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Psoriatic Arthritis

  • Author: Anwar Al Hammadi, MD, FRCPC; Chief Editor: Herbert S Diamond, MD  more...
 
Updated: Jan 21, 2016
 

Practice Essentials

Psoriatic arthritis is most commonly a seronegative oligoarthritis found in patients with psoriasis, with less common, but characteristic, differentiating features of distal joint involvement and arthritis mutilans. Psoriatic arthritis (see the image below) develops in at least 5% of patients with psoriasis.

Swelling and deformity of the metacarpophalangeal Swelling and deformity of the metacarpophalangeal and distal interphalangeal joints in a patient with psoriatic arthritis.

See Psoriasis: Manifestations, Management Options, and Mimics, a Critical Images slideshow, to help recognize the major psoriasis subtypes and distinguish them from other skin lesions.

Signs and symptoms

Onset of psoriasis and arthritis are as follows:

  • Psoriasis appears to precede the onset of psoriatic arthritis in 60-80% of patients (occasionally by as many as 20 years, but usually by less than 10 years)
  • In as many as 15-20% of patients, arthritis appears before the psoriasis
  • Occasionally, arthritis and psoriasis appear simultaneously

In some cases, patients may experience only stiffness and pain, with few objective findings. In most patients, the musculoskeletal symptoms are insidious in onset, but an acute onset has been reported in one third of all patients.

Findings on physical examination are as follows:

  • Enthesopathy or enthesitis, reflecting inflammation at tendon or ligament insertions into bone, is observed more often at the attachment of the Achilles tendon and the plantar fascia to the calcaneus with the development of insertional spurs
  • Dactylitis with sausage digits is seen in as many as 35% of patients
  • Skin lesions include scaly, erythematous plaques; guttate lesions; lakes of pus; and erythroderma
  • Psoriasis may occur in hidden sites, such as the scalp (where psoriasis frequently is mistaken for dandruff), perineum, intergluteal cleft, and umbilicus

Psoriatic nail changes, which may be a solitary finding in patients with psoriatic arthritis, may include the following:

  • Beau lines
  • Leukonychia
  • Onycholysis
  • Oil spots
  • Subungual hyperkeratosis
  • Splinter hemorrhages
  • Spotted lunulae
  • Transverse ridging
  • Cracking of the free edge of the nail
  • Uniform nail pitting

Extra-articular features are observed less frequently in patients with psoriatic arthritis than in those with rheumatoid arthritis (RA) but may include the following:

  • Synovitis affecting flexor tendon sheaths, with sparing of the extensor tendon sheath
  • Subcutaneous nodules are rare
  • Ocular involvement may occur in 30% of patients, including conjunctivitis in 20% and acute anterior uveitis in 7%; in patients with uveitis, 43% have sacroiliitis

Patterns of arthritic involvement

The patterns of psoriatic arthritis involvement are as follows:

  • Asymmetrical oligoarticular arthritis
  • Symmetrical polyarthritis
  • Distal interphalangeal arthropathy
  • Arthritis mutilans
  • Spondylitis with or without sacroiliitis

See Clinical Presentation for more detail.

Diagnosis

Classification of psoriatic arthritis

The Classification Criteria for Psoriatic Arthritis (CASPAR)[1] consist of established inflammatory articular disease with at least 3 points from the following features:

  • Current psoriasis (assigned a score of 2)
  • A history of psoriasis (in the absence of current psoriasis; assigned a score of 1)
  • A family history of psoriasis (in the absence of current psoriasis and history of psoriasis; assigned a score of 1)
  • Dactylitis (assigned a score of 1)
  • Juxta-articular new-bone formation (assigned a score of 1)
  • RF negativity (assigned a score of 1)
  • Nail dystrophy (assigned a score of 1)

Laboratory findings

No specific diagnostic tests are available for psoriatic arthritis.[2] The most characteristic laboratory abnormalities in patients with the condition are as follows:

  • Elevations of the erythrocyte sedimentation rate (ESR) and C-reactive protein level
  • Negative rheumatoid factor in 91-95% of patients
  • In 10-20% of patients with generalized skin disease, the serum uric acid concentration may be increased
  • Low levels of circulating immune complexes have been detected in 56% of patients
  • Serum immunoglobulin A levels are increased in two thirds of patients
  • Synovial fluid is inflammatory, with cell counts ranging from 5000-15,000/µL and with more than 50% of cells being polymorphonuclear leukocytes; complement levels are either within reference ranges or increased, and glucose levels are within reference ranges

Radiographic studies

Radiologic features have helped to distinguish psoriatic arthritis from other causes of polyarthritis. In general, the common subtypes of psoriatic arthritis, such as asymmetrical oligoarthritis and symmetrical polyarthritis, tend to result in only mild erosive disease. Early bony erosions occur at the cartilaginous edge, and cartilage is initially preserved, with maintenance of a normal joint space.

The following radiographic abnormalities are suggestive of psoriatic arthritis:

  • Pencil-in-cup deformity (seen in the image below)
    Arthritis mutilans (ie, "pencil-in-cup" deformitie Arthritis mutilans (ie, "pencil-in-cup" deformities).
  • Joint-space narrowing in the interphalangeal joints, possibly with ankylosis
  • Increased joint space in the interphalangeal joints as a result of destruction
  • Fluffy periostitis
  • Bilateral, asymmetrical, fusiform soft-tissue swelling
  • Unilateral or symmetrical sacroiliitis
  • Large, nonmarginal, unilateral, asymmetrical syndesmophytes (intervertebral bony bridges, seen in the image below) in the cervical, thoracic, and lumbar spine, often sparing some of the segments
    Lateral radiograph of the cervical spine shows syn Lateral radiograph of the cervical spine shows syndesmophytes at the C2-3 and C6-7 levels, with zygapophyseal joint fusion. Courtesy of Bruce M. Rothschild, MD.

Magnetic resonance imaging studies

  • Particularly sensitive for detecting sacroiliitic synovitis, enthesitis, and erosions; can also be used with gadolinium to increase sensitivity
  • May show inflammation in the small joints of the hands, involving the collateral ligaments and soft tissues around the joint capsule, a finding not seen in persons with RA

See Workup for more detail.

Management

Medical treatment regimens include the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs). DMARDs include the following[3] :

  • Methotrexate
  • Sulfasalazine
  • Cyclosporine
  • Leflunomide
  • Biologic agents, such as the anti–TNF-alpha medications

In patients with severe skin inflammation, medications such as methotrexate, retinoic-acid derivatives, and psoralen plus ultraviolet (UV) light should be considered. These agents have been shown to work on skin and joint manifestations. Intra-articular injection of entheses or single inflamed joints with corticosteroids may be particularly effective in some patients. Use DMARDs in individuals whose arthritis is persistent.

Surgical care

  • Arthroscopic synovectomy has been effective in treating severe, chronic, monoarticular synovitis
  • Joint replacement and forms of reconstructive therapy are occasionally necessary
  • Patients in severe pain or with significant contractures may be referred for possible surgical intervention; however, high rates of recurrence of joint contractures have been noted after surgical release, especially in the hand
  • Hip and knee joint replacements have been successful
  • Arthrodesis and arthroplasty have also been used on joints, such as the proximal interphalangeal joint of the thumb
  • The wrist often spontaneously fuses, and this may relieve the patient's pain without surgical intervention
  • For arthritis mutilans, surgical intervention is usually directed toward salvage of the hand; combinations of arthrodesis, arthroplasty, and bone grafts to lengthen the digits may be used

Physical therapy

The rehabilitation treatment program for patients with psoriatic arthritis should be individualized and should be started early in the disease process. Such a program should consider the use of the following:

  • Rest: Local and systemic
  • Exercise: Passive, active, stretching, strengthening, and endurance
  • Modalities: Heat, cold
  • Orthotics: Upper and lower extremities, spinal
  • Assistive devices for gait and adaptive devices for self-care tasks: Including possible modifications to homes and automobiles
  • Education about the disease, energy conservation techniques, and joint protection
  • Possible vocational readjustments

See Treatment and Medication for more detail.

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Background

Psoriatic arthritis is a chronic inflammatory arthritis that develops in at least 5% of patients with psoriasis. The association between psoriasis and arthritis was first made in the mid-19th century, but psoriatic arthritis was not clinically distinguished from rheumatoid arthritis (RA) until the 1960s. (An example of flexion deformity in psoriatic arthritis is shown below.) (See Clinical Presentation and Workup.)

Severe fixed flexion deformity of the interphalang Severe fixed flexion deformity of the interphalangeal joint.

Because of a lack of specific biologic tests, precisely defining psoriatic arthritis remains difficult. The disorder most commonly exists as a seronegative oligoarthritis found in patients with psoriasis. Distal joint involvement and arthritis mutilans are less common, but characteristic, differentiating features. (The first image below compares sites of involvement for psoriatic arthritis with those for RA. The second and third images show distal joint pathology in psoriatic arthritis.)

Comparison between sites of involvements in both h Comparison between sites of involvements in both hands and feet in psoriatic arthritis and rheumatoid arthritis.
Psoriatic arthritis involving the distal phalangea Psoriatic arthritis involving the distal phalangeal joint.
Psoriatic arthritis involving the distal phalangea Psoriatic arthritis involving the distal phalangeal joint.

Because 50% of patients with psoriatic arthritis have evidence of spondyloarthropathy, often human leukocyte antigen (HLA)-B27 associated, psoriatic arthritis has also been classified among the seronegative spondyloarthropathies. (See Pathophysiology and Etiology.)[4, 5, 6, 7, 8]

Peripheral joint disease occurs in 95% of patients with psoriatic arthritis, while in the other 5%, axial spine involvement occurs exclusively. (See Clinical Presentation and Workup.)

Evidence from one study indicated that psoriatic arthritis is more frequent in patients with severe psoriasis than in those with milder cases. While this is true, no evidence indicates that the severity of the psoriasis relates to the pattern of joint involvement. In another study, pustular psoriasis was associated with more severe psoriatic arthritis. (See Prognosis.)

Psoriatic arthritis occurring in patients over age 60 years (elderly onset psoriatic arthritis) has a more severe onset and more a destructive outcome than does psoriatic arthritis in younger patients.

The course of psoriatic arthritis is usually characterized by flares and remissions. The patterns of psoriatic arthritis involvement are as follows:

  • Asymmetrical oligoarticular arthritis
  • Symmetrical polyarthritis
  • Distal interphalangeal arthropathy
  • Arthritis mutilans
  • Spondylitis with or without sacroiliitis

Asymmetrical oligoarticular arthritis

This was previously thought to be the most common type of psoriatic arthritis. The digits of the hands and feet are usually affected first, with inflammation of the flexor tendon and synovium occurring simultaneously, leading to the typical "sausage" appearance (dactylitis) of the fingers and toes. A large joint, such as the knee, is also commonly involved. Usually, fewer than 5 joints are affected at any one time. An asymmetrical arthritis pattern is shown below.

Asymmetrical arthritis pattern of psoriatic arthri Asymmetrical arthritis pattern of psoriatic arthritis (fixed flexion deformity).

Symmetrical polyarthritis

This rheumatoidlike pattern has been recognized as one of the most common types of psoriatic arthritis. The hands, wrists, ankles, and feet may be involved.

It is differentiated from RA by the presence of distal interphalangeal (DIP) joint involvement, relative asymmetry, an absence of subcutaneous nodules, and a negative test result for rheumatoid factor (RF). This condition is also generally milder than RA, with less deformity.

Distal interphalangeal arthropathy

Although DIP joint involvement is considered to be a classic and unique symptom of psoriatic arthritis, it occurs in only 5-10% of patients, primarily men.

Involvement of the nail with significant inflammation of the paronychia and swelling of the digital tuft may be prominent, occasionally making appreciation of the arthropathy more difficult.

Arthritis mutilans

This is a rare form of psoriatic arthritis, being found in only 1-5% of patients (although some reports suggest that arthritis mutilans may occur in as many as 16% of patients and may be as severe as RA).

In arthritis mutilans, resorption of bone (osteolysis), with dissolution of the joint, is observed as the "pencil-in-cup" radiographic finding and leads to redundant, overlying skin with a telescoping motion of the digit. (The effects of arthritis mutilans appear in the images below.)

Arthritis mutilans, a typically psoriatic pattern Arthritis mutilans, a typically psoriatic pattern of arthritis, which is associated with a characteristic "pencil-in-cup" radiographic appearance of digits.
Severe psoriatic arthritis showing involvement of Severe psoriatic arthritis showing involvement of the distal interphalangeal joints, distal flexion deformity, and telescoping of the left third, fourth, and fifth digits due to destruction of joint tissue.
Arthritis mutilans (ie, "pencil-in-cup" deformitie Arthritis mutilans (ie, "pencil-in-cup" deformities).

This "opera-glass hand" is more common in men than in women and is more frequent in early-onset disease.

Spondylitis with or without sacroiliitis

This occurs in approximately 5% of patients with psoriatic arthritis and has a male predominance.

Clinical evidence of spondylitis and/or sacroiliitis can occur in conjunction with other subgroups of psoriatic arthritis.

Spondylitis may occur without radiologic evidence of sacroiliitis, which frequently tends to be asymmetrical, or sacroiliitis may appear radiologically without the classic symptoms of morning stiffness in the lower back. Thus, the correlation between the symptoms and radiologic signs of sacroiliitis can be poor.

Vertebral involvement differs from that observed in ankylosing spondylitis. Vertebrae are affected asymmetrically, and the atlantoaxial joint may be involved with erosion of the odontoid and subluxation (with attendant neurologic complications). Therapy may limit subluxation-associated disability.

Unusual radiologic features may be present, such as nonmarginal asymmetrical syndesmophytes (characteristic), paravertebral ossification, and, less commonly, vertebral fusion with disk calcification.

SAPHO syndrome

First described by Chamot et al in 1987, synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome is characterized by variable bone changes (hyperostosis, arthritis, aseptic osteomyelitis) of the chest wall, sacroiliac joints, and long bones. Dermatologic manifestations include the following:

  • Palmoplantar pustulosis
  • Hidradenitis suppurativa
  • Pustular psoriasis
  • Dissecting cellulitis of the scalp
  • Sweet syndrome
  • Sneddon-Wilkinson disease

Skin and osseous involvement may occur simultaneously or may be separated by as long as 20 years.[9, 10]

Juvenile psoriatic arthritis

Juvenile psoriatic arthritis accounts for 8-20% of childhood arthritis and is monoarticular at onset.

The median age of onset is 4.5 years in girls and 10 years in boys, and there is a female predominance. The disease is usually mild, although occasionally it may be severe and destructive, with the condition progressing into adulthood.

In 50% of children, the arthritis is monoarticular; DIP joint involvement occurs at a similar rate. Tenosynovitis is present in 30% of children, and nail involvement is present in 71%, with pitting being the most common, but least specific, finding.

In 47% of children, disordered bone growth with resultant shortening may result from involvement of the unfused epiphyseal growth plate in the inflammatory process.

Sacroiliitis occurs in 28% of children and is usually associated with HLA-B27 positivity. Although the presence of HLA-B8 may be a marker of more severe disease, HLA-B17 is usually associated with a mild form of psoriatic arthritis.

Children have a higher frequency of simultaneous onset of psoriasis and arthritis than adults do, with arthritis preceding psoriasis in 52% of children.

Classification of psoriatic arthritis

The simple and highly specific Classification Criteria for Psoriatic Arthritis (CASPAR), developed by a large international study group, has a sensitivity and specificity of 98.7% and 91.4%, respectively.[1] The criteria consist of established inflammatory articular disease with at least 3 points from the following features:

  • Current psoriasis (assigned a score of 2)
  • A history of psoriasis (in the absence of current psoriasis; assigned a score of 1)
  • A family history of psoriasis (in the absence of current psoriasis and a history of psoriasis; assigned a score of 1)
  • Dactylitis (assigned a score of 1)
  • Juxta-articular new-bone formation (assigned a score of 1)
  • RF negativity (assigned a score of 1)
  • Nail dystrophy (assigned a score of 1)
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Pathophysiology and Etiology

The etiology of psoriatic arthritis remains unknown, but much information has been gathered. In addition to genetic influences, environmental and immunologic factors are thought to be prominent in the development and perpetuation of the disease. The de novo development or exacerbation of psoriasis and psoriatic arthritis in patients with human immunodeficiency virus (HIV) infection and CD4 deficiency remains controversial.

Psoriasis may remit following allogeneic bone marrow transplantation and may exacerbate with interferon-alfa treatment for hepatitis C.

Slight differences exist in the vascular patterns of joints in psoriatic arthritis, compared with those of RA, suggesting the possibility of different etiologic mechanisms in these diseases.[11]

Genetics

Genetic factors play an important role in susceptibility to psoriasis and psoriatic arthritis[12] ; approximately 40% of patients with either of these conditions have a family history of them in first-degree relatives.[13, 14]

The recurrence risk ratio for psoriatic arthritis, an estimate of the heritability of the disease, is estimated at 30-55 in first-degree relatives of patients with this condition, while that for psoriasis is 8-10.[15] Diseases with higher heritability have a higher likelihood of having genetic factors underlying disease susceptibility.[16, 17, 18, 19, 20]

The following important genetic susceptibility loci have been found (although the exact mechanism of the association between HLA and psoriatic arthritis is not yet clear)[15, 21, 22, 23, 24, 25, 26, 27] :

  • Early-onset psoriasis: HLA-Cw6, HLA-B57, HLA-DR7, and HLA-B17, with HLA-Cw*0602 variant found to be highly associated
  • Psoriasis: HLA-Cw6 (or psoriasis susceptibility 1 [PSOR1] on chromosome 6) and 6 other psoriasis susceptibility loci (PSOR2, PSOR3, PSOR4, PSOR5, PSOR6, PSOR7), transcription factor RUNX1
  • Psoriatic arthritis: HLA-B7, HLA-B27, HLA-DR4, HLA-38, and HLA-DR7
  • Psoriasis and psoriatic arthritis: HLA-Cw6, HLA-B13, HLA-B17, HLA-B57, and HLA-B39
  • Predictors of disease progression: HLA-B39; HLA-B27 in the presence of HLA-DR7; HLA-DQ3 in the absence of HLA-DR7
  • Protective: HLA-B22

Comparing psoriasis with psoriatic arthritis, it has been found that in psoriatic arthritis there is a stronger association with HLA-B alleles than with HLA-C alleles, while psoriasis (particularly early onset psoriasis) is associated with HLA-C.[28, 29]

The following associated gene polymorphisms are also thought to be associated with psoriasis and psoriatic arthritis[15, 21, 24, 30] :

  • Tumor necrosis factor (TNF)-alpha promoter [31]
  • Major histocompatibility complex (MHC) class I chain-related gene A (MICA): Independent of HLA, MICA*016 influences the risk of developing psoriasis without arthritis, while homozygosity for MICA*00801 increases the risk of developing psoriatic arthritis in patients with psoriasis [32, 33]
  • Caspase-activating recruitment domain (CARD) 15
  • Interleukin (IL)-12/IL-23p40 and IL-23 receptor: Studies indicate that HLA-C and IL23R are more strongly associated with psoriasis alone, while IL12B is more strongly associated with psoriatic arthritis [16, 17, 18, 34]

Additional loci that demonstrate an association with psoriatic arthritis include microsatellite polymorphisms in the TNF promoter.

In psoriasis, linkages with loci on 17q, 4q, and 6p have been reported in whole genome scans, with the strongest evidence for linkage on 6p.

It has also been suggested that certain immunoglobulin genes are associated with psoriatic arthritis. Serum levels of immunoglobulin A (IgA) and IgG are higher in psoriatic arthritis patients, whereas IgM levels may be normal or diminished.

Identifying susceptibility genes is likely to aid understanding of disease etiopathogenesis and identify potential therapeutic targets. Although loci identified to date explain only a fraction of the heritability estimates, a model of important pathways in psoriasis pathogenesis is emerging that combines skin barrier function (LCE3B, LCE3C); the TH17 pathway (IL12B, IL23A, IL23R, TRAF3IP2, TYK2); innate immunity involving NFκB and IFN signaling (TNFAIP3, TNIP1, NFKBIA, REL, TYK2, IFIH1, IL23RA), beta-defensin, and TH2 (IL4, IL13), as well as adaptive immunity involving CD8 T cells (ERAP1).[16, 17, 18, 19, 20, 35]

A gene-gene interaction between ERAP1 and HLA-C suggesting that ERAP1 variants only influenced psoriasis susceptibility in individuals carrying the HLA-C risk allele further implicates immune dysregulation in psoriasis pathogenesis.[35]

Immunologic factors

Autoantibodies against nuclear antigens, cytokeratins, epidermal keratins, and heat-shock proteins have been reported in persons with psoriatic arthritis, indicating that the disease has a humoral immune component.

The pathologic process of skin and joint lesions in psoriatic arthritis is an inflammatory reaction, and evidence also indicates the presence of autoimmunity, perhaps mediated by complement activation. The inflammatory nature of the skin and joint lesions in psoriatic arthritis is demonstrated by synovial-lining cell hyperplasia and mononuclear infiltration, resembling the histopathologic changes of RA. However, synovial-lining hyperplasia is less, macrophages are fewer, and vascularity is greater in psoriatic arthritis than in RA synovium.

The cytokine profile for psoriatic arthritis reflects a complex interplay between T cells and monocyte macrophages. Type 1 helper T-cell cytokines (eg, TNF-alpha, IL-1 beta, IL-10) are more prevalent in psoriatic arthritis than in RA, suggesting that these 2 disorders may result from a different underlying mechanism.

Several studies have shown a significant reduction in the number and percentage of CD4+ T cells in the peripheral blood, whereas they are found throughout the skin lesions and synovium.

Dendritic cells have been found in the synovial fluid of patients with psoriatic arthritis and are reactive in the mixed leukocyte reaction; the inference is that the dendritic cells present an unknown antigen to CD4+ cells within the joints and skin of patients with psoriatic arthritis, leading to T-cell activation.[25]

Fibroblasts from the skin and synovia of patients with psoriatic arthritis have an increased proliferative activity and the capability to secrete increased amounts of IL-1, IL-6, and platelet-derived growth factors. Several studies suggest that cytokines secreted from activated T cells and other mononuclear proinflammatory cells induce proliferation and activation of synovial and epidermal fibroblasts.

Psoriatic plaques in skin have increased levels of leukotriene B4. Injections of leukotriene B4 cause intraepidermal microabscesses, suggesting a role for this compound in the development of psoriasis.

Infections

The temporal relationship between certain viral and bacterial infections and the development or exacerbation of psoriasis and psoriatic arthritis suggests a possible pathogenetic role for viruses and bacteria.

Pustular psoriasis is a well-described sequela of streptococcal infections. However, the response to streptococcal antigens by cells from patients with psoriatic arthritis is not different from that of cells from patients with RA, making the role of Streptococcus species in psoriatic arthritis doubtful.

Psoriasis and psoriatic arthritis have been reported to be associated with HIV infection and to be prevalent in some HIV-endemic areas. Although the prevalence of psoriasis in patients infected with HIV is similar to that in the general population, patients with HIV infection usually have more extensive erythrodermic psoriasis, and patients with psoriasis may present with exacerbation of their skin disease after being infected with HIV.

Trauma

A few studies have reported the occurrence of arthritis and acro-osteolysis after physical trauma in patients with psoriasis.

Environmental factors

The theory of environmental factors playing a role in the etiology of psoriatic arthritis involves a process of superantigens reacting with autoantigens.

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Epidemiology

Occurrence in the United States

Psoriasis affects 2.5% of the white population of North America but is less prevalent in the African American and Native American populations.

Psoriatic arthritis is thought to occur in up to 1% of the general population, with survey results indicating that approximately 1 million US adults have the disease. This figure is significantly higher than researchers had previously believed and suggests that many people with psoriasis may not be aware that they have psoriatic arthritis. (This is according to a study conducted by the National Psoriasis Foundation.)

However, prevalence rates vary widely among studies. A random telephone survey of 27,220 US residents found a 0.25% prevalence rate for psoriatic arthritis in the general population and an 11% prevalence rate in patients with psoriasis. However, the exact frequency of the disorder in patients with psoriasis remains uncertain, with the estimated rate ranging from 5-30%.[25, 36]

Moreover, since the late 20th century, the incidence of psoriatic arthritis appears to have been rising in men and women. Reasons for the increase are unknown; it may be related to a true change in incidence or to a greater overall awareness of the diagnosis by physicians.[37]

International occurrence

Depending on the population studied, the prevalence of psoriatic arthritis internationally ranges widely. A 2013 German study found the rate of psoriatic arthritis in patients with psoriasis to be 30.2%.[38]

In a prospective cohort study from Canada that involved psoriasis patients without arthritis at study entry, 51 of 464 patients developed psoriatic arthritis over the course of 8 years of followup. The annual incidence rate was 2.7 cases of psoriatic arthritis per 100 psoriasis patients.[39] Baseline variables associated with the development of psoriatic arthritis in multivariate analysis included the following:

  • Severe psoriasis (relative risk [RR] 5.4, p=0.006)
  • Low level of education (college/university vs. high school incomplete, RR 4.5, p=0.005; high school education vs. high school incomplete, RR 3.3, p=0.049)
  • Use of retinoid medications (RR 3.4, p=0.02)

There is a high prevalence of previously undiagnosed active psoriatic arthritis among patients with psoriasis who are seen by dermatologists. In a 2009 prospective German study, of 1511 patients with plaque-type psoriasis, 20.6% were found to have psoriatic arthritis, with 85% of the cases having been previously undiagnosed.[4]

The number of diagnosed cases of psoriasis and psoriatic arthritis has risen dramatically in sub-Saharan Africa in association with the area’s escalating epidemic of HIV infection. Although HIV is not known to affect the incidence of psoriasis, it may significantly exacerbate otherwise limited disease. The evolution of mild psoriasis to erythroderma in the setting of a flare-up of psoriatic arthritis may be a sign of HIV infection.

Race- and age-related related demographics

Race predilection in psoriatic arthritis has not been well studied. However, whites are known to be affected more commonly than are persons of other racial groups.

Psoriatic arthritis characteristically develops in persons aged 35-55 years, but it can occur at almost any age. In the juvenile form, the age of onset is 9-11 years.

Sex-related demographics

The male-to-female ratio for psoriatic arthritis is 1:1, with the exception of some subsets of patients. Females, however, are more commonly affected with symmetrical polyarthritis resembling RA and the juvenile form.

In contrast, the spondylitic form of psoriatic arthritis, which affects the axial spine, has a male-to-female ratio of 3:1.

In a cross-sectional analysis of a large population of patients with psoriatic arthritis, male patients were found to be more likely to exhibit axial involvement and radiographic joint damage, and female patients were more likely to experience impaired quality of life and severe limitations in function.[40]

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Prognosis

Although psoriatic arthritis was originally thought to be relatively mild, as many as 40% of patients may develop erosive and deforming arthritis. Of patients observed in a large outpatient psoriatic arthritis clinic, 7% required musculoskeletal surgery.

Although a cohort study from the United Kingdom showed no increase in mortality among 453 patients with psoriatic arthritis compared with the general population, the results of another study suggested that psoriatic arthritis is associated with a significantly greater risk of hypertension, obesity, hyperlipidemia, type 2 diabetes mellitus, and cardiovascular events than is psoriasis without arthritis.[41, 42, 43]

Psoriatic arthritis was also associated with infections not treated with antibiotics, neurologic conditions, gastrointestinal disorders, and liver disease.[42]

In another study, by Labitigan et al, the prevalence of obesity, type 2 diabetes, and hypertriglyceridemia was determined to be higher in psoriatic arthritis than in RA. Using data from the Consortium of Rheumatology Researchers of North America (CORRONA) registry, the investigators found type 2 diabetes rates in psoriatic arthritis and RA to be 15% and 11%, respectively, and hypertriglyceridemia rates to be 38% and 28%, respectively.[44]

A pooled analysis of 2 large interventional lipid-lowering trials indicated that lipid-lowering therapy is effective in inflammatory joint disease, including rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis. Furthermore, patients with and without inflammatory joint disease in the study had a 20% reduced risk of cardiovascular disease.[45]

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Patient Education

Education is an important component of the patient's treatment plan, because he or she must be able to manage the symptoms of psoriatic arthritis and be comfortable with self-treatment strategies. Physical therapists provide education and an exercise program developed individually for each patient. Completing the wrong kind of exercise or overexertion can be harmful to patients with psoriatic arthritis.

Instructing patients with psoriatic arthritis in methods of joint protection is necessary and becomes part of the therapy process. Patients need to pace themselves and take adequate rest breaks from activity. Other examples of joint protection include wearing splints on the affected joints, using proper body mechanics and lifting techniques, and incorporating assistive devices or adaptive equipment into the patient's activities of daily living.

For patient education information, see the Skin Conditions and Beauty Center, as well as Psoriatic Arthritis, Psoriasis, Types of Psoriasis, Psoriasis Medications, and Nail Psoriasis.

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Contributor Information and Disclosures
Author

Anwar Al Hammadi, MD, FRCPC Consultant and Head of Dermatology, Rashid Hospital, Dubai Health Authority; Clinical Associate Professor of Dermatology, Dubai Medical College; Clinical Assistant Professor of Dermatology, University of Sharjah, UAE

Anwar Al Hammadi, MD, FRCPC is a member of the following medical societies: American Academy of Dermatology, Royal College of Physicians and Surgeons of Canada, Canadian Dermatology Association, Skin Cancer Foundation

Disclosure: Nothing to disclose.

Coauthor(s)

Humeira Badsha, MD Consultant Rheumatologist, Dr Humeira Badsha Medical Center, UAE

Humeira Badsha, MD is a member of the following medical societies: American College of Rheumatology, Emirates Society for Rheumatology

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, Phi Beta Kappa

Disclosure: Nothing to disclose.

Acknowledgements

Bruce Buehler, MD Professor, Department of Pediatrics and Genetics, Director RSA, University of Nebraska Medical Center

Bruce Buehler, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Pediatrics, American Association on Mental Retardation, American College of Medical Genetics, American College of Physician Executives, American Medical Association, and Nebraska Medical Association

Disclosure: Nothing to disclose.

Denise I Campagnolo, MD, MS Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers

Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers

Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds investigator; Novartis investigator; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

Vinod Chandran, MBBS, MD, PhD Assistant Professor, Department of Medicine, Division of Rheumatology, University of Toronto Faculty of Medicine; Staff Physician, Division of Rheumatology, Toronto Western Hospital, Canada

Disclosure: Nothing to disclose.

Michael J Dans, MD, PhD Clinical Instructor, Department of Dermatology, University of California at San Francisco

Michael J Dans, MD, PhD is a member of the following medical societies: American Academy of Dermatology and American Medical Association

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Patrick M Foye, MD Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

Dafna D Gladman, MD, FRCPC Professor of Medicine, University of Toronto Faculty of Medicine; Staff Physician, Division of Rheumatology, Toronto Western Hospital, Canada

Disclosure: Nothing to disclose.

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology

Disclosure: Nothing to disclose.

Peter D Gorevic, MD, Professor and Chief, Division of Rheumatology, Mount Sinai School of Medicine

Disclosure: Nothing to disclose.

Jeffrey M Heftler, MD Interventional Physiatrist, Orthopaedic and Neurosurgical Specialists, Greenwich, CT

Jeffrey M Heftler, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and International Spine Intervention Society

Disclosure: Nothing to disclose.

Alexa F Boer Kimball, MD, MPH Associate Professor of Dermatology, Harvard University School of Medicine; Vice Chair, Department of Dermatology, Massachusetts General Hospital; Director of Clinical Unit for Research Trials in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital

Alexa F Boer Kimball, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Kristine M Lohr, MD, MS Professor, Department of Internal Medicine, Center for the Advancement of Women's Health and Division of Rheumatology, Director, Rheumatology Training Program, University of Kentucky College of Medicine

Kristine M Lohr, MD, MS is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Nothing to disclose.

Christen M Mowad, MD Associate Professor, Department of Dermatology, Geisinger Medical Center

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Dermatological Association, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Michael F Saulino, MD, PhD Assistant Professor, Department of Physical Medicine and Rehabilitation, MossRehab, Jefferson Medical College of Thomas Jefferson University

Michael F Saulino, MD, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Abby S Van Voorhees, MD Assistant Professor, Director of Psoriasis Services and Phototherapy Units, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania

Abby S Van Voorhees, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, National Psoriasis Foundation, Phi Beta Kappa, Sigma Xi, and Women's Dermatologic Society

Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Merck Salary Management position; Abbott Honoraria Speaking and teaching; Amgen Honoraria Review panel membership; Centocor Honoraria Consulting; Leo Consulting; Merck None Other

Karolyn A Wanat, MD Resident Physician, Department of Dermatology, University of Pennsylvania School of Medicine

Karolyn A Wanat, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and American Medical Women's Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Rajesh R Yadav, MD Associate Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer Center, University of Texas Medical School at Houston

Rajesh R Yadav, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

References
  1. Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H. Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis Rheum. 2006 Aug. 54(8):2665-73. [Medline].

  2. Mease PJ, Reich K. Alefacept with methotrexate for treatment of psoriatic arthritis: open-label extension of a randomized, double-blind, placebo-controlled study. J Am Acad Dermatol. 2009 Mar. 60(3):402-11. [Medline].

  3. Saad AA, Symmons DP, Noyce PR, Ashcroft DM. Risks and benefits of tumor necrosis factor-alpha inhibitors in the management of psoriatic arthritis: systematic review and metaanalysis of randomized controlled trials. J Rheumatol. 2008 May. 35(5):883-90. [Medline].

  4. Reich K, Kruger K, Mossner R, Augustin M. Epidemiology and clinical pattern of psoriatic arthritis in Germany: a prospective interdisciplinary epidemiological study of 1511 patients with plaque-type psoriasis. Br J Dermatol. 2009 May. 160(5):1040-7. [Medline].

  5. Kavanaugh A, McInnes I, Mease P, Krueger GG, Gladman D, Gomez-Reino J, et al. Golimumab, a new human tumor necrosis factor alpha antibody, administered every four weeks as a subcutaneous injection in psoriatic arthritis: Twenty-four-week efficacy and safety results of a randomized, placebo-controlled study. Arthritis Rheum. 2009 Apr. 60(4):976-86. [Medline].

  6. Guttman-Yassky E, Krueger JG. Psoriasis: evolution of pathogenic concepts and new therapies through phases of translational research. Br J Dermatol. 2007 Dec. 157(6):1103-15. [Medline].

  7. Fitzgerald O, Winchester R. Psoriatic arthritis: from pathogenesis to therapy. Arthritis Res Ther. 2009. 11(1):214. [Medline]. [Full Text].

  8. Gladman DD. Psoriatic arthritis. Dermatol Ther. 2009 Jan-Feb. 22(1):40-55. [Medline].

  9. Chamot AM, Benhamou CL, Kahn MF, Beraneck L, Kaplan G, Prost A. [Acne-pustulosis-hyperostosis-osteitis syndrome. Results of a national survey. 85 cases]. Rev Rhum Mal Osteoartic. 1987 Mar. 54(3):187-96. [Medline].

  10. Gmyrek R, Grossman ME, Rudin D, Scher R. SAPHO syndrome: report of three cases and review of the literature. Cutis. 1999 Oct. 64(4):253-8. [Medline].

  11. Fiocco U, Cozzi L, Chieco-Bianchi F, Rigon C, Vezzu M, Favero E, et al. Vascular changes in psoriatic knee joint synovitis. J Rheumatol. 2001 Nov. 28(11):2480-6. [Medline].

  12. Chandran V, Raychaudhuri SP. Geoepidemiology and environmental factors of psoriasis and psoriatic arthritis. J Autoimmun. 2010 May. 34(3):J314-21. [Medline].

  13. Nograles KE, Brasington RD, Bowcock AM. New insights into the pathogenesis and genetics of psoriatic arthritis. Nat Clin Pract Rheumatol. 2009 Feb. 5(2):83-91. [Medline]. [Full Text].

  14. Duffin KC, Chandran V, Gladman DD, Krueger GG, Elder JT, Rahman P. Genetics of psoriasis and psoriatic arthritis: update and future direction. J Rheumatol. 2008 Jul. 35(7):1449-53. [Medline]. [Full Text].

  15. Chandran V, Schentag CT, Brockbank JE, Pellett FJ, Shanmugarajah S, Toloza SM, et al. Familial aggregation of psoriatic arthritis. Ann Rheum Dis. 2009 May. 68(5):664-7. [Medline].

  16. Liu Y, Helms C, Liao W, Zaba LC, Duan S, Gardner J, et al. A genome-wide association study of psoriasis and psoriatic arthritis identifies new disease loci. PLoS Genet. 2008 Mar 28. 4(3):e1000041. [Medline]. [Full Text].

  17. Nair RP, Duffin KC, Helms C, Ding J, Stuart PE, Goldgar D, et al. Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways. Nat Genet. 2009 Feb. 41(2):199-204. [Medline]. [Full Text].

  18. Huffmeier U, Uebe S, Ekici AB, Bowes J, Giardina E, Korendowych E, et al. Common variants at TRAF3IP2 are associated with susceptibility to psoriatic arthritis and psoriasis. Nat Genet. 2010 Nov. 42(11):996-9. [Medline]. [Full Text].

  19. Sun LD, Cheng H, Wang ZX, Zhang AP, Wang PG, Xu JH, et al. Association analyses identify six new psoriasis susceptibility loci in the Chinese population. Nat Genet. 2010 Nov. 42(11):1005-9. [Medline]. [Full Text].

  20. Ellinghaus E, Ellinghaus D, Stuart PE, Nair RP, Debrus S, Raelson JV, et al. Genome-wide association study identifies a psoriasis susceptibility locus at TRAF3IP2. Nat Genet. 2010 Nov. 42(11):991-5. [Medline]. [Full Text].

  21. Cargill M, Schrodi SJ, Chang M, Garcia VE, Brandon R, Callis KP, et al. A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes. Am J Hum Genet. 2007 Feb. 80(2):273-90. [Medline]. [Full Text].

  22. Rozenblit M, Lebwohl M. New biologics for psoriasis and psoriatic arthritis. Dermatol Ther. 2009 Jan-Feb. 22(1):56-60. [Medline].

  23. Huffmeier U, Lascorz J, Bohm B, Lohmann J, Wendler J, Mossner R, et al. Genetic variants of the IL-23R pathway: association with psoriatic arthritis and psoriasis vulgaris, but no specific risk factor for arthritis. J Invest Dermatol. 2009 Feb. 129(2):355-8. [Medline].

  24. Al-Heresh AM, Proctor J, Jones SM, Dixey J, Cox B, Welsh K, et al. Tumour necrosis factor-alpha polymorphism and the HLA-Cw*0602 allele in psoriatic arthritis. Rheumatology (Oxford). 2002 May. 41(5):525-30. [Medline].

  25. Choy E. T cells in psoriatic arthritis. Curr Rheumatol Rep. 2007 Dec. 9(6):437-41. [Medline].

  26. Ho PY, Barton A, Worthington J, Plant D, Griffiths CE, Young HS, et al. Investigating the role of the HLA-Cw*06 and HLA-DRB1 genes in susceptibility to psoriatic arthritis: comparison with psoriasis and undifferentiated inflammatory arthritis. Ann Rheum Dis. 2008 May. 67(5):677-82. [Medline]. [Full Text].

  27. Nickoloff BJ, Nestle FO. Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities. J Clin Invest. 2004 Jun. 113(12):1664-75. [Medline]. [Full Text].

  28. Nair RP, Stuart PE, Nistor I, Hiremagalore R, Chia NV, Jenisch S, et al. Sequence and haplotype analysis supports HLA-C as the psoriasis susceptibility 1 gene. Am J Hum Genet. 2006 May. 78(5):827-51. [Medline]. [Full Text].

  29. Eder L, Pellett F, Chandran V, Shanmugarajah S, Gladman DD. HLA- B*27 and Cw*06 are risk alleles for psoriatic arthritis among psoriasis patients (abstract). Arthritis Rheum. 2010. 62(suppl 10):1974.

  30. Kimball AB, Gordon KB, Langley RG, Menter A, Chartash EK, Valdes J. Safety and efficacy of ABT-874, a fully human interleukin 12/23 monoclonal antibody, in the treatment of moderate to severe chronic plaque psoriasis: results of a randomized, placebo-controlled, phase 2 trial. Arch Dermatol. 2008 Feb. 144(2):200-7. [Medline].

  31. Rahman P, Siannis F, Butt C, Farewell V, Peddle L, Pellett F, et al. TNFalpha polymorphisms and risk of psoriatic arthritis. Ann Rheum Dis. 2006 Jul. 65(7):919-23. [Medline]. [Full Text].

  32. Rahman P, Roslin NM, Pellett FJ, Lemire M, Greenwood CM, Beyene J, et al. High resolution mapping in the major histocompatibility complex region identifies multiple independent novel loci for psoriatic arthritis. Ann Rheum Dis. 2011 Apr. 70(4):690-4. [Medline].

  33. Pollock R, Chandran V, Barrett J, Eder L, Pellett F, Yao C, et al. Differential major histocompatibility complex class I chain-related A allele associations with skin and joint manifestations of psoriatic disease. Tissue Antigens. 2011 Jun. 77(6):554-61. [Medline].

  34. Benson JM, Sachs CW, Treacy G, Zhou H, Pendley CE, Brodmerkel CM, et al. Therapeutic targeting of the IL-12/23 pathways: generation and characterization of ustekinumab. Nat Biotechnol. 2011 Jul. 29(7):615-24. [Medline].

  35. Strange A, Capon F, Spencer CC, Knight J, Weale ME, Allen MH, et al. A genome-wide association study identifies new psoriasis susceptibility loci and an interaction between HLA-C and ERAP1. Nat Genet. 2010 Nov. 42(11):985-90. [Medline]. [Full Text].

  36. Wilson FC, Icen M, Crowson CS, McEvoy MT, Gabriel SE, Kremers HM. Incidence and clinical predictors of psoriatic arthritis in patients with psoriasis: a population-based study. Arthritis Rheum. 2009 Feb 15. 61(2):233-9. [Medline]. [Full Text].

  37. Wilson FC, Icen M, Crowson CS, McEvoy MT, Gabriel SE, Kremers HM. Time trends in epidemiology and characteristics of psoriatic arthritis over 3 decades: a population-based study. J Rheumatol. 2009 Feb. 36(2):361-7. [Medline]. [Full Text].

  38. Henes JC, Ziupa E, Eisfelder M, Adamczyk A, Knaudt B, Jacobs F, et al. High prevalence of psoriatic arthritis in dermatological patients with psoriasis: a cross-sectional study. Rheumatol Int. 2013 Oct 10. [Medline].

  39. Eder L, Haddad A, Rosen CF, Lee KA, Chandran V, Cook R, et al. The incidence and risk factors for psoriatic arthritis in patients with psoriasis - a prospective cohort study. Arthritis Rheumatol. 2015 Nov 10. [Medline].

  40. Eder L, Thavaneswaran A, Chandran V, Gladman DD. Gender difference in disease expression, radiographic damage and disability among patients with psoriatic arthritis. Ann Rheum Dis. 2013 Apr. 72(4):578-82. [Medline].

  41. Buckley C, Cavill C, Taylor G, Kay H, Waldron N, Korendowych E, et al. Mortality in psoriatic arthritis - a single-center study from the UK. J Rheumatol. 2010 Oct. 37(10):2141-4. [Medline].

  42. Husted JA, Thavaneswaran A, Chandran V, Eder L, Rosen CF, Cook RJ, et al. Cardiovascular and other comorbidities in patients with psoriatic arthritis: a comparison with patients with psoriasis. Arthritis Care Res (Hoboken). 2011 Dec. 63(12):1729-35. [Medline].

  43. Torres T, Sales R, Vasconcelos C, Martins da Silva B, Selores M. Framingham Risk Score underestimates cardiovascular disease risk in severe psoriatic patients: Implications in cardiovascular risk factors management and primary prevention of cardiovascular disease. J Dermatol. 2013 Oct 16. [Medline].

  44. Labitigan M, Bahce-Altuntas A, Kremer JM, Reed G, Greenberg JD, Jordan N, et al. Higher rates and clustering of abnormal lipids, obesity, and diabetes in psoriatic arthritis compared with rheumatoid arthritis. Arthritis Care Res (Hoboken). 2013 Oct 7. [Medline].

  45. Semb AG, Kvien TK, DeMicco DA, Fayyad R, Wun CC, LaRosa JC, et al. Effect of intensive lipid-lowering therapy on cardiovascular outcome in patients with and those without inflammatory joint disease. Arthritis Rheum. 2012 Sep. 64(9):2836-46. [Medline].

  46. Augustin M, Blome C, Costanzo A, Dauden E, Ferrandiz C, Girolomoni G, et al. Nail Assessment in Psoriasis and Psoriatic Arthritis (NAPPA): Development and Validation of a Tool for Assessment of Nail Psoriasis Outcomes. Br J Dermatol. 2013 Oct 11. [Medline].

  47. Sanyal K, Stuart B. Osteopoikilosis: spotted bone disease in a patient with psoriatic arthritis. J Clin Rheumatol. 2010 Aug. 16(5):251. [Medline].

  48. Siannis F, Farewell VT, Cook RJ, Schentag CT, Gladman DD. Clinical and radiological damage in psoriatic arthritis. Ann Rheum Dis. 2006 Apr. 65(4):478-81. [Medline]. [Full Text].

  49. Gossec L, Smolen JS, Gaujoux-Viala C, Ash Z, Marzo-Ortega H, van der Heijde D, et al. European League Against Rheumatism recommendations for the management of psoriatic arthritis with pharmacological therapies. Ann Rheum Dis. 2012 Jan. 71(1):4-12. [Medline].

  50. [Guideline] Coates LC, Tillett W, Chandler D, et al, on behalf of BSR Clinical Affairs Committee & Standards, Audit and Guidelines Working Group and the BHPR. The 2012 BSR and BHPR guideline for the treatment of psoriatic arthritis with biologics. Rheumatology (Oxford). October 2013. 52(10):1754-7. [Medline]. [Full Text].

  51. Kelly JC. Psoriatic arthritis: guidelines for treatment with biologics. Medscape Medical News. November 4, 2013. [Full Text].

  52. Mease PJ, McInnes IB, Kirkham B, Kavanaugh A, Rahman P, van der Heijde D, et al. Secukinumab Inhibition of Interleukin-17A in Patients with Psoriatic Arthritis. N Engl J Med. 2015 Oct. 373 (14):1329-39. [Medline].

  53. McInnes IB, Mease PJ, Kirkham B, Kavanaugh A, Ritchlin CT, Rahman P, et al. Secukinumab, a human anti-interleukin-17A monoclonal antibody, in patients with psoriatic arthritis (FUTURE 2): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet. 2015 Sep 19. 386 (9999):1137-46. [Medline].

  54. Brooks M. Ustekinumab approved for psoriatic arthritis in US, Europe. Medscape Medical News [serial online]. September 23, 2013. Medscape. Available at http://www.medscape.com/viewarticle/811496. Accessed: October 25, 2013.

  55. Brooks M. FDA approves certolizumab for psoriatic arthritis. Medscape Medical News. September 30, 2013. [Full Text].

  56. Kavanaugh A, Mease PJ, Gomez-Reino JJ, Adebajo AO, Wollenhaupt J, Gladman DD, et al. Treatment of psoriatic arthritis in a phase 3 randomised, placebo-controlled trial with apremilast, an oral phosphodiesterase 4 inhibitor. Ann Rheum Dis. 2014 Mar 4. [Medline].

  57. Schett G, Wollenhaupt J, Papp K, Joos R, Rodrigues JF, Vessey AR, et al. Oral apremilast in the treatment of active psoriatic arthritis: results of a multicenter, randomized, double-blind, placebo-controlled study. Arthritis Rheum. 2012 Oct. 64(10):3156-67. [Medline].

  58. Brooks M. FDA Clears Apremilast (Otezla) for Psoriatic Arthritis. Medscape Medical News. Available at http://www.medscape.com/viewarticle/822396. Accessed: March 24, 2014.

  59. Otezla (apremilast) prescribing information [package insert]. Summit, NJ.: Celgene Corp. 2014. Available at [Full Text].

  60. Boggs W. Methotrexate Side Effects, Intolerance Common in Arthritis Patients. Medscape Medical News. Available at http://www.medscape.com/viewarticle/818646. Accessed: January 14, 2014.

  61. Bulatovic Calasan M, van den Bosch OF, Creemers MC, Custers M, Heurkens AH, van Woerkom JM, et al. Prevalence of methotrexate intolerance in rheumatoid arthritis and psoriatic arthritis. Arthritis Res Ther. 2013 Dec 18. 15(6):R217. [Medline].

  62. Schrader P, Mooser G, Peter RU, Puhl W. [Preliminary results in the therapy of psoriatic arthritis with mycophenolate mofetil]. Z Rheumatol. 2002 Oct. 61(5):545-50. [Medline].

  63. Mease PJ, Gladman DD, Ritchlin CT, Ruderman EM, Steinfeld SD, Choy EH, et al. Adalimumab for the treatment of patients with moderately to severely active psoriatic arthritis: results of a double-blind, randomized, placebo-controlled trial. Arthritis Rheum. 2005 Oct. 52(10):3279-89. [Medline].

  64. Scarpa R, Peluso R, Atteno M, Manguso F, Spano A, Iervolino S, et al. The effectiveness of a traditional therapeutical approach in early psoriatic arthritis: results of a pilot randomised 6-month trial with methotrexate. Clin Rheumatol. 2008 Jul. 27(7):823-6. [Medline].

  65. Patel S, Veale D, FitzGerald O, McHugh NJ. Psoriatic arthritis--emerging concepts. Rheumatology (Oxford). 2001 Mar. 40(3):243-6. [Medline].

  66. Lindsay K, Fraser AD, Layton A, Goodfield M, Gruss H, Gough A. Liver fibrosis in patients with psoriasis and psoriatic arthritis on long-term, high cumulative dose methotrexate therapy. Rheumatology (Oxford). 2009 May. 48(5):569-72. [Medline].

  67. Antoni C, Krueger GG, de Vlam K, Birbara C, Beutler A, Guzzo C, et al. Infliximab improves signs and symptoms of psoriatic arthritis: results of the IMPACT 2 trial. Ann Rheum Dis. 2005 Aug. 64(8):1150-7. [Medline]. [Full Text].

  68. Helliwell PS, Kavanaugh A. Comparison of composite measures of disease activity in psoriatic arthritis using data from an interventional study with golimumab. Arthritis Care Res (Hoboken). 2013 Oct 14. [Medline].

  69. McInnes IB, Kavanaugh A, Gottlieb AB, Puig L, Rahman P, Ritchlin C, et al. Efficacy and safety of ustekinumab in patients with active psoriatic arthritis: 1 year results of the phase 3, multicentre, double-blind, placebo-controlled PSUMMIT 1 trial. Lancet. 2013 Aug 31. 382(9894):780-9. [Medline].

 
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Severe fixed flexion deformity of the interphalangeal joint.
Comparison between sites of involvements in both hands and feet in psoriatic arthritis and rheumatoid arthritis.
Psoriatic arthritis involving the distal phalangeal joint.
Swelling and deformity of the metacarpophalangeal and distal interphalangeal joints in a patient with psoriatic arthritis.
Psoriatic arthritis involving the distal phalangeal joint.
Psoriatic arthritis involving the distal phalangeal joint.
Asymmetrical arthritis pattern of psoriatic arthritis (fixed flexion deformity).
Arthritis mutilans, a typically psoriatic pattern of arthritis, which is associated with a characteristic "pencil-in-cup" radiographic appearance of digits.
Psoriatic arthritis involving the distal phalangeal joint.
Arthritis mutilans (ie, "pencil-in-cup" deformities).
Severe psoriatic arthritis showing involvement of the distal interphalangeal joints, distal flexion deformity, and telescoping of the left third, fourth, and fifth digits due to destruction of joint tissue.
Psoriatic arthritis showing nail changes, distal interphalangeal joint swelling, and sausage digits.
Left, typical appearance of psoriasis, with silvery scaling on a sharply marginated and reddened area of skin overlying the shin. Right, thimblelike pitting of the nail plate in a 56-year-old woman who had suffered from psoriasis for the previous 23 years. Nail pitting, transverse depressions, and subungual hyperkeratosis often occur in association with psoriatic disease of the distal interphalangeal joint. Courtesy of Ali Nawaz Khan, MBBS.
Lateral radiograph of the cervical spine shows syndesmophytes at the C2-3 and C6-7 levels, with zygapophyseal joint fusion. Courtesy of Bruce M. Rothschild, MD.
A 37-year-old man presents with a 1-year history of an erythematous and intensely pruritic rash at the bilateral soles of feet. He has mild dryness and fissuring at his hands, but no overlying scale, intense erythema, or itching like that at his feet. Diagnosis: Psoriatic arthritis (PsA), with palmoplantar pustulosis variant of psoriasis. Courtesy of Jason Kolfenbach, MD, and Kevin Deane, MD, Division of Rheumatology, University of Colorado Denver School of Medicine.
Table. Comparison of Expected Laboratory Values in Psoriatic Arthritis and Rheumatoid Arthritis
Laboratory Studies Psoriatic Arthritis Rheumatoid Arthritis
Erythrocyte sedimentation rate Elevated (< 100) Elevated (< 100)
Rheumatoid factor Negative Positive (85% of patients)
Antinuclear antibody Negative Positive (30% of patients)
C-reactive protein Elevated Elevated
Synovium WBC count 5000-15,000/µL, >50% polymorphonuclear leukocytes WBC count 2000/µL
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