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Clinical manifestations and diagnosis of psoriatic arthritis

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2017. | This topic last updated: Feb 12, 2016.

INTRODUCTION Psoriatic arthritis (PsA) is an inflammatory arthritis associated with psoriasis [1]. It was initially
considered a variant of rheumatoid arthritis, but subsequently emerged as a distinct clinical entity [2]. Historically,
seronegativity for rheumatoid factor (RF) had been a requirement for the diagnosis; however, over 10 percent of patients with
uncomplicated psoriasis and up to 15 percent of the normal population have RF present in their serum. As a result, the term
usually seronegative arthritis is most suitable for PsA [3,4].

The clinical manifestations and diagnosis of PsA are discussed here. The pathogenesis and treatment of this disorder and
overviews of the clinical manifestations, diagnosis, and treatment of psoriasis are presented separately. (See "Pathogenesis
of psoriatic arthritis" and "Treatment of psoriatic arthritis" and "Epidemiology, clinical manifestations, and diagnosis of
psoriasis" and "Treatment of psoriasis".)

EPIDEMIOLOGY Psoriatic arthritis (PsA) affects women and men equally, with an incidence of approximately 6 per
100,000 per year and a prevalence of about 1 to 2 per 1000 in the general population [1,3,5-8]. Estimates of the prevalence
of psoriatic arthritis among patients with psoriasis have ranged from 4 to 30 percent [8-13]. These estimates have some
limitations, as indicated by a 2008 systematic review of reports from 1987 to 2006 that found marked variability of the
reported incidence and prevalence estimates in the general population and suggested that different definitions, as well as
geography, may contribute to the variability [14]. Similar concerns apply to the analyses of patients with psoriasis.

A multicenter trial in Europe of 1560 patients with psoriasis estimated that 31 percent of the patients would have PsA after 30
years of psoriasis [15]. In this study, the risk of developing PsA did not decrease with time. Another study of 1511 patients
with psoriasis from academic and community dermatology practices in Germany identified 21 percent of the patients as
having PsA [16]. Using the internationally agreed-upon Classification Criteria for Psoriatic Arthritis (CASPAR) criteria
(see 'Classification criteria' below), which were first proposed in 2006, the estimated prevalence of PsA among patients with
psoriasis in two large general practices in the United Kingdom was 14 percent [17]. A prospective, four-year study of patients
with psoriasis who did not have PsA at presentation found an incidence of newly diagnosed PsA, also based upon the
CASPAR criteria, of almost 2 percent per year [18]. In this study, the severity of psoriasis, the presence of nail lesions, and
the presence of scalp and intergluteal lesions were more likely to occur in those with PsA.

The frequency of inflammatory back pain and axial spondyloarthritis in patients with psoriasis were examined using data from
the US Centers for Disease Control and Prevention National Health and Nutrition Examination Survey (NHANES) for 2009 to
2010, which included 148 patients with psoriasis among 5103 patients who were queried regarding issues related to back
pain [19]. The patients with psoriasis exhibited a significantly higher prevalence of inflammatory back pain and
spondyloarthritis (about 17 versus 5 and 14 versus 2 percent, respectively).

Among patients presenting with previously undiagnosed arthritis, PsA is present in a small minority. As an example, in one
prospective study of 1018 patients with early synovitis, PsA was diagnosed in 129 patients (13 percent), a minority of whom
(6 percent) did not have psoriasis at presentation [20].

A prospective study of patients with psoriasis, who did not have arthritis at presentation and were then followed annually,
found the annual incidence of PsA to be 2.7 to 3.2 percent; the lower number was based upon confirmation by a
rheumatologic assessment and use of the CASPAR criteria (see 'Classification criteria' below), while the higher number
included those patients as well as patients screening positive on a validated screening questionnaire (see 'Screening and
classification' below) who were unavailable for confirmatory in-person evaluation by the study rheumatologists [21].

CLINICAL MANIFESTATIONS Patients with psoriatic arthritis (PsA) present with pain and stiffness in the affected joints.
Morning stiffness lasting more than 30 minutes occurs in one-half of patients. The stiffness is accentuated with prolonged
immobility and is alleviated by physical activity. A history of psoriasis is present in about 70 percent of patients presenti ng
with arthritis.

On physical examination, stress pain, joint line tenderness, and effusions in the affected joints are present, often in an
asymmetric distribution [22,23]. The distal interphalangeal (DIP) joints and spine are each affected in 40 to 50 percent of
cases [5]. About 15 percent of patients with PsA will have evidence of psoriasis on examination despite lacking a history of
known psoriatic skin disease.

Patients with PsA may be less tender on physical examination than patients with other inflammatory arthritides such as
rheumatoid arthritis [24]. As a result, they may present with joint deformity without a significant degree of pain.

Major clinical features

Joint manifestations

Patterns of arthritis PsA may involve peripheral joints, axial joints, or both. It most frequently presents as a polyarthritis
or (less often) as an oligoarthritis; however, it has several other patterns of joint involvement that, while less common, are
much more typical of PsA than other disorders. Enthesitis, tenosynovitis, and dactylitis may also occur.

The clinical patterns, which were originally described by Moll and Wright, include [2]:

Distal arthritis, characterized by involvement of the DIP joints (picture 1A-B)


Asymmetric oligoarthritis, in which less than five small and/or large joints are affected in an asymmetric distribution
Symmetric polyarthritis, similar to and, at times, indistinguishable from rheumatoid arthritis
Arthritis mutilans, characterized by deforming and destructive arthritis (picture 2 and image 1)
Spondyloarthritis (SpA), including both sacroiliitis and spondylitis

Some patients present with more than one pattern, and many change the pattern of their arthritis during follow-up [25-27].
Most of the patients in the original description had an oligoarticular presentation [2]. However, subsequent studies have not
found the same distribution in all patient populations [28]. Although the disease may occur as a peripheral
arthritis and/or SpA, the SpA is usually present in association with peripheral joint involvement and occurs alone in only 2 to 4
percent of patients.

Distal arthritis and arthritis mutilans are considered most specific for PsA, but they are not the most common patterns seen
[5,28,29]. Distal involvement alone occurs in less than 20 percent of cases and may be associated with SpA, while arthritis
mutilans can occur with any of the patterns.

Because the clinical patterns described above can change over time in an individual patient, the clinical manifestations of
PsA are most commonly described using the following clinical domains [30]:

Peripheral arthritis
Axial disease
Enthesitis
Dactylitis
Skin and nail disease

Periarticular disease Other common rheumatologic features of PsA include tenosynovitis and soft tissue inflammation
similar to that seen in other forms of SpA (or seronegative arthritides), such as enthesitis and dactylitis:

Enthesitis Enthesitis (inflammation at the site of the insertion of tendons, ligaments, and synovium into bone), eg, of
the Achilles tendon, the plantar fascia, and the pelvic bones. Subclinical Achilles tendinitis, detected
ultrasonographically, is more common in those with psoriasis than in healthy persons [31,32]. Assessment tools for
enthesitis have been developed for use in research. While some work better in enthesitis of ankylosing spondylitis,
others work better for PsA [33].
Tenosynovitis Tenosynovitis of the flexor tendons of the hands, of the extensor carpi ulnaris, or at other sites.
Dactylitis Dactylitis, characterized by diffuse swelling of an entire finger or toe, often termed a sausage digit.
Dactylitis is defined as uniform swelling of the soft tissues between the metacarpophalangeal and interphalangeal
joints, such that the digits are swollen diffusely. In dactylitis, joint swelling, which may be present, can no longer be
recognized independently [34]. Sausage digits occur in nearly one-half of patients with PsA and are associated with an
increased risk of progressive radiographic joint damage [35]. This abnormality is thought to result from inflammation of
soft tissues, including the tendon sheaths, and from the concomitant inflammation of the adjacent joints [36]. This
finding is suggestive of PsA (picture 3). A research tool to quantify dactylitis has been developed and has proven to be
reliable and sensitive to change [37].

Relation between arthritis and skin lesions The arthritis appears after the onset of skin lesions in the majority of
patients. However, the arthritis precedes the skin disease in approximately 13 to 17 percent of patients, and skin lesions are
present but have not been diagnosed in an additional 15 percent [3]. In one study the psoriasis skin phenotypes associated
with a higher risk of PsA were scalp lesions (hazard ratio [HR] 3.9, 95% CI 2.2-6.9), nail dystrophy (HR 2.9, 95% CI 1.7-5.1),
and intergluteal/perianal lesions (HR 2.4, 95% CI 1.3-4.2) [38]. The clinical manifestations of psoriasis are described
separately. (See "Epidemiology, clinical manifestations, and diagnosis of psoriasis", section on 'Clinical manifestations'.)

There is a weak relationship between the severity of skin disease and arthritic involvement [39]. Only a minority of patients
note a relationship between the activity of the skin and joint manifestations [3,4], although some studies have suggested that
PsA occurs more commonly among patients with severe psoriasis [3,10,40]. Many patients with severe PsA have few skin
manifestations, while other patients present with severe skin psoriasis and have either no joint disease or only minimal joint
inflammation.

Nail lesions Characteristic features of psoriasis affecting the nail bed and nail matrix include nail pits, onycholysis, nail
bed hyperkeratosis, and splinter hemorrhages [41]. The nail pits and onycholysis that occur in PsA are indistinguishable from
the nail lesions that occur in uncomplicated psoriasis. Nail lesions occur in 80 to 90 percent of patients with PsA [4,39],
compared with 46 percent of those with psoriasis uncomplicated by arthritis [4]. Nail changes include:

Pits, which are sharply defined depressions in the plate caused by shedding of nail plate cells. They look as if
someone has taken a pin and pricked the nail several times (picture 4). Pits usually occur in large numbers and involve
several nails.
Onycholysis, separation of the nail from its bed, which may involve the whole or only part of the nail. This change
occasionally has to be differentiated from a fungal infection by sending nail scrapings for fungal cultures.
Other lesions, which include leukonychia, red spots in the lunula, and nail plate crumbling [41].

The severity of psoriatic nail involvement may correlate with the extent and severity of both skin and joint disease and has
been reported to be more common in those with DIP joint arthritis [42], although the extent of skin disease, in general, has
not correlated with the degree of joint disease [39]. A study using a validated nail psoriasis severity index found that nail
involvement correlated with many clinical features of PsA, such as global severity and the number of tender or swollen joints
[41].

Pitting edema Swelling of the hands or feet with pitting edema is sometimes a presenting feature of PsA. In a case
control study involving 183 patients with PsA and 366 controls with other rheumatologic disorders (excluding other
spondyloarthropathies), the prevalence of pitting edema was significantly higher in those with PsA (21 versus 5 percent) [43].
The edema was often asymmetrical and occasionally preceded joint involvement.

Clinically apparent chronic lymphedema (which may be nonpitting) is a rare extraarticular manifestation of PsA, and
lymphatic obstruction has been confirmed in some cases using lymphoscintigraphy [44,45]. However, similar symmetrical
swelling of the upper extremities due to extensive tenosynovitis in the absence of impaired lymphatic function has also been
described [45]. (See "Clinical features and diagnosis of peripheral lymphedema", section on 'Inflammatory disorders'.)

Ocular involvement Ocular inflammation, including uveitis and conjunctivitis, occurs in some patients with PsA, as it does
with other chronic inflammatory joint disorders, particularly the spondyloarthritides. In one study, conjunctivitis was reported in
about 20 percent of patients and uveitis in 7 percent [46]. Uveitis may present insidiously with visual impairment or acutely
with a painful red eye.

In one report, compared with the uveitis typically seen in other patients with SpA, the uveitis associated with PsA was more
frequently bilateral, posterior to the lens, insidious in onset, chronic in duration, and more common in females, although all of
these findings were still characteristic of less than half of the patients with uveitis [47]. Uveitis can occur in patients with
peripheral arthritis only; those with axial SpA and PsA are more often male and human leukocyte antigen (HLA)-B*27-
positive. Uveitis is discussed in more detail elsewhere. (See "Uveitis: Etiology, clinical manifestations, and diagnosis", section
on 'Systemic inflammatory diseases'.)

Laboratory findings Laboratory findings in PsA are nonspecific, consistent with the acute phase response and the
degree and chronicity of inflammation; there are no laboratory findings that are characteristic of PsA and distinguish it from
other forms of inflammatory arthritis or systemic autoimmune rheumatic disease. Autoantibodies such as rheumatoid factor
(RF), antinuclear antibodies (ANA), and anti-citrullinated peptide antibodies (ACPA) are present in a minority of patients.

Acute phase reactants are elevated in about 40 percent of patients. An elevated sedimentation rate and leukocytosis are
seen in about one-third of patients, reflecting a nonspecific inflammatory response. Anemia can be induced either by the
chronic disease or by iron deficiency resulting from prolonged use of nonsteroidal antiinflammatory drugs (NSAIDs) [3].

RF is found in 2 to 10 percent of patients with psoriatic arthritis. ANAs are found at low titer (1/40) in nearly 50 percent of
patients and at levels considered clinically significant (1/80) in 14 percent; anti-double-stranded DNA is found in 3 percent of
patients with PsA in the absence of exposure to biologic agents that inhibit tumor necrosis factor (TNF) [48]. Both RF and
ANA also occur in patients with psoriasis uncomplicated by arthritis and may reflect the immunologic response in this
disease.

ACPA, which are associated with rheumatoid arthritis and detected by assays for anti-cyclic citrullinated peptide (anti-CCP)
antibodies, have been found in 8 to 16 percent of patients with PsA; they are most frequently found in patients with
erosive and/or polyarticular disease, but may be present in patients with severe psoriasis in the absence of arthritis [49-52].

HLA-B*27 is associated with PsA, where it is one of the genetic markers that identifies patients destined to develop PsA
among patients with psoriasis [53,54]. It may be useful diagnostically (see 'Diagnosis' below); while HLA-B*27 is associated
with spondylitis, the latter may not be symptomatic. HLA-C*06 and other markers are associated with both psoriasis and PsA.
Although HLA-C*06 is present in lower frequency in patients with PsA than in those with psoriasis alone, and is associated
with later onset of PsA, it is not generally useful diagnostically in routine clinical practice.

Imaging findings Radiographic changes can develop in the course of PsA that exhibit a striking and characteristic pattern
usually not seen in other forms of inflammatory arthritis, with the coexistence of erosive changes and new bone formation
which may occur within the same joint or in different joints within the same digit; other typical radiological changes include
lysis of the terminal phalanges; fluffy periostitis, as well as new bone formation, at the site of enthesitis; gross destruction of
isolated joints; pencil-in-cup appearance; and the occurrence of both joint lysis and ankylosis in the same patient (image 2)
[3,55].

The presence of radiologic changes early in the course of PsA suggests either very aggressive disease or arthritis of longer
duration than that reported by the patient. Radiological damage was observed in two-thirds of patients at their first visit to the
authors (DG) PsA clinic in an academic health center [3], and in 27 percent of early PsA patients seen in Dublin [20].
Magnetic resonance imaging (MRI) may be more sensitive than routine radiography in detecting articular, periarticular, and
soft-tissue inflammation [56,57]. Using MRI, distinct abnormalities characterized by marked inflammation in the adjacent bone
marrow and soft tissues, combined with the detection of inflammation of entheses in joints felt to be clinically not inflamed,
suggest that enthesitis may be the primary lesion in PsA, although this interpretation is controversial [58,59]. While MRI
findings suggestive of moderate to severe sacroiliitis are found in more than one-third of patients, these imaging findings are
poor predictors of clinical symptoms; MRI evidence of sacroiliitis does correlate with decreased spinal mobility and with
longer duration of disease [60].

PsA is associated with a decrease in bone mass, as indicated by bone mineral density testing; this may lead to osteoporosis
and to an increased risk of fractures [61].

Comorbidities The risk of cardiovascular disease is increased in patients with PsA [62,63]. This has been further
documented in a large population-based longitudinal study of patients in the United Kingdom, which involved 8706 patients
with PsA, 41,752 patients with rheumatoid arthritis, 138,424 patients with psoriasis, and 81,573 controls [64]. The risk of
major adverse cardiovascular events (cardiovascular death, myocardial infarction, and stroke) was significantly increased in
patients with PsA who had not received disease-modifying antirheumatic drugs (DMARDs) compared with controls, after
adjustment for traditional cardiovascular risk factors (HR 1.24, 95% CI 1.03-1.49). A similar trend among DMARD-treated
patients with PsA did not reach statistical significance. Results were similar to those seen among patients with rheumatoid
arthritis and severe psoriasis.

Psoriasis is associated with a number of comorbidities, including an increased risk of the metabolic syndrome, hypertension,
diabetes, atherosclerosis, malignancy, hepatic and pulmonary disorders, and psychiatric disease. These conditions may also
be increased in patients with PsA, but are not as well-studied in this population. The comorbidities of psoriasis are reviewed
in detail separately. (See "Comorbid disease in psoriasis".)

DIAGNOSIS

Diagnosis The diagnosis of psoriatic arthritis (PsA) can generally be made in a patient who has both psoriasis and an
inflammatory arthritis in a pattern typical of PsA (see 'Patterns of arthritis' above). Several additional factors also require
consideration before establishing or excluding the diagnosis:

Other forms of arthritis can occur in patients with psoriasis. These conditions, such as rheumatoid arthritis,
osteoarthritis, gout, reactive arthritis, and the arthritis of inflammatory bowel disease should be excluded as the cause
of the patients syndrome. This can generally be done based upon the pattern of joint involvement, laboratory testing,
imaging, and synovial fluid analysis (see 'Differential diagnosis' below). Gout may occasionally coexist with PsA.
Certain clinical features suggest psoriatic arthritis in the absence of psoriasis (psoriatic arthritis sine psoriasis) [65]:
Distal joint involvement
Asymmetric distribution
The presence of nail lesions (eg, pitting or onycholysis) or hidden psoriatic plaques (eg, in the scalp, gluteal fold,
or umbilicus)
Dactylitis
Family history of psoriasis
Presence of human leukocyte antigen (HLA)-C*06, although it is not commonly used in routine clinical practice

The diagnostic evaluation depends in part upon the clinical presentation and initial findings that may raise suspicion for
particular alternative diagnoses, but should generally include:

History A thorough medical history should be obtained, with particular attention to a history of skin disease,
description of involved joints, symptoms of enthesitis (eg, Achilles tendinopathy or plantar fasciitis) or sausage digits
(ie, dactylitis), eye disease, a history consistent with inflammatory back pain (eg, onset under age 40, worse at night
with morning stiffness that is better with activity), history of gout or nephrolithiasis, response to medications, medication
use for other conditions (eg, diuretics, which may predispose to gout), and family history of psoriasis, PsA, and other
arthritic disorders.
Physical examination A thorough physical examination should be performed, with particular attention to the
pattern of peripheral and axial joint involvement, characteristics of involved joints (eg, presence of active inflammation
or alternatively of chronic bone changes such as Heberdens nodes), enthesitis, dactylitis, skin disease, and
rheumatoid nodules or tophi. Hidden psoriatic lesions should be sought if there is no overt evidence or history of
psoriasis.
Laboratory testing Laboratory testing should be obtained to determine if there is evidence of systemic
inflammation and to exclude other conditions. The following tests should be obtained, although none are diagnostic:
Complete blood count with differential and platelet count
Blood urea nitrogen, creatinine, uric acid, and a urinalysis
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
Rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) antibody, and antinuclear antibody (ANA)
HLA-B27 testing, which should be obtained in patients with psoriasis who present with arthritis and in patients in
whom PsA is suspected despite the absence of psoriasiform skin lesions
In patients with psoriasis who present with arthritis and others in whom PsA is suspected, HLA-B27 testing may be
helpful, as it is one of the genetic markers that identify patients likely to develop PsA, even though it is not diagnostic.
Additionally, spondylitis, for which risk is increased in the presence of the HLA-B*27 allele, may not be symptomatic.
Arthrocentesis and synovial fluid analysis - Synovial fluid testing should include cell count and differential, Gram
stain and culture, and crystal examination.
Imaging Radiographs of affected joints and the spine (if affected) should be obtained. Additional imaging may be
useful if there is uncertainty regarding whether enthesitis is present, such as ultrasonography (if adequate expertise is
available) or magnetic resonance imaging (MRI).

Screening and classification

Screening questionnaires A number of screening questionnaires have been developed to identify patients with PsA in
dermatology or general practice [66]. Several were developed to identify PsA among patients with psoriasis [67-70], while the
Toronto Psoriatic Arthritis Screen (ToPAS) was developed to identify patients with PsA regardless of the setting [71]. These
instruments are similar in terms of sensitivity and specificity and should be used to identify patients who should be seen by a
rheumatologist.

Classification criteria Classification criteria have been developed for use in epidemiologic studies and clinical trials.
(See 'Classification criteria' below.)

DIFFERENTIAL DIAGNOSIS Psoriatic arthritis (PsA) can mimic the findings in other arthritides, but can usually be
distinguished from these conditions based upon the clinical and laboratory evaluation, sometimes aided by imaging findings
in patients with more longstanding disease. Major conditions that should be considered in the differential diagnosis include:

Rheumatoid arthritis Patients with PsA in the form of a polyarthritis can present in a fashion that may be
indistinguishable from rheumatoid arthritis. However, involvement of the distal interphalangeal (DIP) joints, an
asymmetric distribution of joint disease, spondyloarthritis (SpA), sausage digits, new bone formation on radiographs,
cutaneous findings, and the characteristic nail manifestations of PsA all help to distinguish it from rheumatoid arthritis
[72]. Only a small number of patients with PsA will test positive for rheumatoid factor (RF) or anti-citrullinated peptide
(anti-CCP) antibodies, while these tests are positive in a majority of patients with rheumatoid arthritis. (See "Diagnosis
and differential diagnosis of rheumatoid arthritis".)
Reactive arthritis - Asymmetric oligoarthritis, enthesitis, sausage digits, and back pain can be seen in patients with
either reactive arthritis (formerly called Reiter syndrome) or PsA. However, unlike reactive arthritis, a history of an
antecedent infectious illness, with either genitourinary symptoms of urethritis or a dysenteric illness, would not be
characteristic of PsA. In addition, some skin lesions may differ (although others may be similar), and human leukocyte
antigen (HLA)-B27 positivity occurs more commonly in patients with reactive arthritis, but can also occur in PsA.
(See "Reactive arthritis".)
Arthritis of inflammatory bowel disease The peripheral and axial arthritis associated with inflammatory bowel
disease may occur in a very similar pattern to that seen in PsA; patients with either may exhibit symmetric or
asymmetric oligoarthritis or sacroiliitis. Uveitis may occur in either condition and the frequency of psoriasis may be
increased in patients with Crohns disease. Additionally, patients with PsA without bowel symptoms can have
microscopic lesions in the bowel even when the gut mucosa is macroscopically normal. However, inflammatory bowel
disease can usually be suspected based upon clinical findings and confirmed with endoscopic investigation and biopsy.
Additionally, the nail disease and DIP joint involvement that may occur in PsA are not characteristics of arthritis
associated with inflammatory bowel disease, and radiographic findings may differ. (See "Dermatologic and ocular
manifestations of inflammatory bowel disease", section on 'Rare dermatologic diseases' and "Dermatologic and ocular
manifestations of inflammatory bowel disease", section on 'Uveitis' and "Clinical manifestations and diagnosis of
arthritis associated with inflammatory bowel disease and other gastrointestinal diseases".)
Ankylosing spondylitis - Spinal disease that occurs in patients with PsA may be difficult to distinguish from
ankylosing spondylitis [72,73]. Peripheral features of SpA, such as enthesitis and dactylitis, can occur in either
condition. However, the presence of psoriasis and some radiographic features may help distinguish the two disorders.
PsA is more often associated with the presence of asymmetric sacroiliitis, non-marginal syndesmophytes, asymmetric
syndesmophytes, more frequent involvement of the cervical spine, and less frequent involvement of the lumbar spine.
(See "Diagnosis and differential diagnosis of axial spondyloarthritis (ankylosing spondylitis and non-radiographic axial
spondyloarthritis) in adults".)
Gout Both PsA and gout can present as an acute monoarthritis or oligoarthritis, and psoriasis can be associated
with hyperuricemia. The diagnosis of gout can be confirmed by finding monosodium urate crystals on examination of
the synovial fluid. However, PsA and gout can coexist, and recognition of other findings that suggest PsA, such as nail
changes, prominent DIP joint disease (especially in the absence of distal lower extremity joint disease), enthesitis,
dactylitis, and axial disease would support the diagnosis of PsA in addition to gout in patients with positive findings on
crystal examination (See "Clinical manifestations and diagnosis of gout".)
Osteoarthritis Both PsA and osteoarthritis may be characterized by involvement of the DIP joints, which may
sometimes exhibit some inflammatory characteristics and can mimic PsA. PsA as the cause of DIP joint involvement
can generally be distinguished from osteoarthritis with Heberdens nodes by the nodular bony change of osteoarthritis,
the more diffuse swelling of the joint in PsA, and the presence of other findings of PsA, such as characteristic nail
changes, inflammatory oligoarticular, polyarticular, and or axial disease, enthesitis, and dactylitis. (See "Clinical
manifestations and diagnosis of osteoarthritis".)

CLASSIFICATION CRITERIA Criteria that can be used to classify a patient as having psoriatic arthritis (PsA) are valuable
in scientific communication and in clinical trials. The criteria proposed in 2006 based upon the international Classification of
Psoriatic Arthritis (CASPAR) study, which included 588 patients with PsA and 536 patients with other forms of inflammatory
arthritis [74]; these represent the first generally agreed-upon set of classification criteria for PsA.

CASPAR criteria - The CASPAR study concluded that a patient with an inflammatory musculoskeletal disease
(peripheral arthritis, spondylitis, or enthesitis) can be classified as having PsA if a total of at least three points is
accumulated from the presence of the following list of features (each of which is assigned a certain number of points):
Skin psoriasis that is:
-Present two points, OR
-Previously present by history one point, OR
-A family history of psoriasis, if the patient is not affected one point
Nail lesions (onycholysis, pitting) one point
Dactylitis (present or past, documented by a rheumatologist) one point
Negative rheumatoid factor (RF) one point
Juxtaarticular bone formation on radiographs (distinct from osteophytes) one point
These classification criteria should facilitate studies in PsA and may function well in diagnosing PsA, given sensitivity
and specificity in four studies, including two of early arthritis patients, ranging from 91 to 100 percent and 97 to 99
percent, respectively [74-78]. However, these criteria can only be applied to individuals who demonstrate evidence for
inflammatory musculoskeletal disease (peripheral arthritis, axial disease, or enthesitis).

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SUMMARY AND RECOMMENDATIONS

Psoriatic arthritis (PsA) is a form of inflammatory arthritis that may occur in up to 30 percent of patients with psoriasis,
although it is relatively uncommon in the general population. The arthritis may be peripheral, axial, or both. It can
present as a symmetrical polyarthritis, an asymmetric oligoarthritis, arthritis of the distal interphalangeal (DIP) joints, as
a destructive arthritis termed arthritis mutilans, or as a spondyloarthritis (SpA). Patterns often overlap. Enthesitis,
dactylitis (sausage digits), and tenosynovitis can occur. (See 'Epidemiology' above and 'Patterns of arthritis' above.)
Arthritis appears after the onset of skin lesions in the majority of patients with PsA. However, the arthritis precedes the
skin disease in approximately 13 to 17 percent of patients, and skin lesions are present but have not been diagnosed in
an additional 15 percent. (See 'Relation between arthritis and skin lesions' above.)
Characteristic features of uncomplicated psoriasis may affect the nail bed in patients with PsA, including nail pits and
onycholysis. Nail lesions occur in 80 to 90 percent of patients with PsA. The severity of psoriatic nail involvement
correlates closely with the extent and severity of both skin and joint disease and is more common in those with DIP
joint arthritis, although the extent of skin disease does not generally correlate with the degree of joint disease.
(See 'Nail lesions' above.)
Laboratory findings in PsA are nonspecific, consistent with the acute phase response and the degree and chronicity of
inflammation; acute phase reactants are elevated in only about 40 percent of the patients; there are no laboratory
findings characteristic of PsA that distinguish it from other forms of inflammatory arthritis. Radiographic changes can
develop in the course of PsA that exhibit a pattern usually not seen in other forms of inflammatory arthritis, including
the coexistence of erosive changes and new bone formation. (See 'Laboratory findings' above and 'Imaging
findings' above.)
The diagnosis of PsA can generally be made in a patient who has both psoriasis and an inflammatory arthritis in a
pattern typical of PsA. Other forms of arthritis can occur in patients with psoriasis, such as rheumatoid arthritis,
osteoarthritis, gout, reactive arthritis, and the arthritis of inflammatory bowel disease, and should be excluded as the
cause of the patients syndrome. This can generally be done based upon the pattern of joint involvement, laboratory
testing, imaging, and synovial fluid analysis. Certain clinical features may suggest PsA in the absence of psoriasis
(psoriatic arthritis sine psoriasis), such as distal joint involvement, an asymmetric distribution, nail lesions, dactylitis,
and the family history. (See 'Diagnosis' above and 'Differential diagnosis' above.)