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Clinical manifestations and diagnosis of psoriatic arthritis

Clinical manifestations and diagnosis of psoriatic arthritis
Literature review current through: Jan 2024.
This topic last updated: Apr 12, 2023.

INTRODUCTION — Psoriatic arthritis (PsA) is an inflammatory musculoskeletal disease associated with psoriasis [1] that was initially considered a variant of rheumatoid arthritis, but subsequently emerged as a distinct clinical entity [2]. Historically, seronegativity for rheumatoid factor (RF) was required 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. Several reports also documented positive cyclic citrullinated peptide (CCP) antibodies in PsA patients. 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 "Psoriasis: Epidemiology, clinical manifestations, and diagnosis" and "Treatment of psoriasis in adults".)

EPIDEMIOLOGY AND RELATION OF ARTHRITIS TO SKIN DISEASE

Overall incidence and prevalence – Psoriatic arthritis (PsA) affects females and males equally, with an incidence of approximately 6 per 100,000 per year and a prevalence of approximately 1 to 2 per 1000 in the general population [1,3,5-8]. A Canadian population study from 2019 reported the cumulative prevalence estimate for PsA of 0.17 percent, with an incidence of 15 per 100,000 population [9]. A 2019 meta-analysis described an overall pooled prevalence of PsA of 20 percent in patients with psoriasis and 25 percent in the subset with moderate to severe psoriasis [10]. Estimates of the prevalence of PsA among patients with psoriasis have ranged from 4 to 30 percent [8,10-15]. 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 [16]. Similar concerns apply to the analyses of patients with psoriasis.

Incidence and prevalence among patients with psoriasis – Estimates of the prevalence of PsA among patients with psoriasis range from 14 to 31 percent [13,14,17-21]. Patients with psoriasis are also more likely to report inflammatory back pain [22].

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 [23]. In this study, the severity of psoriasis, the presence of nail lesions, low level of education, and the presence of uveitis were predictors for the development of PsA among patients with psoriasis.

A retrospective study of 15,501 patients with psoriasis found that the risk of progression to PsA was lower in patients prescribed interleukin (IL) 12/23 inhibitors (adjusted hazard ratio [HR] 0.57) or IL-23 inhibitors (adjusted HR 0.41) compared with patients treated with tumor necrosis factor (TNF) inhibitors [24].

Risk factors for development of psoriatic arthritis – In one study, the psoriasis skin phenotypes associated with a higher risk of PsA were scalp lesions (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) [25]. The clinical manifestations of psoriasis are described separately. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

There is a weak relationship between the severity of skin disease and arthritic involvement [26]. 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 [3,12,27]. 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.

Timing of onset of arthritis versus skin disease – In the majority of patients with PsA, psoriasis precedes the onset of arthritis with a median time between the diagnosis of skin and joint disease of seven to eight years [28]. However, the arthritis precedes the skin disease in approximately 7 to 15 percent of patients (although skin disease may be present but undetected in some of these patients) [28]; in an additional 15 percent, the skin and joint manifestations occur simultaneously [3]. The time interval between the onset of arthritis following psoriasis diagnosis was more than 15 years, and in some patients, as high as 40 years. The risk of developing PsA is linear and may occur even in patients with a prolonged history of psoriasis [17,29].

CLINICAL MANIFESTATIONS — The clinical features of psoriatic arthritis (PsA) are characterized by a high degree of heterogeneity and complexity in that involvement of multiple domains is often observed in a single patient. The severity of involvement ranges from mild to severe, with some patients experiencing advanced joint damage and functional disability.

The domains that are most commonly involved include:

Peripheral joints

Axial skeleton

Skin

Entheses (areas where ligaments, tendons, and joint capsules attach to bone and soft tissues)

Dactylitis, a diffuse swelling of a whole digit, results from both joint and soft tissue inflammation

In addition, multiple comorbidities are associated with PsA (see 'Comorbidities' below) that often negatively impact therapeutic response.

Patients with PsA present with pain and stiffness in the affected joints. Fatigue occurs in 22 percent of patients with PsA [23]; it has been identified as a symptom that is associated with the development of PsA among patients with psoriasis. Morning stiffness lasting more than 30 minutes occurs in one-half of patients. Stiffness is accentuated with prolonged immobility and alleviated by physical activity. A history of psoriasis is present in approximately 70 percent of patients presenting with arthritis.

On physical examination, stress pain, joint line tenderness, and effusions in the affected joints are present, often in an asymmetric distribution [30,31]. The distal interphalangeal (DIP) joints and spine are each affected in 40 to 50 percent of cases [5]. Approximately 15 percent of patients with PsA are diagnosed with concomitant psoriasis on examination despite lacking a history of known psoriatic skin disease.

Patients with PsA may demonstrate less joint tenderness on physical examination compared with patients with other inflammatory arthritides such as rheumatoid arthritis [32]. As a result, they may present with joint deformities without a significant degree of pain.

Bony fusion across a joint (ankylosis), which is often noted in the spine of patients with axial spondyloarthritis (SpA) and with axial involvement in PsA, can also take place in the peripheral joints of PsA patients (picture 1). These findings can be observed in the interphalangeal joints of the fingers and toes.

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 also are commonly present in combinations that vary widely from patient to patient.

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

Distal arthritis, characterized by involvement of the DIP joints (picture 2A-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 3 and image 1)

SpA, including both sacroiliitis (image 2) and spondylitis (image 3)

Some patients present with more than one pattern, and many change the pattern of their musculoskeletal involvement during follow-up [33-35]. 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 [36]. 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. A prospective study demonstrated that while 47 percent of the patients presented with oligoarthritis at their initial visit, 39 percent of those patients progressed to polyarticular disease over the follow-up period [37].

In a prospective cross-sectional observational study, the frequency on plain radiographs of axial involvement in patients with PsA was 42 percent [38]. The frequency of involvement of the spine as measured by MRI findings in the sacroiliac joints is not known. The patients with axial involvement were more likely to present with an earlier onset of arthritis, more severe nail onycholysis, symptoms of axial inflammation (eg, symptoms of inflammatory back pain), and inflammatory bowel disease. In this cohort, the prevalence of the human leukocyte antigen (HLA)-B*27 allele was 32 percent in patients with sacroiliitis alone and 67 percent in patients with sacroiliitis and spondylitis. Axial disease was associated with clinically impactful measures of disease activity, disability, and spinal motion that were equal in magnitude to those observed in patients with ankylosing spondylitis.

Distal arthritis and arthritis mutilans are considered most specific for PsA, but they are not the most common patterns seen [5,36,39]. 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 [40]:

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 [41,42]. Assessment tools for enthesitis have been developed for use in research. While some work better for assessment of enthesitis of ankylosing spondylitis, others work better for PsA [43]. One study identified enthesitis in 35 percent of the patients [44].

Tenosynovitis – Tenosynovitis of the flexor tendons of the hands, the extensor carpi ulnaris, and the posterior tibial and peroneus longus tendons in the feet are frequently involved.

Dactylitis – Dactylitis, characterized by diffuse swelling of an entire finger or toe, often termed a "sausage digit" (picture 4). 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 [45]. Sausage digits occur in nearly one-half of patients with PsA and are associated with an increased risk of progressive radiographic joint damage [46]. This abnormality is thought to result from inflammation of soft tissues, including the tendon sheaths, and from the concomitant inflammation of the adjacent joints [47]. This finding is suggestive of PsA (picture 5). A research tool to quantify dactylitis has been developed and has proven to be reliable and sensitive to change [48].

Nail lesions — Characteristic features of psoriasis affecting the nail bed and nail matrix include nail pits, onycholysis, nail bed hyperkeratosis, and splinter hemorrhages [49]. 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 [4,26], 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 6). 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 [49].

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 [50], although the extent of skin disease, in general, has not correlated with the degree of joint disease [26]. 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 [49].

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) [51]. 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 [52,53]. However, similar symmetrical swelling of the upper extremities due to extensive tenosynovitis in the absence of impaired lymphatic function has also been described [53]. (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 [54]. 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 [55]. Uveitis can occur in patients with peripheral arthritis only; patients with uveitis with axial SpA and PsA are more often male and HLA-B*27-positive than those with peripheral arthritis alone. Uveitis is more common among patients with PsA than those with psoriasis alone [56]. Uveitis is discussed in more detail elsewhere. (See "Uveitis: Etiology, clinical manifestations, and diagnosis", section on 'Systemic inflammatory diseases' and "Dermatologic and ocular manifestations of inflammatory bowel disease", section on 'Uveitis'.)

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 deoxyribonucleic acid (DNA) is found in 3 percent of patients with PsA in the absence of exposure to biologic agents that inhibit tumor necrosis factor (TNF) [57]. 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 [58-61].

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 [62,63]. 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. 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; however, it is not generally useful diagnostically in routine clinical practice [63,64].

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 4) [3,65].

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. Radiologic damage was observed in two-thirds of patients at their first visit (disease duration of 9 years on average) to the author's (DG) PsA clinic in an academic health center [3], and in 27 percent of early PsA patients seen in Dublin (duration of symptoms for 10 months on average) [66]. Axial radiographs in patients with PsA may reveal changes identical to those seen in ankylosing spondylitis with symmetric grade 2 or unilateral grade 3 or 4 sacroiliitis. However, many patients with PsA present with unilateral grade 2 sacroiliitis. Syndesmophytes are also seen in patients with PsA. These are often bulkier than those seen in ankylosing spondylitis, may be paramarginal, and may skip vertebral levels. (See "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults", section on 'Musculoskeletal imaging'.)

Magnetic resonance imaging (MRI) may be more sensitive than routine radiography in detecting articular, periarticular, and soft-tissue inflammation [67,68]. Using MRI, distinct abnormalities characterized by marked inflammation in the adjacent bone marrow (osteitis) 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 [69,70].

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 [71]. Findings on MRI in the axial sacroiliac joints include bone marrow edema in the iliac and sacral bones, erosions, chronic changes in periarticular fat accumulation, sclerosis, and new bone formation [72]. Similar MRI features are observed in the spine with the addition of asymmetric chunky syndesmophytes and erosive discovertebral (Andersson) lesions [73]. MRI can also provide detailed soft tissue and bone images of the chest wall and sternoclavicular region, an area frequently involved in PsA [74].

Power Doppler ultrasound is gaining widespread use for point-of-care evaluation of joint inflammation in PsA. Grayscale findings of synovitis, tenosynovitis, and joint effusions can be readily identified, along with hypervascularity characteristic of synovial inflammation in large and small joints. Ultrasound is particularly helpful in distinguishing inflammatory activity from fibromyalgia in patients with PsA [75].

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 [76].

Comorbidities — The risk of cardiovascular disease is increased in patients with PsA [77,78]. 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 [79]. 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. In a longitudinal study, 19.8 percent of the patients with PsA developed a cardiovascular event by the age of 70 and 30 percent by the age of 80. Cardiovascular risk factors and disease-related factors were predictors for cardiovascular events [29]. Use of TNF inhibitors was associated with reduced indices of subclinical atherosclerosis in patients with PsA [80].

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 (particularly prevalent are anxiety and depression). Metabolic syndrome occurs commonly among patients with PsA, and it is related to disease severity [81,82]. Diabetes is also more common among patients with PsA than the general population and is also associated with disease severity [83]. Atherosclerosis is more common among patients with PsA than the general population [29]. By contrast, there is no increased prevalence of malignancy among patients with PsA [84]. Depression and anxiety occur more commonly among patients with PsA compared with those with psoriasis alone [85]. The prevalence of nonalcoholic fatty liver disease is also increased in psoriasis and PsA patients [86]. The comorbidities of psoriasis are reviewed in detail separately. (See "Comorbid disease in psoriasis".)

DIAGNOSIS

Diagnosis — Psoriatic arthritis (PsA) is a leading diagnostic consideration 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 (both erosive and nonerosive), gout, acute calcium pyrophosphate (CPP) crystal arthritis, reactive arthritis, and the arthritis of inflammatory bowel disease should be excluded as part of the comprehensive evaluation. Differentiation of PsA from other disorders is 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) [87]:

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, (which occurs in 42 percent of patients with PsA compared with 17 percent of the general population [88]) although it is not commonly used in routine clinical practice

Mutilans deformities

Peripheral and axial involvement

Enthesitis (medial and lateral epicondyles, Achilles tendon, plantar fasciitis)

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 Heberden's nodes), enthesitis, dactylitis, skin disease, and rheumatoid nodules or tophi. Hidden psoriatic lesions in the scalp, axillae, umbilical area, and groin 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. HLA-B27 occurs in the same frequency as the general population in psoriasis (4 to 8 percent and in 25 to 30 percent of patients with PsA). 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. Power Doppler ultrasound may reveal synovitis, tendonitis, enthesitis, or joint effusions. Additional imaging may be useful if there is uncertainty regarding whether enthesitis is present, such as ultrasonography (if adequate expertise is available) or MRI.

Screening and classification

Screening questionnaires — A number of screening questionnaires have been developed to identify patients with PsA in dermatology or general practice [89]. Several were developed to identify PsA among patients with psoriasis [90-93], while the Toronto Psoriatic Arthritis Screen (ToPAS) and its modification (ToPAS2) were developed to identify patients with PsA regardless of the setting [94,95]. This instrument is copyrighted to the University Health Network in Toronto but is available upon request. The Psoriasis Epidemiology Screening Tool (PEST) is available and may work well in clinical practice. These instruments have similar sensitivity and specificity and can 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 [96]. 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 Crohn 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 [96,97]. 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 nonradiographic 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".)

Acute CPP crystal arthritis (formerly pseudogout)/pyrophosphate arthropathy – Acute inflammation, particularly of the knee, may present with a warm swollen knee, a presentation that may also be seen in PsA. The clue to the diagnosis is the presence of calcium pyrophosphate (CPP) crystals in the synovial fluid and chondrocalcinosis on joint films, which is often noted in the cartilage of the knee or the wrist. A chronic form of this disorder is pyrophosphate arthropathy, a well-known mimic of other forms of inflammatory and osteoarthritis.

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 Heberden's 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 [98]; 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 [98-102]. However, these criteria can only be applied to individuals who demonstrate evidence for inflammatory musculoskeletal disease (peripheral arthritis, axial disease, or enthesitis).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Psoriatic arthritis in adults".)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Psoriatic arthritis in adults (The Basics)")

Beyond the Basics topic (see "Patient education: Psoriatic arthritis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Epidemiology and patterns of arthritis – Psoriatic arthritis (PsA) is a form of inflammatory arthritis that may occur in up to 30 percent of patients with psoriasis, although it is less prevalent than rheumatoid arthritis 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 and relation of arthritis to skin disease' above and 'Patterns of arthritis' above.)

Relation of arthritis to psoriatic skin disease – Arthritis appears after the onset of skin lesions in the majority of patients with PsA. However, the arthritis precedes the skin disease in approximately 7 to 15 percent of patients, and skin lesions are present but have not been diagnosed in an additional 15 percent. (See 'Epidemiology and relation of arthritis to skin disease' above.)

Nail lesions – Characteristic features of uncomplicated psoriasis may affect the nail bed in patients with PsA, including nail pits and onycholysis (picture 6). 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 and imaging findings – 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 (image 4). (See 'Laboratory findings' above and 'Imaging findings' above.)

Diagnosis and differential diagnosis – The diagnosis of PsA should be considered 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 patient's syndrome. Accurate diagnosis can generally be achieved 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.)

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References

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