
patients with PsA, several simple and easy-to-
administer screening questionnaires have been
developed, including the Psoriasis Epidemiology
Screening Tool (Fig 2),44 the Toronto Psoriatic
Arthritis Screen (Fig 3),45 the Psoriatic Arthritis
Screening and Evaluation (Fig 4),46 and Early
Arthritis for Psoriatic Patients (Fig 4).47 These ques-
tionnaires help identify symptoms associated with
inflammatory arthritis (eg, swelling/stiffness) and
PsA (sausage digit) that might suggest referral to a
rheumatologist. Although these tools are not specific
for axial PsA, they can capture some information on
axial disease. For example, the Toronto Psoriatic
Arthritis Screen asks about back/neck pain and
stiffness history, the Psoriatic Arthritis Screening
and Evaluation asks about current back pain, and
Early Arthritis for Psoriatic Patients asks about
nocturnal back pain. The Psoriasis Epidemiology
Screening Tool does not include questions about
axial disease, but the accompanying figure allows
patients to mark any joints in the neck, upper/lower
portions of the back, or hips that have caused
discomfort; however, the figure is not commonly
used in clinical practice. Because most of these tools
are not free and take time to administer, patients may
not always be screened during medical visits.
Additionally, these tools have been found to have
only moderate accuracy (sensitivity, 65%-87%; spec-
ificity, 34%-85%).48,49 To help improve screening, we
have previously proposed using the mnemonic PSA
(for joint pain, stiffness after a period of inactivity/
sausage digit [dactylitis], axial involvement) before a
formal screening (Fig 5).30 The presence of 2 of these
features suggests PsA; stiffness (S) and axial involve-
ment (A) suggest axial PsA and should lead to formal
screening and/or referral to a rheumatologist.
JUVENILE AXIAL PsA
PsA may also develop in children, with axial
involvement occurring in approximately 20% of
patients and being more common in later-onset
than in early-onset juvenile PsA.50 Findings from
the Childhood Arthritis and Rheumatology Research
Alliance patient registry suggest that juvenile PsA is
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Fig 1. Characteristics of inflammatory neck or back pain and sacroiliac joint pain.27,28,33,34
an aggressive disease; 24.6% of children have joint
damage 4.6 years after symptom onset, despite more
than 50% of patients being treated with a biologic
disease-modifying anti-rheumatic drug (DMARD).50
Although juvenile SpA is more common in boys and
is associated with HLA-B27,51 juvenile PsA is more
common in girls and is not significantly associated
with HLA-B27.50 Uveitis, one of the criteria for
enthesitis/spondylitis-related juvenile idiopathic
arthritis,52 was present in 11% of patients with
juvenile PsA compared with 24% of patients with
juvenile SpA and 9% of those with juvenile periph-
eral PsA.53
PATHOGENESIS
The trigger for inflammation in axial PsA remains
unknown; however, evidence suggests a role for the
interleukin (IL) 23/IL-17 pathway. Dysregulation of
the IL-23/IL-17 axis has been observed in patients
with axSpA and those with AS.54,55 In addition,
preclinical studies have shown that genes associated
with axial disease, such as HLA-B27, may contribute
to excess tumor necrosis factor-a (TNFa) and IL-17
production.56 Therefore, development of therapies
for axial PsA has focused on TNF inhibitors (TNFis)
and agents targeting molecules in the IL-23/IL-17
pathway.
Gottlieb and Merola 95
TREATMENT
Treatment is based on international guidelines
developed by the Group for Research and
Assessment of Psoriasis and Psoriatic Arthritis, the
European League Against Rheumatism, Assessment of
SpondyloArthritis International SocietyeEuropean
League Against Rheumatism, and the American
College of Rheumatology/Spondylitis Association of
America/Spondyloarthritis Research and Treatment
Network.10,57-59 Most of the evidence supporting
treatment recommendations for axial PsA is derived
from studies in AS. Goals of treatment include
reducing pain, stiffness, and fatigue; improving and
maintaining spinal flexibility and normal posture;
improving functional capability; and maintaining the
ability to work, with a target of remission or minimal/
low disease activity.10,57-59
Nonsteroidal anti-inflammatory drugs (NSAIDS)
are the first-line recommended treatment for pain
and stiffness.10,57-59 Physiotherapy and sacroiliac
joint injections (if appropriate) can also be part of
the initial treatment approach; however, patients
should not be treated long term with systemic
glucocorticoids. If symptoms are not controlled by
NSAIDs, or if patients have high disease activity,
the guidelines recommend initiation of biologic
DMARDs. However, conventional DMARDs (eg,
methotrexate) are not routinely prescribed for
96 Gottlieb and Merola
Fig 2. The PEST screening questionnaire.44 Each positive
answer is assigned 1 point. A total of 3 or more points
indicates psoriatic arthritis. The axial joints that might be
affected are highlighted. PEST, Psoriasis Epidemiology
Screening Tool. (Reproduced from Ibrahim et al. Clin
Exp Rheumatol 2009;27:469-74. Copyright Clinical and
Experimental Rheumatology 2009.44)
patients with axial disease because they are not
efficacious.58
TNFis are usually recommended in patients who
do not respond to or are intolerant of NSAIDs.10,57-59
No data show the efficacy of TNFis specifically in
patients with axial PsA; however, a meta-analysis
found that TNFis improved disease activity and
functional capacity in both patients with AS and
those with nonradiographic axSpA.60 Available
TNFis include adalimumab, certolizumab pegol,
etanercept, golimumab, and infliximab.10,57-59 No
TNFi is recommended over another, although mono-
clonal antibodies (eg, infliximab, certolizumab
pegol, or adalimumab [which is approved in the
United States for uveitis]) are recommended over
etanercept in patients with IBD or recurrent
iritis.58,59,61 Furthermore, etanercept is less effective
for skin clearance in patients with PsA and psoriasis:
J AM ACAD DERMATOL
JANUARY 2021
at 24 weeks, a 75% improvement in the Psoriasis Area
and Severity Index (PASI75) was achieved by only
23% of patients using etanercept,62 whereas PASI75
rates in trials of other TNFis have been in the range of
59% to 65%.63-66 Etanercept is also associated with
lower PASI75 rates in patients with psoriasis (49% at
week 12)67; in contrast, PASI75 rates with infliximab,
certolizumab pegol, and adalimumab have ranged
from 71% to 88% (week 10 or 16).68-70 Interestingly,
very little variability has been observed in the pro-
portion of patients achieving a 20% improvement in
the American College of Rheumatology response
criteria in patients with PsA treated with these 4
agents (52%-59%).62-65 However, approximately 40%
of patients do not respond to TNFi therapy.71 In
these cases, patients can switch to a different TNFi58;
however, efficacy may be lower than that with the
first TNFi.72
Studies in AS also suggested that IL-17 inhibitors
could be effective in treating axial PsA.73 The phase 3
studies MEASURE1 (16 Week Efficacy and 2 Year
Long Term Safety and Efficacy of Secukinumab in
Patients With Active Ankylosing Spondylitis) (N =
371) and MEASURE2 (16 Week Efficacy and 5 Year
Long Term Efficacy, Safety and Tolerability of
Secukinumab in Patients With Active Ankylosing
Spondylitis) (N = 219) showed that secukinumab, a
selective IL-17A inhibitor, was superior to placebo in
reducing signs and symptoms of AS.73,74 To deter-
mine efficacy specifically in axial PsA, secukinumab
was evaluated in MAXIMISE (Study of the Efficacy
and Safety of Secukinumab in Participants With
Active Psoriatic Arthritis With Axial Skeleton
Involvement) (N = 498), the first randomized
controlled study to evaluate a biologic in axial
PsA.75 Patients with axial PsA and inadequate
response to NSAIDs were randomized to secukinu-
mab 300 mg, secukinumab 150 mg, or placebo.
Secukinumab provided rapid and significant
improvement of axial function and symptoms versus
placebo, with the proportion of patients achieving
an Assessment of SpondyloArthritis International
Society 20% response at week 12 being 63.1% with
secukinumab 300 mg and 66.3% with secukinumab
150 mg versus 31.3% with placebo (P \.0001).75 The
safety profile was similar across groups, and IBD was
uncommon in patients with PsA or AS treated with
secukinumab.76
Ixekizumab, a second IL-17A inhibitor, is also
approved for PsA and was recently approved for AS,
suggesting that ixekizumab could benefit patients
with axial PsA. Ixekizumab led to clinical improve-
ment and was better than placebo at improving AS in
patients who were naive to biologic DMARDs
(COAST-V [A Study of Ixekizumab (LY2439821) in
J AM ACAD DERMATOL Gottlieb and Merola 97
VOLUME 84, NUMBER 1

Fig 3. The Toronto Psoriatic Arthritis Screen.45 A score of 8 or more points indicates psoriatic
arthritis. The questions that refer to axial involvement are highlighted. Not available for free.
(Reproduced from Gladman et al45 with permission from BMJ Publishing Group Ltd and the
European League Against Rheumatism.)

Fig 4. The PASE and EARP questionnaires.46,47 Questions that can help identify axial
involvement are highlighted. Questionnaires not available for free. EARP, Early Arthritis for
Psoriatic Patients; PASE, Psoriatic Arthritis Screening and Evaluation.
98 Gottlieb and Merola J AM ACAD DERMATOL
JANUARY 2021

Fig 5. Psoriatic arthritis mnemonic: It’s as easy as PSA.30 (Photograph of the hand showing
dactylitis reproduced with permission of Dove Medical Press from Yamamoto T. Optimal
management of dactylitis in patients with psoriatic arthritis. Open Access Rheumatol 2015;7:55-
62.)

bDMARD-Naive Participants With Radiographic clinically meaningful improvements versus pla-

Axial Spondyloarthritis] [N = 341])77 and in those
previously treated with TNFis (COAST-W [A Study
of Ixekizumab (LY2439821) in TNF Inhibitor
Experienced Participants With Radiographic Axial
Spondyloarthritis] [N = 316]).78 Injection-site reac-
tions, upper respiratory tract infections, and naso-
pharyngitis were common adverse events. Although
these findings are promising for the treatment of
axial PsA, ixekizumab had not been evaluated
specifically in axial PsA at the time of this writing.
Findings from an open-label proof-of-concept
study suggested that ustekinumab, an antibody
targeting IL-12 and IL-23, might be efficacious in
AS.79 Ustekinumab was associated with a reduction
in symptoms of active disease, with 35% of patients
achieving inactive disease after 24 weeks of
treatment. However, subsequent phase 3 studies
evaluating ustekinumab in patients with radio-
graphic or nonradiographic axSpA were termi-
nated because ustekinumab did not achieve
key endpoints.80 Similarly, treatment with risanki-
zumab, a p19/IL-23 inhibitor, did not lead to
cebo in patients with active AS.81 These findings
suggest that IL-23 may not be a relevant target in
patients with axial PsA.
CONCLUSIONS
PsA, with or without axial involvement, is an
underdiagnosed and potentially debilitating disease
that greatly reduces patients’ functioning and QOL.
Early and appropriate treatment is essential in
delaying structural joint damage and maintaining
patient QOL and well-being. Dermatologists play a
crucial role in detecting PsA in their patients and in
treating or promptly referring patients to a rheuma-
tologist. Therefore, it is important for dermatologists
to proactively screen patients with psoriasis for
symptoms of PsA and to understand how to identify
signs of axial involvement in PsA (Figs 2-5), espe-
cially inflammatory back pain (Fig 1). Dermatologists
are encouraged to partner with patients, rheumatol-
ogists, and other specialists to achieve optimal
patient management.
J AM ACAD DERMATOL
VOLUME 84, NUMBER 1
The authors thank Karen Chinchilla, PhD, of
ArticulateScience LLC, Hamilton, NJ, for providing medical
writing support/editorial support, which was funded by
Novartis Pharmaceuticals Corporation, East Hanover, NJ, in
accordance with Good Publication Practice (GPP3) guide-
lines (http://www.ismpp.org/gpp3).
REFERENCES
1. Helmick CG, Lee-Han H, Hirsch SC, Baird TL, Bartlett CL.
Prevalence of psoriasis among adults in the U.S.: 2003-2006
and 2009-2010 National Health and Nutrition Examination
Surveys. Am J Prev Med. 2014;47:37-45.
2. Krueger G, Koo J, Lebwohl M, Menter A, Stern RS, Rolstad T.
The impact of psoriasis on quality of life: results of a 1998
National Psoriasis Foundation patient-membership survey.
Arch Dermatol. 2001;137:280-284.
3. Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis preva-
lence among adults in the United States. J Am Acad Dermatol.
2014;70:512-516.
4. Elmets CA, Leonardi CL, Davis DMR, et al. Joint AAD-NPF
guidelines of care for the management and treatment of
psoriasis with awareness and attention to comorbidities. J Am
Acad Dermatol. 2019;80:1073-1113.
5. Alinaghi F, Calov M, Kristensen LE, et al. Prevalence of psoriatic
arthritis in patients with psoriasis: a systematic review and
meta-analysis of observational and clinical studies. J Am Acad
Dermatol. 2019;80:251-265.
6. Mease PJ, Gladman DD, Papp KA, et al. Prevalence of
rheumatologist-diagnosed psoriatic arthritis in patients with
psoriasis in European/North American dermatology clinics. J
Am Acad Dermatol. 2013;69:729-735.
7. Taylor W, Gladman D, Helliwell P, et al. Classification criteria for
psoriatic arthritis: development of new criteria from a large
international study. Arthritis Rheum. 2006;54:2665-2673.
8. Sieper J, Poddubnyy D. Axial spondyloarthritis. Lancet. 2017;
390:73-84.
9. Coates LC, Helliwell PS. Psoriatic arthritis: state of the art
review. Clin Med (Lond). 2017;17:65-70.
10. Coates LC, Kavanaugh A, Mease PJ, et al. Group for Research
and Assessment of Psoriasis and Psoriatic Arthritis 2015
treatment recommendations for psoriatic arthritis. Arthritis
Rheumatol. 2016;68:1060-1071.
11. Gottlieb A, Korman NJ, Gordon KB, et al. Guidelines of care for
the management of psoriasis and psoriatic arthritis: section 2.
Psoriatic arthritis: overview and guidelines of care for treat-
ment with an emphasis on the biologics. J Am Acad Dermatol.
2008;58:851-864.
12. Ogdie A, Schwartzman S, Husni ME. Recognizing and man-
aging comorbidities in psoriatic arthritis. Curr Opin Rheumatol.
2015;27:118-126.
13. Kane D, Stafford L, Bresnihan B, FitzGerald O. A prospective,
clinical and radiological study of early psoriatic arthritis: an
early synovitis clinic experience. Rheumatology (Oxford). 2003;
42:1460-1468.
14. Husted JA, Tom BD, Farewell VT, Schentag CT, Gladman DD. A
longitudinal study of the effect of disease activity and clinical
damage on physical function over the course of psoriatic
arthritis: does the effect change over time? Arthritis Rheum.
2007;56:840-849.
15. Mease P, van der Heijde D, Landewe R, et al. Secukinumab
improves active psoriatic arthritis symptoms and inhibits
radiographic progression: primary results from the rando-
mised, double-blind, phase III FUTURE 5 study. Ann Rheum Dis.
2018;77:890-897.
Gottlieb and Merola 99
16. Gladman DD. Axial disease in psoriatic arthritis. Curr Rheuma-
tol Rep. 2007;9:455-460.
17. Baraliakos X, Coates LC, Braun J. The involvement of the spine
in psoriatic arthritis. Clin Exp Rheumatol. 2015;33:S31-S35.
18. Chandran V, Barrett J, Schentag CT, Farewell VT, Gladman DD.
Axial psoriatic arthritis: update on a longterm prospective
study. J Rheumatol. 2009;36:2744-2750.
19. Tascilar K, Aydin SZ, Akar S, et al. Delay between the onset of
psoriasis and arthritis in PsA patients from the PsART international
cohort [abstract]. Arthritis Rheumatol. 2019;71(Suppl 10):2854.
20. Christophers E, Barker JN, Griffiths CE, et al. The risk
of psoriatic arthritis remains constant following initial
diagnosis of psoriasis among patients seen in European
dermatology clinics. J Eur Acad Dermatol Venereol. 2010;24:
548-554.
21. Haroon M, Kirby B, FitzGerald O. High prevalence of psoriatic
arthritis in patients with severe psoriasis with suboptimal
performance of screening questionnaires. Ann Rheum Dis.
2013;72:736-740.
22. Jadon DR, Sengupta R, Nightingale A, et al. Axial disease in
psoriatic arthritis study: defining the clinical and radiographic
phenotype of psoriatic spondyloarthritis. Ann Rheum Dis. 2017;
76:701-707.
23. Mease PJ, Palmer JB, Liu M, et al. Influence of axial
involvement on clinical characteristics of psoriatic arthritis:
analysis from the Corrona Psoriatic Arthritis/Spondyloarthritis
Registry. J Rheumatol. 2018;45:1389-1396.
24. Ritchlin CT, Colbert RA, Gladman DD. Psoriatic arthritis. N Engl
J Med. 2017;376:957-970.
25. Merola JF, Li T, Li WQ, Cho E, Qureshi AA. Prevalence of
psoriasis phenotypes among men and women in the USA. Clin
Exp Dermatol. 2016;41:486-489.
26. Perez Alamino R, Maldonado Cocco JA, Citera G, et al. Differ-
ential features between primary ankylosing spondylitis and
spondylitis associated with psoriasis and inflammatory bowel
disease. J Rheumatol. 2011;38:1656-1660.
27. Rudwaleit M, Metter A, Listing J, Sieper J, Braun J. Inflamma-
tory back pain in ankylosing spondylitis: a reassessment of the
clinical history for application as classification and diagnostic
criteria. Arthritis Rheum. 2006;54:569-578.
28. Sieper J, van der Heijde D, Landewe R, et al. New criteria for
inflammatory back pain in patients with chronic back pain: a
real patient exercise by experts from the Assessment of
SpondyloArthritis International Society (ASAS). Ann Rheum
Dis. 2009;68:784-788.
29. Queiro R, Belzunegui J, Gonzalez C, et al. Clinically asymp-
tomatic axial disease in psoriatic spondyloarthropathy. A
retrospective study. Clin Rheumatol. 2002;21:10-13.
30. Cohen JM, Husni ME, Qureshi AA, Merola JF. Psoriatic arthritis:
it’s as easy as ‘‘PSA’’. J Am Acad Dermatol. 2015;72:905-906.
31. Gladman DD. Clinical, radiological, and functional assess-
ment in psoriatic arthritis: is it different from other inflam-
matory joint diseases? Ann Rheum Dis. 2006;65(Suppl 3):iii22-
iii24.
32. Haroon M, Winchester R, Giles JT, Heffernan E, FitzGerald O.
Clinical and genetic associations of radiographic sacroiliitis
and its different patterns in psoriatic arthritis. Clin Exp
Rheumatol. 2017;35:270-276.
33. Williamson L, Dockerty JL, Dalbeth N, McNally E, Ostlere S,
Wordsworth BP. Clinical assessment of sacroiliitis and HLA-B27
are poor predictors of sacroiliitis diagnosed by magnetic
resonance imaging in psoriatic arthritis. Rheumatology (Ox-
ford). 2004;43:85-88.
34. van den Berg R, de Hooge M, Rudwaleit M, et al. ASAS
modification of the Berlin algorithm for diagnosing axial
100 Gottlieb and Merola
spondyloarthritis: results from the Spondyloarthritis Caught
Early (SPACE)-cohort and from the Assessment of Spondyloar-
thritis international Society (ASAS)-cohort. Ann Rheum Dis.
2013;72:1646-1653.
35. Paiva ES, Macaluso DC, Edwards A, Rosenbaum JT. Character-
isation of uveitis in patients with psoriatic arthritis. Ann Rheum
Dis. 2000;59:67-70.
36. Chandran V, Tolusso DC, Cook RJ, Gladman DD. Risk factors for
axial inflammatory arthritis in patients with psoriatic arthritis. J
Rheumatol. 2010;37:809-815.
37. Fragoulis GE, Liava C, Daoussis D, Akriviadis E, Garyfallos A,
Dimitroulas T. Inflammatory bowel diseases and spondyloar-
thropathies: from pathogenesis to treatment. World J Gastro-
enterol. 2019;25:2162-2176.
38. Halling ML, Kjeldsen J, Knudsen T, Nielsen J, Hansen LK.
Patients with inflammatory bowel disease have increased risk
of autoimmune and inflammatory diseases. World J Gastro-
enterol. 2017;23:6137-6146.
39. Eder L, Haddad A, Rosen CF, et al. The incidence and risk
factors for psoriatic arthritis in patients with psoriasis: a
prospective cohort study. Arthritis Rheumatol. 2016;68:915-
923.
40. Brewerton DA, Caffrey M, Nicholls A, Walters D, James DC. HL-
A 27 and arthropathies associated with ulcerative colitis and
psoriasis. Lancet. 1974;1:956-958.
41. Feld J, Chandran V, Haroon N, Inman R, Gladman D. Axial
disease in psoriatic arthritis and ankylosing spondylitis: a
critical comparison. Nat Rev Rheumatol. 2018;14:363-371.
42. Queiro R, Morante I, Cabezas I, Acasuso B. HLA-B27 and
psoriatic disease: a modern view of an old relationship.
Rheumatology (Oxford). 2016;55:221-229.
43. Queiro R, Sarasqueta C, Belzunegui J, Gonzalez C, Figueroa M,
Torre-Alonso JC. Psoriatic spondyloarthropathy: a comparative
study between HLA-B27 positive and HLA-B27 negative dis-
ease. Semin Arthritis Rheum. 2002;31:413-418.
44. Ibrahim GH, Buch MH, Lawson C, Waxman R, Helliwell PS.
Evaluation of an existing screening tool for psoriatic arthritis in
people with psoriasis and the development of a new instru-
ment: the Psoriasis Epidemiology Screening Tool (PEST)
questionnaire. Clin Exp Rheumatol. 2009;27:469-474.
45. Gladman DD, Schentag CT, Tom BD, et al. Development and
initial validation of a screening questionnaire for psoriatic
arthritis: the Toronto Psoriatic Arthritis Screen (ToPAS). Ann
Rheum Dis. 2009;68:497-501.
46. Dominguez PL, Husni ME, Holt EW, Tyler S, Qureshi AA.
Validity, reliability, and sensitivity-to-change properties of
the psoriatic arthritis screening and evaluation questionnaire.
Arch Dermatol Res. 2009;301:573-579.
47. Tinazzi I, Adami S, Zanolin EM, et al. The early psoriatic arthritis
screening questionnaire: a simple and fast method for the
identification of arthritis in patients with psoriasis. Rheuma-
tology (Oxford). 2012;51:2058-2063.
48. Iragorri N, Hazlewood G, Manns B, Danthurebandara V,
Spackman E. Psoriatic arthritis screening: a systematic review
and meta-analysis. Rheumatology (Oxford). 2019;58:692-707.
49. Karreman MC, Weel A, van der Ven M, et al. Performance of
screening tools for psoriatic arthritis: a cross-sectional study in
primary care. Rheumatology (Oxford). 2017;56:597-602.
50. Zisman D, Gladman DD, Stoll ML, et al. The juvenile psoriatic
arthritis cohort in the CARRA registry: clinical characteristics,
classification, and outcomes. J Rheumatol. 2017;44:342-351.
51. Goirand M, Breton S, Chevallier F, et al. Clinical features of
children with enthesitis-related juvenile idiopathic arthritis/ju-
venile spondyloarthritis followed in a French tertiary care
J AM ACAD DERMATOL
JANUARY 2021
pediatric rheumatology centre. Pediatr Rheumatol Online J.
2018;16:21.
52. Martini A, Ravelli A, Avcin T, et al. Toward new classification
criteria for juvenile idiopathic arthritis: first steps, Pediatric
Rheumatology International Trials Organization international
consensus. J Rheumatol. 2019;46:190-197.
53. Hayworth JL, Turk MA, Nevskaya T, Pope JE. The frequency of
uveitis in patients with juvenile inflammatory rheumatic
diseases. Joint Bone Spine. 2019;86:685-690.
54. Wendling D. Interleukin-17 targeted therapies in axial spon-
dyloarthritis. Immunotherapy. 2015;7:1125-1128.
55. McGonagle DG, McInnes IB, Kirkham BW, Sherlock J, Moots R.
The role of IL-17A in axial spondyloarthritis and psoriatic
arthritis: recent advances and controversies. Ann Rheum Dis.
2019;78:1167-1178.
56. Glatigny S, Fert I, Blaton MA, et al. Proinflammatory Th17 cells
are expanded and induced by dendritic cells in
spondylarthritis-prone HLA-B27-transgenic rats. Arthritis
Rheum. 2012;64:110-120.
57. Gossec L, Smolen JS, Ramiro S, et al. European League Against
Rheumatism (EULAR) recommendations for the management
of psoriatic arthritis with pharmacological therapies: 2015
update. Ann Rheum Dis. 2016;75:499-510.
58. van der Heijde D, Ramiro S, Landewe R, et al. 2016 update of
the ASAS-EULAR management recommendations for axial
spondyloarthritis. Ann Rheum Dis. 2017;76:978-991.
59. Ward MM, Deodhar A, Akl EA, et al. American College of
Rheumatology/Spondylitis Association of America/Spondy-
loarthritis Research and Treatment Network 2015 recommen-
dations for the treatment of ankylosing spondylitis and
nonradiographic axial spondyloarthritis. Arthritis Rheum.
2016;68:282-298.
60. Callhoff J, Sieper J, Weiss A, Zink A, Listing J. Efficacy of
TNFalpha blockers in patients with ankylosing spondylitis and
non-radiographic axial spondyloarthritis: a meta-analysis. Ann
Rheum Dis. 2015;74:1241-1248.
61. Menter A, Strober BE, Kaplan DH, et al. Joint AAD-NPF
guidelines of care for the management and treatment of
psoriasis with biologics. J Am Acad Dermatol. 2019;80:1029-
1072.
62. Mease PJ, Kivitz AJ, Burch FX, et al. Etanercept treatment of
psoriatic arthritis: safety, efficacy, and effect on disease pro-
gression. Arthritis Rheum. 2004;50:2264-2272.
63. Mease PJ, Gladman DD, Ritchlin CT, et al. Adalimumab for the
treatment of patients with moderately to severely active
psoriatic arthritis: results of a double-blind, randomized,
placebo-controlled trial. Arthritis Rheum. 2005;52:3279-3289.
64. Mease PJ, Fleischmann R, Deodhar AA, et al. Effect of
certolizumab pegol on signs and symptoms in patients with
psoriatic arthritis: 24-week results of a phase 3 double-blind
randomised placebo-controlled study (RAPID-PsA). Ann Rheum
Dis. 2014;73:48-55.
65. Antoni C, Krueger GG, de Vlam K, et al. Infliximab improves
signs and symptoms of psoriatic arthritis: results of the
IMPACT 2 trial. Ann Rheum Dis. 2005;64:1150-1157.
66. Kavanaugh A, Husni ME, Harrison DD, et al. Safety and efficacy
of intravenous golimumab in patients with active psoriatic
arthritis: results through week twenty-four of the GO-VIBRANT
study. Arthritis Rheumatol. 2017;69:2151-2161.
67. Leonardi CL, Powers JL, Matheson RT, et al. Etanercept as
monotherapy in patients with psoriasis. New Engl J Med. 2003;
349:2014-2022.
68. Gottlieb AB, Evans R, Li S, et al. Infliximab induction therapy
for patients with severe plaque-type psoriasis: a randomized,
J AM ACAD DERMATOL
VOLUME 84, NUMBER 1
double-blind, placebo-controlled trial. J Am Acad Dermatol.
2004;51:534-542.
69. Menter A, Tyring SK, Gordon K, et al. Adalimumab therapy for
moderate to severe psoriasis: a randomized, controlled phase
III trial. J Am Acad Dermatol. 2008;58:106-115.
70. Gottlieb AB, Blauvelt A, Thaci D, et al. Certolizumab pegol for
the treatment of chronic plaque psoriasis: results through 48
weeks from 2 phase 3, multicenter, randomized, double-
blinded, placebo-controlled studies (CIMPASI-1 and CIMPASI-
2). J Am Acad Dermatol. 2018;79:302-314.
71. Noureldin B, Barkham N. The current standard of care and the
unmet needs for axial spondyloarthritis. Rheumatology (Ox-
ford). 2018;57:vi10-vi17.
72. Lie E, van der Heijde D, Uhlig T, et al. Effectiveness of
switching between TNF inhibitors in ankylosing spondylitis:
data from the NOR-DMARD register. Ann Rheum Dis. 2011;70:
157-163.
73. Baeten D, Sieper J, Braun J, et al. Secukinumab, an interleukin-
17A inhibitor, in ankylosing spondylitis. N Engl J Med. 2015;
373:2534-2548.
74. Braun J, Baraliakos X, Deodhar A, et al. Secukinumab shows
sustained efficacy and low structural progression in ankylosing
spondylitis: 4-year results from the MEASURE 1 study. Rheu-
matology (Oxford). 2019;58:859-868.
75. Baraliakos X, Coates LC, Gossec L, et al. Secukinumab improves
axial manifestations in patients with psoriatic arthritis and
inadequate response to NSAIDs: primary analysis of the
MAXIMISE trial. Ann Rheum Dis. 2019;78:195-196.
76. Schreiber S, Colombel JF, Feagan BG, et al. Incidence rates of
inflammatory bowel disease in patients with psoriasis,
Gottlieb and Merola 101
psoriatic arthritis and ankylosing spondylitis treated with
secukinumab: a retrospective analysis of pooled data from
21 clinical trials. Ann Rheum Dis. 2019;78:473-479.
77. van der Heijde D, Cheng-Chung Wei J, Dougados M, et al.
Ixekizumab, an interleukin-17A antagonist in the treatment of
ankylosing spondylitis or radiographic axial spondyloarthritis
in patients previously untreated with biological disease-
modifying anti-rheumatic drugs (COAST-V): 16 week results
of a phase 3 randomised, double-blind, active-controlled and
placebo-controlled trial. Lancet. 2018;392:2441-2451.
78. Deodhar A, Poddubnyy D, Pacheco-Tena C, et al. Efficacy and
safety of ixekizumab in the treatment of radiographic axial
spondyloarthritis: sixteen-week results from a phase III ran-
domized, double-blind, placebo-controlled trial in patients
with prior inadequate response to or intolerance of tumor
necrosis factor inhibitors. Arthritis Rheumatol. 2018;71:
599-611.
79. Poddubnyy D, Hermann KG, Callhoff J, Listing J, Sieper J.
Ustekinumab for the treatment of patients with active
ankylosing spondylitis: results of a 28-week, prospective,
open-label, proof-of-concept study (TOPAS). Ann Rheum Dis.
2014;73:817-823.
80. Deodhar A, Gensler LS, Sieper J, et al. Three multicenter,
randomized, double-blind, placebo-controlled studies evalu-
ating the efficacy and safety of ustekinumab in axial spondy-
loarthritis. Arthritis Rheumatol. 2019;71:258-270.
81. Baeten D, Ostergaard M, Wei JC, et al. Risankizumab, an IL-23
inhibitor, for ankylosing spondylitis: results of a randomised,
double-blind, placebo-controlled, proof-of-concept, dose-
finding phase 2 study. Ann Rheum Dis. 2018;77:1295-1302.