Psoriatic arthritis: Difference between revisions
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===Age=== | ===Age=== | ||
* [[Psoriatic arthritis (patient information)|Psoriatic arthritis]] may commonly occur in age groups 40-50 yrs with mean age at [[diagnosis]] is 40.7 years.<ref name="pmid10813295">{{cite journal |vauthors=Shbeeb M, Uramoto KM, Gibson LE, O'Fallon WM, Gabriel SE |title=The epidemiology of psoriatic arthritis in Olmsted County, Minnesota, USA, 1982-1991 |journal=J. Rheumatol. |volume=27 |issue=5 |pages=1247–50 |date=May 2000 |pmid=10813295 |doi= |url=}}</ref> | * [[Psoriatic arthritis (patient information)|Psoriatic arthritis]] may commonly occur in age groups 40-50 yrs with mean age at [[diagnosis]] is 40.7 years.<ref name="pmid10813295">{{cite journal |vauthors=Shbeeb M, Uramoto KM, Gibson LE, O'Fallon WM, Gabriel SE |title=The epidemiology of psoriatic arthritis in Olmsted County, Minnesota, USA, 1982-1991 |journal=J. Rheumatol. |volume=27 |issue=5 |pages=1247–50 |date=May 2000 |pmid=10813295 |doi= |url=}}</ref> | ||
===Gender=== | |||
===Gender=== | |||
* In general, there is no gender predilection to [[Psoriatic arthritis (patient information)|psoriatic arthritis]].<ref name="pmid4715537">{{cite journal |vauthors=Moll JM, Wright V |title=Familial occurrence of psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=32 |issue=3 |pages=181–201 |date=May 1973 |pmid=4715537 |pmc=1006078 |doi= |url=}}</ref> | * In general, there is no gender predilection to [[Psoriatic arthritis (patient information)|psoriatic arthritis]].<ref name="pmid4715537">{{cite journal |vauthors=Moll JM, Wright V |title=Familial occurrence of psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=32 |issue=3 |pages=181–201 |date=May 1973 |pmid=4715537 |pmc=1006078 |doi= |url=}}</ref> | ||
===Race=== | ===Race=== | ||
* There is insufficient data to support the racial dominance of [[Psoriatic arthritis (patient information)|psoriatic arthritis]]. | * There is insufficient data to support the racial dominance of [[Psoriatic arthritis (patient information)|psoriatic arthritis]]. | ||
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** [[Ankylosis]] | ** [[Ankylosis]] | ||
** [[Edema]] of [[bone marrow]] | ** [[Edema]] of [[bone marrow]] | ||
* '''[[Medical ultrasonography|Ultrasonography]]''': [[Medical ultrasonography|Ultrasonography]] may reveal following findings.<ref name="pmid10451072">{{cite journal |vauthors=Kane D, Greaney T, Bresnihan B, Gibney R, FitzGerald O |title=Ultrasonography in the diagnosis and management of psoriatic dactylitis |journal=J. Rheumatol. |volume=26 |issue=8 |pages=1746–51 |date=August 1999 |pmid=10451072 |doi= |url=}}</ref> | * '''[[Medical ultrasonography|Ultrasonography]]''': [[Medical ultrasonography|Ultrasonography]] may reveal following findings.<ref name="pmid10451072">{{cite journal |vauthors=Kane D, Greaney T, Bresnihan B, Gibney R, FitzGerald O |title=Ultrasonography in the diagnosis and management of psoriatic dactylitis |journal=J. Rheumatol. |volume=26 |issue=8 |pages=1746–51 |date=August 1999 |pmid=10451072 |doi= |url=}}</ref> | ||
** Joint effusions and widening of [[joint]] space | ** Joint effusions and widening of [[joint]] space | ||
Revision as of 17:09, 25 April 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Chandrakala Yannam, MD [2]
Overview
Historical Perspective
- [Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
- In [year], [gene] mutations were first identified in the pathogenesis of [disease name].
- In [year], the first [discovery] was developed by [scientist] to treat/diagnose [dis
Classification
- The CASPAR classification criteria (ClASsification criteria for Psoriatic ARthritis):[1]
- 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.
- 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 xray 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
- Psoriatic arthritis must be differentiated from other arthritides including[5][6][7][8]
- Rheumatoid arthritis
- Reactive arthritis
- Ankylosing spondylitis
- Arthritis associated with inflammatory bowel disease
- Osteoarthritis
- Gout
- Pseudogout
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.
- The incidence of psoriatic arthritis is 3.6-6 per 100,000 individuals.[10]
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
- Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
Natural History, Complications and Prognosis
- Psoriatic arthritis goes through the following stages of progression during its course, defined by the change in clinical damage:[13]
- Common complications or comorbid conditions associated with psoriatic arthritis include:[14][15][16][17][18][19][20]
- 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.[21][22]
Diagnosis
Diagnostic Criteria
- The diagnosis of psoriatic arthritis is easily confirmed when the cutaneous manifestations of psoriasis coexist with arthritis.[23][24][5][25]
- 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.[26]
- 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
Symptoms
- Common symptom may be associated with psoriatic arthritis include:[27][28][29][25]
- 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:
- 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:[30][31]
- Joint tenderness
- Joint swelling may or may not be present
- 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[32]
- Dactylitis: sausage digit due to swelling of the whole finger or toe.[33]
- Skin:[34][35]
- 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.[36]
- Nails:[37][38]
- Nail pits
- Onycholysis
- Subungual hyperkeratosis
- Splinter hemorrhages
- Beau lines
- Leukonychia
- Oil drop patches
- Nail crumbling
- Nail destruction
- Involvement of eyes:[39][40]
- Edema of hands or feet: Swelling of hands and feet which is asymmetrical with pitting edema may be found in some cases.[41]
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:[42]
- CBC with differential count
- Elevated ESR
- Elevated CRP (C- reactive protein)
- Autoantibodies: The following autoantibodies may be found in patients with psoriatic arthritis.[43]
- Rheumatoid factor
- ANA (Antinuclear antibodies)
- Anti-citrullinated peptide antibodies (ACPA)
- Genetic markers:[44][45]
- Synovial fluid analysis: Elevated WBC count suggestive of inflammation.
Imaging Findings
- X-ray of digits:[46][47][48]
- 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:[49]
- enthesitis
- Periostitis
- Joint erosions
- Synovitis (articular or flexor tendon sheath)
- Ankylosis
- Edema of bone marrow
- Ultrasonography: Ultrasonography may reveal following findings.[50]
- 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. [51]
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.[52][53]
- 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[54]
- British Society of Rheumatology (BSR)[55]
- 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.[56][57]
- 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[58][59]: 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[59]: 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[60]
- Preferred regimen (1): Methotrexate[58][59]: 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[61]: It is a human anti-TNF alpha monoclonal antibody. Dosage: 40 mg can be given s.c every 2 weeks
- Preferred regimen (2): Etanercept[62]: It is a TNF receptor p75-IgG1 fusion protein. Dosage: 50 mg can be given s.c every week.
- Preferred regimen (3): Infliximab[63]: 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[64]: it is a human IgG1k anti-TNF alpha antibody. Dosage: 50 mg can be given s.c and monthly.
- Preferred regimen (5): Certolizumab pegol[65]: 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[66]: 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[67] : Dosage: 160 mg initially, then 80 mg every two or four weeks can be given subcutaneously.
- Anti-IL-12/23 therapy:
- Ustekinumab[68]: 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[69]: 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.[56][57]
- Axial disease/ spondylitis:[70]
- 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:[71]
- 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:[72]
- 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:[73]
- 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.[74]
- 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
- ↑ Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H (August 2006). "Classification criteria for psoriatic arthritis: development of new criteria from a large international study". Arthritis Rheum. 54 (8): 2665–73. doi:10.1002/art.21972. PMID 16871531.
- ↑ 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.
- ↑ Barnas JL, Ritchlin CT (November 2015). "Etiology and Pathogenesis of Psoriatic Arthritis". Rheum. Dis. Clin. North Am. 41 (4): 643–63. doi:10.1016/j.rdc.2015.07.006. PMID 26476224.
- ↑ 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.
- ↑ 5.0 5.1 Helliwell PS, Taylor WJ (March 2005). "Classification and diagnostic criteria for psoriatic arthritis". Ann. Rheum. Dis. 64 Suppl 2: ii3–8. doi:10.1136/ard.2004.032318. PMC 1766878. PMID 15708931.
- ↑ McEwen C, DiTata D, Lingg C, Porini A, Good A, Rankin T (1971). "Ankylosing spondylitis and spondylitis accompanying ulcerative colitis, regional enteritis, psoriasis and Reiter's disease. A comparative study". Arthritis Rheum. 14 (3): 291–318. PMID 5562018.
- ↑ 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.
- ↑ Moll JM, Haslock I, Macrae IF, Wright V (September 1974). "Associations between ankylosing spondylitis, psoriatic arthritis, Reiter's disease, the intestinal arthropathies, and Behcet's syndrome". Medicine (Baltimore). 53 (5): 343–64. PMID 4604133.
- ↑ 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.
- ↑ 10.0 10.1 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.
- ↑ 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.
- ↑ Gladman DD, Antoni C, Mease P, Clegg DO, Nash P (2005). "Psoriatic arthritis: epidemiology, clinical features, course, and outcome". Ann. Rheum. Dis. 64 Suppl 2: ii14–7. doi:10.1136/ard.2004.032482. PMC 1766874. PMID 15708927.
- ↑ Han C, Robinson DW, Hackett MV, Paramore LC, Fraeman KH, Bala MV (November 2006). "Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis". J. Rheumatol. 33 (11): 2167–72. PMID 16981296.
- ↑ Labitigan M, Bahče-Altuntas A, Kremer JM, Reed G, Greenberg JD, Jordan N, Putterman C, Broder A (April 2014). "Higher rates and clustering of abnormal lipids, obesity, and diabetes mellitus in psoriatic arthritis compared with rheumatoid arthritis". Arthritis Care Res (Hoboken). 66 (4): 600–7. doi:10.1002/acr.22185. PMC 3969762. PMID 24115739.
- ↑ Eder L, Wu Y, Chandran V, Cook R, Gladman DD (September 2016). "Incidence and predictors for cardiovascular events in patients with psoriatic arthritis". Ann. Rheum. Dis. 75 (9): 1680–6. doi:10.1136/annrheumdis-2015-207980. PMID 26493817.
- ↑ Rohekar S, Tom BD, Hassa A, Schentag CT, Farewell VT, Gladman DD (January 2008). "Prevalence of malignancy in psoriatic arthritis". Arthritis Rheum. 58 (1): 82–7. doi:10.1002/art.23185. PMID 18163513.
- ↑ McDonough E, Ayearst R, Eder L, Chandran V, Rosen CF, Thavaneswaran A, Gladman DD (May 2014). "Depression and anxiety in psoriatic disease: prevalence and associated factors". J. Rheumatol. 41 (5): 887–96. doi:10.3899/jrheum.130797. PMID 24692521.
- ↑ Ciacli C, Cojocaru M (2012). "Systemic osteoporosis--major complication of psoriatic arthritis". Rom J Intern Med. 50 (2): 173–8. PMID 23326962.
- ↑ Curtis JR, Beukelman T, Onofrei A, Cassell S, Greenberg JD, Kavanaugh A, Reed G, Strand V, Kremer JM (January 2010). "Elevated liver enzyme tests among patients with rheumatoid arthritis or psoriatic arthritis treated with methotrexate and/or leflunomide". Ann. Rheum. Dis. 69 (1): 43–7. doi:10.1136/ard.2008.101378. PMC 2794929. PMID 19147616.
- ↑ McLaughlin M, Ostör A (December 2014). "Early treatment of psoriatic arthritis improves prognosis". Practitioner. 258 (1777): 21–4, 3. PMID 25603589.
- ↑ Buckley C, Cavill C, Taylor G, Kay H, Waldron N, Korendowych E, McHugh N (October 2010). "Mortality in psoriatic arthritis - a single-center study from the UK". J. Rheumatol. 37 (10): 2141–4. doi:10.3899/jrheum.100034. PMID 20682670.
- ↑ Liu JT, Yeh HM, Liu SY, Chen KT (September 2014). "Psoriatic arthritis: Epidemiology, diagnosis, and treatment". World J Orthop. 5 (4): 537–43. doi:10.5312/wjo.v5.i4.537. PMC 4133459. PMID 25232529.
- ↑ WRIGHT V (December 1956). "Psoriasis and arthritis". Ann. Rheum. Dis. 15 (4): 348–56. PMC 1006908. PMID 13395269.
- ↑ 25.0 25.1 Punzi L, Pianon M, Rossini P, Schiavon F, Gambari PF (April 1999). "Clinical and laboratory manifestations of elderly onset psoriatic arthritis: a comparison with younger onset disease". Ann. Rheum. Dis. 58 (4): 226–9. PMC 1752862. PMID 10364901.
- ↑ Scarpa R, Cosentini E, Manguso F, Oriente A, Peluso R, Atteno M, Ayala F, D'Arienzo A, Oriente P (December 2003). "Clinical and genetic aspects of psoriatic arthritis "sine psoriasis"". J. Rheumatol. 30 (12): 2638–40. PMID 14719207.
- ↑ Sankowski AJ, Lebkowska UM, Cwikła J, Walecka I, Walecki J (January 2013). "Psoriatic arthritis". Pol J Radiol. 78 (1): 7–17. doi:10.12659/PJR.883763. PMC 3596149. PMID 23493653.
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