Clinics in Dermatology (2018) 36, 551–560

Psoriatic arthritis and the dermatologist: An

approach to screening and clinical evaluation
Arianna Zhang, BA a , Drew J.B. Kurtzman, MD b,c,⁎, Lourdes M. Perez-Chada, MD d ,
Joseph F. Merola, MD, MMSc e
a
Department of Dermatology, Brigham and Women's Hospital, Harvard University, Cambridge, Massachusetts, USA
b
Division of Dermatology, The University of Arizona College of Medicine, Tucson, Arizona, USA
c
Division of Dermatology, St. Elizabeth Physicians, Florence, Kentucky, USA
d
Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
e
Department of Dermatology, Division of Rheumatology, and Department of Medicine, Brigham and Women’s Hospital, Harvard
Medical School, Boston, Massachusetts, USA

Abstract Psoriatic arthritis is a common form of inflammatory arthritis that frequently accompanies psoriasis
of the skin—up to 30% of patients with psoriasis are affected. Recognition of the clinical features of psori-
atic arthritis is critical, as delayed detection and untreated disease may result in irreparable joint injury, im-
paired physical function, and a significantly reduced quality of life. Recent epidemiologic studies have also
supported that psoriatic arthritis is associated with cardiometabolic and cerebrovascular comorbidities, in-
cluding coronary heart disease, diabetes mellitus, hypertension, dyslipidemia, and cerebrovascular acci-
dents, further highlighting the importance of identifying affected patients. Dermatologists are poised for
the early detection of psoriatic arthritis, as psoriasis predates its development in as many as 80% of patients.
In an effort to further acquaint dermatologists and other clinicians with psoriatic arthritis, this review pro-
vides a detailed overview, emphasizing its salient clinical features, and discusses classification criteria, val-
idated screening tools, and simple musculoskeletal examination maneuvers that may facilitate earlier
detection and treatment of the disorder.
© 2018 Elsevier Inc. All rights reserved.

Introduction
Psoriatic arthritis (PsA) is an inflammatory arthritis that
commonly accompanies plaque psoriasis of the skin with a
prevalence as high as 30% among this patient group.1 The
spectrum of psoriatic disease encompasses involvement of
the skin, nails, peripheral and axial joints, points of enthesis
⁎ Corresponding author. Tel.: +1 859 371 3376.
E-mail address: drewkurtzman@gmail.com (D.J.B. Kurtzman).
(sites of tendon insertion into bone and/or ligaments), and dac-
tylitis (“sausage digit”). PsA often leads to a marked reduction
in patient quality of life due to physical disability from joint
damage, fatigue, cardiovascular (and other) comorbidity, and
psychologic stress, particularly when left untreated.2,3 In the
majority of cases (84%), patients experience skin manifesta-
tions before clinical manifestations of arthritis develop. As a
result, patients initially seek treatment from dermatologists.1
For this reason, dermatologists represent the first line of care
in psoriatic disease diagnosis and intervention. Emerging

https://doi.org/10.1016/j.clindermatol.2018.04.011
0738-081X/© 2018 Elsevier Inc. All rights reserved.
552
evidence has shown that delays in PsA diagnosis are
associated with worse functional and physical outcomes
for patients.4
PsA is likely underdiagnosed—as many as 30% of patients
with psoriasis have undiagnosed PsA.5 Greater vigilance in
screening for PsA in psoriasis patients visiting the dermatolo-
gy clinic could significantly reduce the rate of undiagnosed
PsA and thus improve patient quality of life and outcomes.
The focus of this review is to provide an overview of PsA
for the dermatologist, and to promote PsA awareness and
screening in dermatology clinics. To that end, we review the
toolset that the dermatologist has at her or his disposal for
PsA screening and diagnosis, including classification criteria,
validated screening tools, and musculoskeletal examination
maneuvers that may be used in clinic to facilitate earlier detec-
tion and treatment of PsA.
Why should dermatologists screen for PsA?
PsA is a systemic, potentially disabling, and destructive
disease. Although at one point thought to be a relatively be-
nign and nonprogressive condition compared with rheumatoid
arthritis, PsA results in chronic systemic inflammation and has
been shown to lead to erosive joint damage in 40% to 57% of
patients and significantly affects quality of life.2,6
In addition to the risk of joint damage leading to physical
disability and psychological stress, PsA is coprevalent with
cardiovascular and cerebrovascular disease, as well as type 2
diabetes mellitus, hyperlipidemia, and hypertension and is as-
sociated with increased mortality.2 The multiplicity of comor-
bidities associated with PsA makes treatment decisions for
patients complex.3 The co-occurrence of PsA with these vari-
ous comorbid diseases often necessitates multidisciplinary
care that requires coordination between the rheumatologist
and dermatologist, as well as the primary care physician, car-
diologist, mental health provider, and other specialists to mon-
itor and appropriately formulate an effective treatment plan.
Delays in diagnosis of PsA are associated with worse
physical functional outcomes
Destructive arthritis tends to develop early in PsA patients,
with an estimated 67% of patients demonstrating at least one
joint erosion at initial presentation to a rheumatologist.4,7 In
a prospective study conducted in 2003, erosive joint damage
was observed in 27% of patients at initial assessment and in
47% of patients within 2 years.2,6 The same study reported that
the remission rate for patients prescribed disease-modifying
antirheumatic drug (DMARD) was 26% after 1 year, whereas
spontaneous (ie, DMARD-free) remission was less than half
of that, occurring in only 11% to 12% of patients. There was
a substantial reduction in patient-reported Health Assessment
Questionnaire (HAQ) assessments of pain and disability with
treatment from a mean score of 0.63 at initial assessment to
A. Zhang et al.
0.13 after 1 year that was associated with an increase in
DMARD prescription from 12% to 59% in the same period.6
These findings were further supported by a retrospective
study conducted in 2015, in which investigators divided PsA
patients into two groups—early or late consulters—depending
on whether the patient was seen by a rheumatologist within or
beyond 6 months from the onset of clinical manifestations.4
Results from the multivariate regression analysis used in this
study indicated significantly worse peripheral joint disease
(eg, erosive changes) as well as poorer HAQ scores among
those presenting later in the course of disease, which was con-
sistent with the previous report. Such findings highlight the re-
lationship between early detection and improved patient
outcomes and, conversely, late detection with worse
outcomes.
The dermatologist is particularly well situated for
early detection of PsA
A number of studies have highlighted the critical role der-
matologists play in early PsA detection. PsA is uncommon
in the general population, with an overall prevalence of
0.25%; however, it is common among patients with plaque
psoriasis.8 Estimates of PsA prevalence rates among patients
with plaque psoriasis range between 6% and 41% depending
on diagnostic parameters and study designs.9 An estimated
80% to 84% of PsA patients have psoriatic skin disease that
precedes clinical manifestations of arthritis.1,10 As a result,
most patients initially seek treatment from a dermatologist.11
This pattern of presentation, in which psoriasis predates PsA,
positions dermatologists at the front line for the early detection
of PsA.
Indeed, ample evidence suggests that greater vigilance in
PsA screening at dermatology clinics could reduce the rate
of undiagnosed PsA among psoriasis patients. In one study,
949 patients diagnosed with psoriasis in a dermatology clinic
were subsequently seen by a rheumatologist. Out of this sam-
ple, 285 (30%) had PsA according to rheumatologist assess-
ment, and of these patients, only 59% had been previously
diagnosed with PsA by a dermatologist. 5 In a subsequent
study, 29% of psoriasis patients visiting a dermatology clinic
had undiagnosed PsA.12 One of the explanations behind the
historically significant rates of unidentified PsA is a lack of fa-
miliarity with the tools to identify PsA among primary care
physicians and dermatologists.13 Taken together, these find-
ings suggest that dermatologists may play a crucial role in ad-
dressing the high rates of undiagnosed PsA, which in turn
would ameliorate the burden of the disease.
Overview of PsA
PsA is a polygenic disorder that is influenced by genetic,
immunologic, and environmental factors. Although the patho-
genesis of PsA remains poorly understood, it has been
Psoriatic arthritis and the dermatologist
proposed that the process driving PsA is similar to that of pla-
que psoriasis, in which environmental stressors, such as infec-
tion, drug use, or trauma, may trigger a systemic inflammatory
reaction in susceptible hosts. The point of enthesis, in which T-
cells, dendritic cells, mast cells, macrophages, and neutrophils
infiltrate the enthesium, plays an important role in the onset of
PsA and has been suggested as the site of origin.2,14 Cellular
and inflammatory mediators are involved in both psoriasis
and PsA. In particular, tumor necrosis factor (TNF)-α and in-
terleukin (IL)-1β, IL-9, IL-17, IL-18, IL-22, and IL-23 repre-
sent important proinflammatory cytokines that are
upregulated at the sites of skin lesions, synovial membranes,
and joint fluid of psoriasis and PsA patients.15–17
Several human leukocyte antigen (HLA) genes (a part of
the major histocompatibility complex) have been shown to
be associated with specific PsA phenotypes. Axial phenotypes
of PsA have been strongly associated with HLA-B27 haplo-
types, whereas peripheral arthritis has been associated with
HLA-B39. In addition, HLA-B39 haplotypes have been asso-
ciated with progressive disease, whereas HLA-Cw6 and HLA-
DRB1*07 have been associated with more mild PsA, but ear-
lier onset and more severe skin disease.2 The heritability of
PsA has also been described, with first-degree relatives of
PsA patients in Iceland, Finland, and Canada having a 30- to
55-fold greater risk of developing PsA compared with the gen-
eral population.2,18,19 Unsurprisingly, the prevalence of PsA
varies by country—among the respective general populations,
it is as low as 0.001% in Japan and as high as 0.42% in Italy.20
Psoriasis phenotypes associated with an increased PsA risk
include nail, scalp, and inverse (or flexural) phenotypes. By
contrast, the presence of other disease phenotypes (eg, palmo-
plantar disease) do not appear to increase the risk of PsA de-
velopment above baseline.21,22 Obesity is also linked to a
higher risk of developing PsA and appears to be associated
with unfavorable responses to biologic agents.22 In particular,
a study has shown that each additional unit of BMI above 25
was associated with a 5.3% increase in risk of PsA and that
an elevated BMI (N30) at 18 years of age predicted a threefold
greater probability of developing PsA later in adulthood.23
This finding is consistent with preclinical data demonstrating
that adipocytes are capable of secreting inflammatory cyto-
kines such as TNF-α, which promotes proinflammatory
Table 1 Differentiating inflammatory from noninflammatory arthritis
Inflammatory arthritis
Stiffness after a period of inactivity N30-60 min
Improves with activity
Redness, warmth, swelling (inflammatory signs)
Episode/flare duration
Presence of systemic clinical manifestations (fatigue, uveitis, etc)
Response to anti-inflammatory therapy
Family history of inflammatory arthritis or related condition
(rheumatoid arthritis, psoriasis/psoriatic arthritis, inflammatory bowel disease, etc)
553
activity in synovial tissues in PsA joint models.24 Additional-
ly, there appears to be a positive relationship between percent-
age of affected body surface area of plaque psoriasis and risk
of PsA.22
Classification and identification of PsA
Because PsA is an inflammatory arthritis, it most common-
ly presents with redness, warmth, swelling, and pain of affect-
ed joints, along with stiffness after inactivity for longer than 30
to 60 minutes that improves with activity. By contrast, clinical
manifestations of noninflammatory arthritis (eg, osteoarthritis)
tend to worsen with activity, particularly toward the end of day
(Table 1). Tracking the duration of morning stiffness experi-
enced by a patient over time can be a useful measure of disease
activity, and the development of joint pain and stiffness in a
patient with plaque psoriasis should prompt a more thorough
evaluation. Differentiating inflammatory from noninflammato-
ry arthritis clinical manifestations is a key clinical consideration
that can aid the dermatologist in deciding whether to screen
and refer a patient with psoriasis with possible PsA to a rheuma-
tologist. A simple screening mnemonic, “PSA,” has been pub-
lished to remind dermatologists and other clinicians of the
most basic clinical features that may help to distinguish inflam-
matory from noninflammatory arthritis (Figure 1). The presence
of two out of three of these features should prompt the use of a
formal validated screening tool (see below) and/or referral to a
rheumatologist for evaluation.25
Although specific diagnostic criteria for PsA have not yet
been developed, the Classification Criteria for Psoriatic Arthri-
tis (CASPAR) is currently used to classify cases of PsA for
clinical trial enrollment. Familiarity with these criteria may
further acquaint the dermatologist with some of the key fea-
tures of PsA. In addition to signs or clinical manifestations
of inflammatory joint disease (presence of joint, spine, or
entheseal inflammatory arthritis), a score ≥3 based on evi-
dence of skin psoriasis, psoriatic nail dystrophy, a negative test
result for rheumatoid factor (seronegativity), presence of dac-
tylitis, and radiologic evidence of juxta-articular new bone for-
mation is required for a patient to meet these criteria (Table 2).
Degenerative/osteoarthritis
No significant period of stiffness after inactivity
Worsens with activity, end of the day
Specific joints patterns (eg, base of thumb
involvement with hand osteoarthritis)
554 A. Zhang et al.

Fig. 1 A useful mnemonic developed to promote awareness of psoriatic arthritis clinical manifestations. Psoriatic arthritis is a clinical diagnosis,
and clinical manifestations that characterize the disease include joint pain, joint stiffness, “sausage digit,” and/or axial spine involvement.25

Screening for PsA active PsA in psoriasis patients. It consists of five binary (yes
or no) questions and allows the patient to mark affected joints
Driven by the need for early identification and treatment of on a caricature figure. Derived from the longer Psoriatic Ar-
PsA, a number of screening tools have been developed and thritis Questionnaire, the PEST design has the advantage of
validated, including the Psoriasis Epidemiology Screening simplicity and ease-of-use. During its development, the
Tool (PEST),26 Psoriatic Arthritis Screening and Evaluation PEST showed 94% and 78% sensitivity and specificity, re-
(PASE),27 and Toronto Psoriatic Arthritis Screening (2) spectively, for detecting active PsA.26
[ToPAS (2)],28,29 compared in the CONTEST study.13,30 The Psoriatic Arthritis Screening and Evaluation (PASE)
These are patient-reported questionnaires that can be adminis- questionnaire can also be administered to psoriasis patients
tered in advance of or during office visits. These screening to screen for PsA. This self-reported assessment consists of
tools showed moderate-to-high sensitivity and specificity in 15 questions, scored on a 1 (strongly disagree) to 5 (strongly
the initial validation studies, but subsequent validation studies agree) Likert scale, assessing both clinical manifestations and
in other populations showed mixed results with somewhat functional impairment.27,31 It is capable of quantifying the se-
lower sensitivity and specificity for detecting PsA.9 In the case verity of PsA and has been validated for use in both rheumatol-
of a negative result, but with a strong clinical suspicion of PsA, ogy and dermatology clinics.31 The PASE has a sensitivity of
patients should still be referred to a rheumatologist for evalua- 82% and specificity of 73% for identifying PsA.13
tion. Details on the sensitivity and specificity as well as char- The Toronto Psoriatic Arthritis Screening (2) [ToPAS (2)]
acteristics of each instrument are presented in Table 3. questionnaire differs from the PASE instrument in that it can
The Psoriasis Epidemiology Screening Tool (PEST) is a be used to assess for PsA in both psoriasis patients and the gen-
concise, patient-completed instrument designed to screen for eral population. The ToPAS (2) is a self-assessment consisting
of 13 binary (yes or no) questions, with each question having
additional subsections. The ToPAS (2) survey includes pic-
Table 2 CASPAR criteria tures that depict skin lesions of psoriasis, dactylitis, and arthrit-
ic joints to help the patient with answering questions about the
CASPAR criteria for identifying psoriatic arthritis: patient has
presence of psoriasis spectrum disease.29 ToPAS (2) has a sen-
joint, spine, or entheseal inflammatory articular disease AND a
score ≥3 points according to following categories:
sitivity and specificity of 87% and 93%, respectively, for
PsA.13
Points
1 Evidence of psoriasis (choose one)
Table 3 Comparison of psoriatic arthritis screening question-
a) Current psoriasis 2
naires [PEST, PASE, and ToPAS (2)]13
b) Personal history of psoriasis 1
c) Family history of psoriasis 1 PEST PASE ToPAS (2)
d) No history of psoriasis 0
No. of true positive 36 35 36
2 Psoriatic nail dystrophy—pitting, onycholysis, 1
No. of false positive 93 91 104
hyperkeratosis
No. of true negative 55 57 44
3 Negative test result for rheumatoid factor 1
No. of false negative 11 12 11
4 Dactylitis (choose one)
Sensitivity 0.766 0.745 0.766
a) Current swelling of an entire digit 1
Specificity 0.372 0.385 0.297
b) History of dactylitis 1
AUC 0.61 0.594 0.554
c) No history of dactylitis 0
5 Radiologic evidence of juxta-articular new bone 1 PEST, Psoriasis Epidemiology Screening Tool; PASE, Psoriatic Arthritis
formation Screening and Evaluation; ToPAS, Toronto Psoriatic Arthritis Screening;
AUR, Area Under Curve.
CASPAR, Classification Criteria for Psoriatic Arthritis. Adapted from Coates et al.13
Psoriatic arthritis and the dermatologist
The CONTEST study13 compared the utility of PEST, PASE,
and ToPAS (2). The results from this study showed that the
performance differences between PEST, PASE, and ToPAS
(2) questionnaires were negligible and not significant, con-
cluding that either of the three assessments were effective
screening instruments; however, the CONTEST study investi-
gators did note high false-positive rates with each survey, often
resulting in the identification of other musculoskeletal dis-
eases, particularly noninflammatory arthritis. Despite high
false-positive rates, the authors ultimately argued in favor of
casting a wider net (ie, screening with higher false-positive
rates may be acceptable) to avoid overlooking individuals with
PsA to ensure that they are appropriately referred to a rheuma-
tologist. Importantly, the CONTEST study results indicated
that cases of entheseal and axial PsA in particular are more dif-
ficult to identify using these questionnaires.
Clinical evaluation of PsA
The diagnosis of PsA relies mainly on clinical evaluation.
In addition to the patient clinical manifestations reviewed
above, clinical signs and physical examination can further sup-
port the diagnosis; where originally described, there were 5
clinical patterns of PsA: oligo- and polyarthritis, distal inter-
phalangeal (DIP) joint predominant disease, arthritis mutilans,
spine or axial predominant disease (spondyloarthropathy), and
symmetrical/asymmetric disease (Table 4).32
Some of the classic subtypes of PsA are easily recogniz-
able, including oligoarthritis, DIP disease, and arthritis muti-
lans (Figure 2). Although some discrepancy remains
regarding the proportion of oligoarthritis to polyarthritis (gen-
erally held that oligoarthritis is the most common presentation
of the disorder), one analysis suggested that the pattern may
change with disease progression and therefore these patterns
may reflect the stage of disease at the time of diagnosis rather
than disparate phenotypes.33
Oligoarthritis appears to be the predominant pattern at ini-
tial diagnosis, which may be seen in up to 60% of PsA pa-
tients, but one longitudinal cohort study found that up to
67% of oligoarthritis PsA later demonstrated features of poly-
arthritis.34 Axial involvement (inflammatory back disease/
spondylitis) is generally estimated to occur in 30% to 50% of
PsA patients and can be identified through detailed history-
taking and simple musculoskeletal examinations.35
Table 4 Clinical presentation patterns of psoriatic arthritis32
Clinical pattern Percentage of patients
Asymmetric oligoarthritis 50
Symmetrical polyarthritis 40
Spinal column involvement 40
Distal interphalangeal arthritis 5 instructed to bend forward fully (in full flexion), while keeping
Arthritis mutilans 5 the knees extended. The distance between the two marks is
555
A targeted musculoskeletal examination for the
dermatologist
Dermatologists should feel comfortable going beyond
history-gathering alone to determine whether or not a patient
has PsA. With some practice, even a rudimentary musculo-
skeletal examination can yield very helpful information about
the presence of inflammatory arthritis, enthesitis, and other
PsA features that will aid in workup, referral, and treatment
decisions. Performing a musculoskeletal examination is
particularly warranted in a patient presenting with nail, scalp,
and inverse psoriasis, phenotypes known to be associated with
a greater risk of PsA. The presence of psoriasis of the nails is
common among PsA patients. A retrospective analysis
showed that, of 1661 patients with PsA, 739 (44.5%) had
psoriatic nail disease.36 Some experts even believe that
psoriasis involving the nails is synonymous with enthesitis/
DIP joint disease and may even predict enthesitis at distant
sites.37,38 Joint examination of the fingers and toes, entheseal
points, and spinal column is important when evaluating for
PsA.
Dactylitis, or a “sausage digit,” is characterized by two or
more contiguous swollen small joints of a single digit on the
hands or feet and can be assessed for by a simple examination
(Figure 2). Comparing affected versus unaffected contralateral
sides of the hands and feet can be particularly helpful when
assessing for dactylitis. The Leeds Dactylitis Index (LDI) takes
into account the circumference of affected and unaffected fin-
gers to provide a useful quantitative measure of dactylitis.39,40
Enthesitis refers to inflammation of sites of tendon, liga-
ment, and joint capsule fiber insertions into bone. An assess-
ment for enthesitis can be performed by applying pressure to
entheseal points, including the knee, foot, pelvis, spine, ribc-
age, shoulder, Achilles tendon, and elbow and determining
whether or not tenderness is present.40 A number of indices
that measure the presence and/or severity of enthesitis are
available and include the Leeds Enthesitis Index (LEI),41 the
Spondyloarthritis Research Consortium of Canada (SPARCC)
Enthesitis Index,42 and the Maastricht Ankylosing Spondylitis
Enthesitis Score (MASES).43
Assessment for axial disease involves examination of the
spinal column. This can be accomplished by a number of val-
idated maneuvers, including the lateral lumbar flexion and the
modified Schober’s test.44,45 The lateral lumbar flexion test is
administered by measuring the distance between the patient’s
middle finger and the floor when the patient’s back is posi-
tioned against a wall, and again when the patient bends to
the side while maintaining straight knees (Figure 3). The two
measurements are averaged to produce a score that can be
followed over time. The modified Schober’s test involves the
examiner marking the midpoint of an artificial line joining
the patient’s posterior and superior iliac crests, followed by a
second mark made 10 cm above the first while the patient is
remeasured, and the difference between the original
556 A. Zhang et al.

Fig. 2 Clinical depictions of classic subtypes of psoriatic arthritis. Distal interphalangeal (DIP) arthritis of the middle finger (A); note concurrent
psoriasis plaques of the skin. Arthritis mutilans form of psoriatic arthritis with “telescoping” change of the fourth digit of the left hand (B). Rheu-
matoid arthritis–like pattern of psoriatic arthritis (C). Pencil-in-cup deformity of the thumb noted by plain film radiography (D). Nail changes
(onycholysis and oil spots) of the affected nail (E). Dactylitis (sausage digit) of the second toe in a patient with psoriatic arthritis (F).

measurement and the second measurement constitutes the final
score (Figure 4). Ranges for a healthy individual are 4 cm or
more, whereas individuals with axial disease display reduced
excursion. An additional simple screening maneuver includes
evaluation of the patient’s neck range of motion in all direc-
tions, with restriction suggesting the need for further evalua-
tion for axial involvement.
Some other important principles to keep in mind for pa-
tients with PsA include defining joint tenderness and swelling,
determining which anatomic sites are to be examined (includ-
ing entheseal points), and assessing range of motion (including
of the axial spine). Peripheral PsA tends to involve the
shoulders, proximal interphalangeal and metacarpal joints,
wrists, knees, ankles, and midtarsal and metatarsal joints, and
these sites are particularly important to examine in a patient
suspected of having PsA. In addition to range of motion exam-
inations, routine palpation while assessing for joint tenderness
and swelling are helpful.
To determine tenderness in a joint, the examiner should use
their thumb to exert ~4 kg/cm2 of pressure on the joint, which
is enough pressure to cause the whitening of the examiner’s
nailbeds.40 Pain that is elicited is defined as tenderness. Joint
swelling is defined as swelling of the soft tissues of a joint
along the joint margins, often reducing the range of motion
Psoriatic arthritis and the dermatologist 557

Fig. 3 Lateral lumbar flexion test. (A) Measure the distance between the patient’s middle finger and the floor when the patient’s back is posi-
tioned against a wall. (B) Ask the patient to bend to the left, holding her/his knees extended, trying to edge as far as the knee. (C) Ask the patient to
bend to the right, holding her/his knees extended, trying to edge as far as the knee. Average the two measurements to obtain a final score.

Fig. 4 Modified Schober’s test. (A) Mark the midpoint of an artificial line joining the patient’s posterior and superior iliac crests, followed by a
second mark made 10 cm above the first. (B) Ask the patient to bend forward fully (in full flexion), while keeping the knees extended. Remeasure
the distance between the two marks. Calculate the difference between the original measurement and the second measurement to obtain a final
score.
558
at that joint. Joint swelling indicates synovial effusion. It
should be noted that joint swelling is not synonymous with
bony swelling and deformity of the joint. Joint swelling can
be determined by inquiring about decreased range of motion,
such as decreased dorsiflexion of the wrist or decreased elbow
extension. Fluctuation in the degree of swelling is also a com-
mon feature that may be patient-reported or clinician-detected.
Other assessments that can support the diagnosis
of PsA
Several tests can be helpful in parsing out the differential
diagnosis of other arthritides as well as potentially offering
some diagnostic and prognostic information to the treating cli-
nician. Tests alone cannot be used to exclude the possibility of
PsA. Commonly used but sometimes confusing laboratory ab-
normalities in PsA may include the presence of hyperuricemia
(increased incidence among psoriasis/PsA patients) and posi-
tive rheumatoid factor and anticyclic citrullinated peptide anti-
body (anti-CCP) testing, which may be positive in 8% to 12%
of patients with PsA despite being commonly thought of as
rheumatoid arthritis specific-testing.32 In addition, serum in-
flammatory markers such as C-reactive protein (CRP) may
be elevated and erythrocyte sedimentation rates (ESR) may
be prolonged in individuals with PsA, although this is not uni-
formly true for all PsA patients. According to a retrospective
analysis examining 1306 Italian patients with PsA, only
52.2% and 52.6% of patients with PsA demonstrated elevated
levels of ESR or CRP, respectively.2,46,47 Elevated inflamma-
tory markers, however, are useful for predicting more aggres-
sive disease and erosive PsA, which may inform treatment
decisions.47
The differential diagnosis of PsA is broad and can be chal-
lenging. For this reason, we often emphasize the need to at
least distinguish between features of inflammatory and nonin-
flammatory disease as an important primary consideration
when first evaluating the psoriasis patient. Once the nature of
the arthritis (ie, inflammatory or not) has been determined,
the subsequent evaluation and/or referral to the rheumatologist
should be directed toward clarifying musculoskeletal com-
plaints. Further complicating the clinical picture is the in-
creased coprevalence with PsA of conditions that may mimic
PsA, such as fibromyalgia, gout, and osteoarthritis.9,48
Radiographically, PsA differs from several other forms of
arthritis—the simultaneous presence of erosions and concur-
rent new bone formation at joint margins appears to be specific
to PsA2; however, inflammatory osteoarthritis and some other
osteoarthritic changes, particularly at the distal interphalangeal
joints, can lead to diagnostic confusion. Radiographic changes
need to be considered in the context of other clinical signs and
clinical manifestations, including the presence of nail changes
or supportive imaging modalities such as ultrasonography or
magnetic resonance imaging (MRI). Patterns of joint involve-
ment may also be helpful to distinguish PsA from other forms
of inflammatory arthritis; for example, involvement of the base
A. Zhang et al.
of the thumb is commonly associated with osteoarthritis and not
PsA.49 Ultrasonography and MRI can also play an important
role in both early detection and monitoring of progression in
the peripheral joints and spinal structures.50 Ultrasonography
has a particularly unique role in the evaluation of enthesitis
when performed by experienced sonographers.51
Treatment
The presence of PsA affects therapeutic decisions in a pa-
tient with preexisting plaque psoriasis. Treatments should be
tailored to achieve clinical remission, improving patients’
health and quality of life, and limiting the extent of erosive
damage.52 Such choices for the psoriatic disease patient can
be complex, because patients may present with comorbid
and other coprevalent conditions. Potential drug interactions
must also be considered. Importantly, some therapies that are
effective for plaque psoriasis and rheumatoid arthritis may be
ineffective or less effective for PsA, or for certain specific fea-
tures of PsA.2
A detailed discussion of the management of PsA is beyond
the scope of this review, but certain management principles
should be kept in mind. Monitoring for the activity and pro-
gression of disease by tracking the duration of stiffness in the
morning as well as other assessments of pain and range of mo-
tion can inform treatment decisions. For more mild clinical
manifestations and nonerosive disease, nonsteroidal anti-
inflammatory drugs (NSAIDs) and other conservative mea-
sures are typically indicated. In individuals with moderate or
more severe disease, nonbiologic DMARDs (such as
methotrexate) as well as a newer targeted synthetic oral and bi-
ologic DMARDs (eg, phosphodiesterase inhibitors, TNF-α in-
hibitors, and inhibitors of IL-17A and IL-12/23) should be
considered.2 Although a precise understanding of the patho-
physiology of PsA remains unknown, clinical benefits
of TNF-α inhibitor therapy appear to extend beyond relief of
joint clinical manifestations in the long-term (eg, halt erosive
disease) and may possibly attenuate cardiovascular
comorbidities.2,53
In cases of rapidly progressive, advanced disease, and/or
lack of comfort with management, immediate referral to rheu-
matology is warranted. In 2015 the members of the Group for
Research and Assessment of Psoriasis and Psoriatic Arthritis
(GRAPPA) performed a formal literature review to publish a
set of updated treatment recommendations for the major clini-
cal manifestation patterns of PsA, to which the reader is re-
ferred for a more in-depth treatment discussion.52 Additional
resources with detailed treatment plans can also be found on
the GRAPPA and National Psoriasis Foundation websites. Fi-
nally, new treatment guidelines for PsA from the American
College of Rheumatology (ACR) were proposed at the 2017
annual meeting in San Diego, California, and will be forth-
coming in an upcoming publication.
Psoriatic arthritis and the dermatologist
Conclusions
PsA remains underdiagnosed among psoriasis patients.
Left untreated, PsA can result in severe morbidity and irrevers-
ible physical limitations. Because PsA is often preceded by
skin manifestations, dermatologists are well positioned to
mitigate the impact of PsA by recognizing the early signs of
PsA, monitoring for its development in patients with estab-
lished plaque psoriasis, and ensuring that patients receive
disease-modifying treatments soon after the onset of clinical
manifestations. After minimal training, simple musculoskele-
tal examinations can be performed by dermatologists to aid
in the clinical diagnosis of PsA. The treatment of PsA is
nuanced and requires consideration of a variety of factors,
often necessitating multidisciplinary care from dermatologists,
rheumatologists, and other specialists working collectively to
minimize the impact of the disease.
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