Psoriatic arthritis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Chandrakala Yannam, MD [2]
Overview
Psoriatic arthritis is a systemic, immune- mediated inflammatory arthritis, associated with psoriasis. The etiology is not clearly understood. It may be caused by complex interaction between genetic, immunologic and environmental mechanisms which act as triggers for the disease development. Both psoriatic arthritis and psoriasis have been shown to have strong familial predisposition. Psoriatic arthritis present with pain and stiffness in the affected joints. According to Moll and Wright criteria, joint involvement pattern in psoriatic arthritis include distal arthritis usually involving distal interphalangeal joints, asymmetric oligoarthritis, symmetric polyarthritis, arthritis mutilans, spondylitis, and sacroiliitis. Other symptoms include enthesitis (pain and tenderness at the insertion of tendons and ligaments to the bone), dactylitis ( sausage like finger or toe swelling), nail changes (pitting, hyperkeratosis, and nail destruction). The pathophysiology of psoriatic arthritis consists of interactions between cytokines, dendritic cells, and T lymphocytes. Psoriatic arthritis must be differntiated from other inflammatory arthritides including rheumatoid arthritis, ankylosing spondylitis, reactive arthritis, gout, pseudogout, osteoarthritis, arthritis associated with inflammatory bowel disease. The prevalence of psoriatic arthritis in general population ranges from 60 - 250 cases per 100,000 individuals and the prevalence of psoriatic arthritis among psoriasis patients is 11,000 per 100,000 individuals. The mainstay of therapy for psoriatic arthritis NSAIDs, conventional DMARDs (eg, methotrexate, sulfasalazine, cyclosporine) and biologic DMARDs (eg, TNF inhibitors), anti IL therapy (eg, secukinumab, ustekinumab). Other treatment options include physiotherapy, patient education about disease and joint preservation and surgery. Psoriatic arthritis is associated with a number of comorbid conditions due to circulating immunoglobulins, antibodies including metabolic syndrome, increased insulin resistance, atherosclerosis, stroke, hypertension, uveitis, osteoporosis and depression. Patients are monitored regularly for disease activity, drug efficacy, adverse effects and associated comorbid conditions.
Historical Perspective
- In 1822, the association between psoriasis and psoriatic arthritis was noticed by Dr. Alibert.
- In 1948 after the discovery of rheumatoid factor, psoriatic arthritis was considered as a separate entity from rheumatoid arthritis by UK physician Wright.[1]
Classification
- Based on the severity, psoriatic arthritis may be classified into following categories:[2]
- Mild
- Moderate
- Severe
| Organ system involvement | Mild psoriatic arthritis | Moderate psoriatic arthritis | Severe psoriatic arthritis |
|---|---|---|---|
| Peripheral arthritis | <5 joints involvement
No damage can be seen on x-ray No loss of physical function Minimal impact on patient's quality of life |
⩾5 joints involvement
Damage can be visible on x-ray Non-responsive to NSAIDs Moderate impact on patient's quality of life |
⩾5 joints involvement
Severe damage may be seen on x-ray Nonresponsive to NSAIDs, standard DMARDs Severe impact on patient's quality of life |
| Axial joint involvement | Mild pain present
No loss of physical function |
Loss of physical function
Bath Ankylosing Spondylitis Disability Activity Index (BASDAI) >4 |
Failure of response |
| Skin | Body Surface Area ( BSA) <5
Psoriasis area and severity index (PASI) <5 |
Resistant to topical therapy
Dermatology Life Quality Index (DLQI)<10 PASI<10 |
BSA>10, DLQI>10PASI>10 |
| Dactylitis | +/- Pain
Normal activity/ function |
Presence of erosive disease or loss of physical function | Failure of response to NSAIDs and conventional DMARDs |
| Enthesitis | Number of sites involved:1–2
No loss of physical function |
Number of sites involved >2
or Loss of function |
Loss of function
>2 sites involvement and failure of response |
Causes
There are no established causes of psoriatic arthritis. The occurrence of psoriatic arthritis is secondary to a combination of genes, immune mechanisms and exposure to specific external factors or triggers, which increase an individual's risk of developing psoriatic arthritis. These risk factors lead to complex interactions between the genetics, immune system, and the environment.[3]
Pathophysiology
The pathogenesis of psoriatic arthritis (PsA) involves the following events:[4]
- In joints there is a prominent lymphocytic infiltrate, limited to the dermal papillae in skin and to the underlying stroma.
- T lymphocytes, particularly CD4 cells, are the most common inflammatory cells in the skin and joints, with a CD4/CD8 ratio of 2:1.
- High levels of tumor necrosis factor alpha (TNF), IL-8, IL-6, IL-1, IL-10, and matrix metalloproteinases are present in the joint fluid of patients with early PsA.
- Collagenase mediated degradation of cartilage collagen begins in early phases of the disease and may be the result of the proteases produced as a result of above mentioned cytokines.
Osteoclast mediated joint destruction
- The elevated levels of TNF leads to a high number of osteoclast precursor cells circulating in the blood.
- Osteoclast precursors migrate to the joint where they encounter increased expression of receptor activator of nuclear factor kappa B ligand ( NF-κB), which favors the differentiation and activation of osteoclasts.
- Osteoclasts eventually lead to the joint destruction seen in psoriatic arthritis.
Differentiating psoriatic arthritis from other Diseases
Epidemiology and Demographics
- The prevalence of psoriatic arthritis in general population ranges from 60 - 250 cases per 100,000 individuals in United states.[9]
- The prevalence ranges in genreal population from 50 - 210 cases per 100,000 individuals in Europe.[10]
- The prevalence among psoriasis patients is 11,000 per 100,000 individuals.
- Incidence of psoriatic arthritis is approximately 6 per 100,000 individuals.[11]
Age
- Psoriatic arthritis may commonly occur in age groups 40-50 yrs with mean age at diagnosis is 40.7 years.[11]
Gender
- In general, there is no gender predilection to psoriatic arthritis.[12]
Race
- There is insufficient data to support the racial dominance of psoriatic arthritis.
Risk Factors
- Genetic factors:[13][14][15]
- Both psoriasis and psoriatic arthritis have been shown to have strong familial distribution among first degree relatives.
- psoriatic arthritis is frequently associated with HLA-B alleles than with HLA-C alleles, when compared to psoriasis.
- In patients with psoriatic arthritis when compared to general population, HLA antigens that are expressed more oftenly including HLA-B13, HLA-B17, HLA-B57, and HLA-Cw*0602.
- HLA CLASS 1 antigens that are related to psoriatic arthritis include HLA-B13, HLA-B38, HLA-B27, HLA-B39, and HLA-B57.
- HLA-B38 and HLA-B39 have a strong association with peripheral inflammatory articular disease, while HLA-B27 is strongly associated with spondylitis.
- HLA class 2 antigens that are associated with psoriatic arthritis including HLA-DRB1*04 and HLA-DRB1*07.
- HLA antigens, HLA-B27 along with HLA-DR7, HLA-DQ3 and in the absence of HLA-DR7, and HLA-B39 may be considered as predictors for disease progression. HLA-B22 antigen is protective for psoriatic arthritis.[16]
- Increased risk for both psoriatic arthritis and psoriasis may be associated with following gene polymorphisms:
- TNF-alpha polymorphisms[17]
- CARD15 gene on chrosome 16q: Pleiotropic autoimmune gene. It is the first non-MHC gene that can be associated with psoriatic arthritis.[18]
- Polymorphisms involving IL-23 receptor and IL-12 beta genes.[19]
- Interleukin 2 (IL2) and interleukin 21 (IL21)
- MHC class I chain-related gene A (MICA)[20]
- IL-1 gene cluster polymorphism
- IL-13 polymorphism
- Increased risk for deveoping poriatic arthritis may also be related to interactions between certain HLA-class I alleles and killer inhibitory receptors (KIRs) located on chromosome 19. Psoriatic arthritis susceptibility is correlated with the presence of KIR2DS1 and/or KIR2DS2, and HLA-Cw alleles.[21]
- Immune mechanisms:[22][23][3]
- Presence of increased levels immunoglobulins and antinuclear antibodies in the serum may be found in patients with psoriatic arthritis.
- In patients with psoriatic arthritis, the synovial fluid contains reactive dendritic cells, which lead to activation of T lymphocytes by presenting an unknown antigen to CD4 positive T cells.
- Cytokines produced as a result of T cell activation and activation of other inflammatory precursors lead to proliferation and activation of synovial and epidermal fibroblasts.
- Excessively proliferated fibroblasts from epiderm and synovium may produce excess IL-1, IL-6, and platelet-derived growth factors.
- T lymphocytes may express HLA-DR and IL-2 receptor, and receptors to several adhesive molecules and cytokines particularly IL-6.
- Synovial fluid of patients with psoriatic arthritis will show increased levels of tumor necrosis factor (TNF)-alpha, IL-1, IL-6, and IL-8.
- Elevated concentrations of serum interleukins including IL-10, IL-13, interferons particularly INF- alpha, chemokines such as CCL19, vascular endothelial growth factor, fibroblast growth factor, and decreased levels of granulocyte-colony stimulating factor may be found.
- Environmental factors:
Natural History, Complications and Prognosis
- If left untreated psoriatic arthritis may lead to severe joint destruction and deformity resulting in loss of physical function and reduced quality of life.
- Common complications or comorbid conditions associated with psoriatic arthritis include:[29][30][31][32][33][34][35]
- Metabolic syndrome
- Progressive joint destruction and deformity
- Hypertension
- Increase insulin resistance and diabetes mellitus
- Dyslipidemia
- Increased atherosclerotic risk
- Myocardial infarction
- Congestive heart failure
- Arrythmias
- Stroke
- Inflammatory bowel disease
- Osteoporosis
- Depression
- Increased risk for malignancy (breast, prostate, and lung)
- uveitis
- Non alcoholic fatty liver disease
- Decreased quality of life
- Prognosis is generally good with early diagnosis and treatment with DMARDs and TNF inhibitors. Overall survival rate also depends on management of comorbid conditions along with arthritis treatment.[36][37]
Diagnosis
Diagnostic Criteria
- The diagnosis of psoriatic arthritis is easily confirmed when the cutaneous manifestations of psoriasis coexist with arthritis.[38][39][5][40]
- It must be differentiated from other arthritides based on the joint involvement patterns, clinical features, imaging and laboratory studies.
- The following manifestations may be helpful in diagnosing psoriatic arthritis in an individual in the absence of psoriatic skin lesions.[41]
- Family history of psoriasis in first degree relatives
- Asymmetric joint distribution
- Involvement of distal joints
- Nail involvement (eg, pitting, nail bed destruction, onycholysis)
- Dactylitis
- Hidden psoriatic plaques
- The CASPAR criteria (ClASsification criteria for Psoriatic ARthritis):[42]
- The CASPAR study stated that a patient present with inflammatory articular disease (inflammatory peripheral arthritis, enthesitis, spondylitis) can be diagnosed as having psoriatic arthritis if a total of at least three points are present from the presence of the following possibilities.
- Skin lesions:
- dactylitis (1 point)
- Nail dystrophy (1 point)
- Juxta-articular new bone formation (1point)
- Absence of rheumatoid factor (1 point)
- The specificity is approximately 98.7% and sensitivity is approximately 91.4%.
- The CASPAR study stated that a patient present with inflammatory articular disease (inflammatory peripheral arthritis, enthesitis, spondylitis) can be diagnosed as having psoriatic arthritis if a total of at least three points are present from the presence of the following possibilities.
Symptoms
- Common symptom may be associated with psoriatic arthritis include:[43][44][45][40]
- Joint pain and swelling
- Joint stiffness
- Morning stiffness: May lasts more than 30 mins. It is aggravated by prolonged rest and relieved by physical activity.
- Decreased range of motion and quality of life depending on the severity of the disease.
- Enthesitis: Pain can be felt in areas where tendons, ligaments, and synovium attach to bones.
- Common locations include:
- Achilles tendinitis: Pain at the heel, tibial tuberosity and other tendon insertion.
- Plantar fasciitis
- Common locations include:
- Dactylitis: Sausage-like swelling of the entire finger or toe.
- Skin lesions: Scaly, erythematous papules and plaques
- Dystrophic nails
- Ocular symptoms include redness and tearing due to conjunctivitis, blepharitis, and uveitis.
- Fatigue
Physical Examination
- Patients with psoriatic arthritis usually appear normal.
- Physical examination of a patient with psoriatic arthritis may include:
- Joint involvement:[46][47]
- Joint tenderness
- Joint swelling may or may not be present
- Redness and warmth
- Patterns of joint involvement in psoriatic arthritis may include according to moll and wright :
- Distal arthritis: Involving mostly DIP joints, may be symmetric or asymmetric. It may involve multiple joints or only few joints.
- Asymmetric oligoarthritis: Most common pattern can be seen in psoriatic arthritis. It is characterized by asymmetric involvement of less than 5 small or large joints.
- Symmetric polyarthritis
- Arthritis mutilans: Resorption of phalanges, metatarsals and, metacarpals.
- Spondylitis
- Sacroiliitis
- Joint effusion
- Achilles tendinitis[48]
- Dactylitis: sausage digit due to swelling of the whole finger or toe.[49]
- Skin:[50][51]
- Psoriatic arthritis may occur after the onset of psoriasis in most of the patients. However, in some cases, arthritis precede psoriasis. The phenotypes of skin psoriasis that are associated with an increased risk of psoriatic arthritis are the lesions in the scalp, nail, intergluteal, and perianal regions.[52]
- Nails:[53][54]
- Nail pits
- Onycholysis
- Subungual hyperkeratosis
- Splinter hemorrhages
- Beau lines
- Leukonychia
- Oil drop patches
- Nail crumbling
- Nail destruction
- Involvement of eyes:[55][56]
- Edema of hands or feet: Swelling of hands and feet which is asymmetrical with pitting edema may be found in some cases.[57]
Laboratory Findings
- There are no specific laboratory findings associated with psoriatic arthritis and most the tests are non-specific.
- However, there are certain laboratory tests that can check for markers of inflammation and to exclude other diseases. These include:[58]
- CBC with differential count
- Elevated ESR
- Elevated CRP (C- reactive protein)
- Autoantibodies: The following autoantibodies may be found in patients with psoriatic arthritis.[59]
- Rheumatoid factor
- ANA (Antinuclear antibodies)
- Anti-citrullinated peptide antibodies (ACPA)
- Genetic markers:[60][14]
- Synovial fluid analysis: Elevated WBC count suggestive of inflammation.
Imaging Findings
- X-ray of digits:[61][62][63]
- Bone destructive changes including formation of subchondral cyst and erosions
- Fluffy periostitis
- Ankylosis
- Phalangeal tuft acroosteolysis
- New bone formation: Perisoteal and endosteal bone formation may result in increased bone density of an entire phalanx resulting in so called ivory phalanx.
- Pencil-in-cup deformity (osteolytic lesions) usually involving DIP joints but also affects PIP joints
- Osteolysis and ankylosis both coexists in the same joints of hands and foot
- Enthesitis
- Dactylitis (sausage digit)
- Gross finger deformity
- Arthritis mutilans: It may lead to telescoping of fingers caused by marked bony resorption and the subsequent collapse of soft tissue
- Asymmetrical sacroiliitis
- Spondylitis: Asymmetric paravertebral ossifications and relative sparing of the facet joints
- MRI: MRI may reveal the following findings:[64]
- enthesitis
- Periostitis
- Joint erosions
- Synovitis (articular or flexor tendon sheath)
- Ankylosis
- Edema of bone marrow
- Ultrasonography: Ultrasonography may reveal following findings.[65]
- Joint effusions and widening of joint space
- Synovitis (articular and flexor tenosynovitis)
- Dactylitis
- Thickening of the joint capsule
Other Diagnostic Studies
- Bone mineral density (BMD) testing: Bone density may be decreased in psoriatic arthritis resulting in osteoporosis and increased risk for fractures. [66]
Treatment
Medical Therapy
- Medical therapy for psoriatic arthritis is according to the guidelines proposed by
- European League Against Rheumatism (EULAR): Guidelines were first proposed in 2012 and they were updated in 2015.[67][68]
- Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA)[2]
- American College of Rheumatology (ACR)
- National Psoriasis Foundation (NPF)
- American Academy of Dermatology (AAD) Psoriasis Guidelines of Care[69]
- British Society of Rheumatology (BSR)[70]
- Pharmacologic therapy for psoriatic arthritis include, non-steroidal anti-inflammatory drugs (NSAIDs), conventional synthetic DMARDs (eg, methotrexate, sulfasalazine, cyclosporin A, leflunomide), biologicDMARDs including, TNF inhibitors (eg, etanercept, infliximab, adalimumab, golimumab), phosphodiesterase (PDE) inhibitors (eg, apremilast), interleukin(IL) inhibitors (eg, secukinumab, ixekizumab, abatacept) and intraarticular glucocorticoid injections.
- Peripheral arthritis:
- Mild disease: Nonsteroidal antiinflammatory drugs (NSAIDs) are the most commonly used drugs for the management of mild active psoriatic arthritis.[71][72]
- Preferred regimen (1): Naproxen: 375-500 mg/twice a day
- Preferred regimen (2): Celecoxib: 200 mg/twice a day
- Preferred regimen (3): Nimesulide: 200 and 400 mg/day
- Preferred regimen (4): Ibuprofen: Max dose of up to 2400 mg/day
- Adverse effects of non-steroidal anti-inflammatory drugs include increased cardiovascular risk, gastritis, ulcers and low renal clearance.
- Moderate to severe disease: Conventional synthetic disease-modifying antirheumatic drugs (DMARDs) may be considered in patients with moderate to severe active peripheral arthritis. These are also considered in patients who are resistant or not responding to NSAIDs, and local corticosteroid injections.
- Preferred regimen (1): Methotrexate[73][74]: 15 to 25 mg/week
- Adverse effects of methotrexate: Liver toxicity, immunosuppression, interstitial pneumonitis, increased infection risk.
- Folic acid supplementation should be given to all patients taking methotrexate.
- Preferred regimen (2): Leflunomide: 20 mg/day
- Adverse effects of Leflunomide: Liver toxicity, diarrhea, rash, alopecia, pneumonitis.
- Preferred regimen (3): Sulfasalazine[74]: 2-3 gms/day
- Adverse effects of sulfasalazine: Nausea, diarrhea, abdominal pain, rash, and neutropenia.
- Preferred regimen (4): Cyclosporine A: 3.5 mg/kg per day[75]
- Preferred regimen (1): Methotrexate[73][74]: 15 to 25 mg/week
- Severe disease and the presence of adverse prognostic factors: TNF inhibitors (eg, etanercept, infliximab, adalimumab, golimumab), interleukin(IL) inhibitors (eg, secukinumab, ixekizumab, abatacept).
- Biologic DMARDs are considered for patients who fail to respond or contraindication to conventional synthetic DMARDs. It is also administered in patients with presence of poor prognosis factors, even if they have not failed a standard DMARDs therapy.
- TNF inhibitors:
- Preferred regimen (1): Adalimumab[76]: It is a human anti-TNF alpha monoclonal antibody. Dosage: 40 mg can be given s.c every 2 weeks
- Preferred regimen (2): Etanercept[77]: It is a TNF receptor p75-IgG1 fusion protein. Dosage: 50 mg can be given s.c every week.
- Preferred regimen (3): Infliximab[78]: It is a chimeric monoclonal antibody against TNF alpha. Dosage: 5 mg/kg at weeks 0, 2, and 6 and after that 5 mg/kg every 6-8 weeks.
- Preferred regimen (4): Golimumab[79]: it is a human IgG1k anti-TNF alpha antibody. Dosage: 50 mg can be given s.c and monthly.
- Preferred regimen (5): Certolizumab pegol[80]: It is a Fab fragment of anti-TNF alpha monoclonal antibody. Dosage: 400 mg at 0, 2, and 4 weeks can be given s.c and then 200 mg every 2 weeks sub cutaneously.
- Adverse effects: Reactivation of latent tuberculosis, increased risk for infections including bacterial and opportunistic infection. Therefore, before starting treatment with TNF inhibitors screening for TB, Hepatitis B, and C should be done.
- IL inhibitor therapy: This is considered in patients with severe peripheral arthritis, where TNF therapy is contraindicated or not responding even after switching to different TNF inhibitor.
- Anti-IL-17 therapies :
- Preferred regimen (1): Secukinumab[81]: It is a monoclonal antibody against IL-17A. Dosage: 150 mg at weeks 0, 1, 2, 3, and 4 and then every 4 weeks can be given subcutaneously.
- Preferred regimen (2): Ixekizumab[82] : Dosage: 160 mg initially, then 80 mg every two or four weeks can be given subcutaneously.
- Anti-IL-12/23 therapy:
- Ustekinumab[83]: It is a IgG1 monoclonal antibody against the shared P40 subunit of human IL-12 and IL-23. Dosage: 45 mg at weeks 0 and 4 and then for every 12 weeks can be given subcutaneously.
- Anti-IL-17 therapies :
- Abatacept[84]: It is a costimulatory T-cell molecule, blocking signal activation of the CD28 receptor on the T cell inhibiting T-cell activation. Dosage: 125 mg can be given subcutaneously once in a week.
- TNF inhibitors:
- Biologic DMARDs are considered for patients who fail to respond or contraindication to conventional synthetic DMARDs. It is also administered in patients with presence of poor prognosis factors, even if they have not failed a standard DMARDs therapy.
- Mild disease: Nonsteroidal antiinflammatory drugs (NSAIDs) are the most commonly used drugs for the management of mild active psoriatic arthritis.[71][72]
- Axial disease/ spondylitis:[85]
- Mild disease: Non-steroidal anti-inflammatory drugs (NSAIDs), local corticosteroid injections, patient education, exercise and physiotherapy may be recommended to treat mild axial involvement.
- Moderate to severe disease: TNF inhibitors
- Skin disease:[86]
- Phototherapy: First line of treatment including UVB, PUVA.
- Fumeric esters, retinols, calcipotriol
- Conventional DMARDs and TNF inhibitors, and retinoic acid derivatives (eg, acitretin) may be used in combinatination with phototherapy.
- Nail disease:[87]
- Topical corticosteroids, calcipotriol creams, DMARDs and TNF inhibitors may be helpful.
- Enthesitis:
- Mild disease: NSAIDs, local corticosteroid injection, physical therapy may be helpful.
- Moderate to severe disease: TNF inhibitors
- Dactylitis:[88]
- NSAIDs, steroid injections, conventional DMARDs and TNF inhibitors can be helpful.
- Biologic DMARDs can be considered for treatment of dactylitis if, therapy with NSAIDs, steroid injections, conventional DMARDs fails.
- Non pharmacologic therapy:
- Exercise
- Weight reduction
- Physical therapy
- Occupational therapy
- Educating the patient about disease course, joint protection and comorbid conditions.
- Orthotics
Surgery
- Surgery may be indicated in patients of psoriatic arthritis with severe joint damage that limit mobility.[89]
- Common procedures include hand joint surgery involving PIP and DIP joints, hip or knee surgery.
Prevention
- There are no established preventive measures for psoriatic arthritis.
- Patients are monitored regularly for disease activity, drug efficacy, adverse effects and associated comorbid conditions.
References
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- ↑ 2.0 2.1 Ritchlin CT, Kavanaugh A, Gladman DD, Mease PJ, Helliwell P, Boehncke WH, de Vlam K, Fiorentino D, Fitzgerald O, Gottlieb AB, McHugh NJ, Nash P, Qureshi AA, Soriano ER, Taylor WJ (September 2009). "Treatment recommendations for psoriatic arthritis". Ann. Rheum. Dis. 68 (9): 1387–94. doi:10.1136/ard.2008.094946. PMC 2719080. PMID 18952643.
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- ↑ Ritchlin CT, Haas-Smith SA, Li P, Hicks DG, Schwarz EM (2003). "Mechanisms of TNF-alpha- and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis". J. Clin. Invest. 111 (6): 821–31. doi:10.1172/JCI16069. PMC 153764. PMID 12639988.
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- ↑ Helliwell PS, Hickling P, Wright V (March 1998). "Do the radiological changes of classic ankylosing spondylitis differ from the changes found in the spondylitis associated with inflammatory bowel disease, psoriasis, and reactive arthritis?". Ann. Rheum. Dis. 57 (3): 135–40. PMC 1752543. PMID 9640127.
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- ↑ Gelfand JM, Gladman DD, Mease PJ, Smith N, Margolis DJ, Nijsten T, Stern RS, Feldman SR, Rolstad T (October 2005). "Epidemiology of psoriatic arthritis in the population of the United States". J. Am. Acad. Dermatol. 53 (4): 573. doi:10.1016/j.jaad.2005.03.046. PMID 16198775.
- ↑ Hanova P, Pavelka K, Holcatova I, Pikhart H (August 2010). "Incidence and prevalence of psoriatic arthritis, ankylosing spondylitis, and reactive arthritis in the first descriptive population-based study in the Czech Republic". Scand. J. Rheumatol. 39 (4): 310–7. doi:10.3109/03009740903544212. PMID 20476864.
- ↑ 11.0 11.1 Shbeeb M, Uramoto KM, Gibson LE, O'Fallon WM, Gabriel SE (May 2000). "The epidemiology of psoriatic arthritis in Olmsted County, Minnesota, USA, 1982-1991". J. Rheumatol. 27 (5): 1247–50. PMID 10813295.
- ↑ Moll JM, Wright V (May 1973). "Familial occurrence of psoriatic arthritis". Ann. Rheum. Dis. 32 (3): 181–201. PMC 1006078. PMID 4715537.
- ↑ Nograles KE, Brasington RD, Bowcock AM (February 2009). "New insights into the pathogenesis and genetics of psoriatic arthritis". Nat Clin Pract Rheumatol. 5 (2): 83–91. doi:10.1038/ncprheum0987. PMC 2790861. PMID 19182814.
- ↑ 14.0 14.1 Eder L, Chandran V, Pellet F, Shanmugarajah S, Rosen CF, Bull SB, Gladman DD (January 2012). "Human leucocyte antigen risk alleles for psoriatic arthritis among patients with psoriasis". Ann. Rheum. Dis. 71 (1): 50–5. doi:10.1136/ard.2011.155044. PMID 21900282.
- ↑ Gladman DD, Cheung C, Ng CM, Wade JA (March 1999). "HLA-C locus alleles in patients with psoriatic arthritis (PsA)". Hum. Immunol. 60 (3): 259–61. PMID 10321964.
- ↑ Gladman DD, Farewell VT, Kopciuk KA, Cook RJ (April 1998). "HLA markers and progression in psoriatic arthritis". J. Rheumatol. 25 (4): 730–3. PMID 9558177.
- ↑ Rahman P, Siannis F, Butt C, Farewell V, Peddle L, Pellett F, Gladman D (July 2006). "TNFalpha polymorphisms and risk of psoriatic arthritis". Ann. Rheum. Dis. 65 (7): 919–23. doi:10.1136/ard.2005.039164. PMC 1798211. PMID 16284098.
- ↑ Rahman P, Bartlett S, Siannis F, Pellett FJ, Farewell VT, Peddle L, Schentag CT, Alderdice CA, Hamilton S, Khraishi M, Tobin Y, Hefferton D, Gladman DD (September 2003). "CARD15: a pleiotropic autoimmune gene that confers susceptibility to psoriatic arthritis". Am. J. Hum. Genet. 73 (3): 677–81. doi:10.1086/378076. PMC 1180694. PMID 12879366.
- ↑ Filer C, Ho P, Smith RL, Griffiths C, Young HS, Worthington J, Bruce IN, Barton A (December 2008). "Investigation of association of the IL12B and IL23R genes with psoriatic arthritis". Arthritis Rheum. 58 (12): 3705–9. doi:10.1002/art.24128. PMC 3001112. PMID 19035472.
- ↑ Gonzalez S, Martinez-Borra J, Torre-Alonso JC, Gonzalez-Roces S, Sanchez del Río J, Rodriguez Pérez A, Brautbar C, López-Larrea C (May 1999). "The MICA-A9 triplet repeat polymorphism in the transmembrane region confers additional susceptibility to the development of psoriatic arthritis and is independent of the association of Cw*0602 in psoriasis". Arthritis Rheum. 42 (5): 1010–6. doi:10.1002/1529-0131(199905)42:5<1010::AID-ANR21>3.0.CO;2-H. PMID 10323458.
- ↑ Williams F, Meenagh A, Sleator C, Cook D, Fernandez-Vina M, Bowcock AM, Middleton D (July 2005). "Activating killer cell immunoglobulin-like receptor gene KIR2DS1 is associated with psoriatic arthritis". Hum. Immunol. 66 (7): 836–41. doi:10.1016/j.humimm.2005.04.005. PMID 16112031.
- ↑ Partsch G, Steiner G, Leeb BF, Dunky A, Bröll H, Smolen JS (March 1997). "Highly increased levels of tumor necrosis factor-alpha and other proinflammatory cytokines in psoriatic arthritis synovial fluid". J. Rheumatol. 24 (3): 518–23. PMID 9058659.
- ↑ Szodoray P, Alex P, Chappell-Woodward CM, Madland TM, Knowlton N, Dozmorov I, Zeher M, Jarvis JN, Nakken B, Brun JG, Centola M (March 2007). "Circulating cytokines in Norwegian patients with psoriatic arthritis determined by a multiplex cytokine array system". Rheumatology (Oxford). 46 (3): 417–25. doi:10.1093/rheumatology/kel306. PMID 16936328.
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