Psoriatic arthritis: Difference between revisions

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__NOTOC__
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{{SI}}                                                                  
                                                                  
{{CMG}}; {{CK}}
'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
==Overview==


==Historical Perspective==
{{Psoriatic arthritis}}
*[Disease name] was first discovered by [scientist name], a [nationality + occupation], in [year] during/following [event].
{{CMG}}; {{AE}} {{CK}}
*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==
* Based on the severity, psoriatic arthritis may be classified into following categories:<ref name="pmid18952643">{{cite journal |vauthors=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 |title=Treatment recommendations for psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=68 |issue=9 |pages=1387–94 |date=September 2009 |pmid=18952643 |pmc=2719080 |doi=10.1136/ard.2008.094946 |url=}}</ref>
** Mild
** Moderate
** Severe
{| class="wikitable"
!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
==[[Psoriatic arthritis overview|Overview]]==


Minimal impact on patient's quality of life
==[[Psoriatic arthritis historical perspective|Historical Perspective]]==
|⩾5 joints involvement


Damage can be visible on ''x''ray
==[[Psoriatic arthritis classification|Classification]]==


Non-responsive to NSAIDs
==[[Psoriatic arthritis pathophysiology|Pathophysiology]]==


Moderate impact on patient's quality of life
==[[Psoriatic arthritis causes|Causes]]==
|⩾5 joints involvement


Severe damage may be seen on x-ray Nonresponsive to NSAIDs, standard DMARDs
==[[Psoriatic arthritis differential diagnosis|Differentiating Psoriatic arthritis from Other Diseases]]==


Severe impact on patient's quality of life
==[[Psoriatic arthritis epidemiology and demographics|Epidemiology and Demographics]]==
|-
|Axial joint involvement
|Mild pain present
No loss of physical function
|Loss of physical function


Bath Ankylosing Spondylitis Disability Activity Index (BASDAI) >4
==[[Psoriatic arthritis risk factors|Risk Factors]]==
|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
==[[Psoriatic arthritis screening|Screening]]==


PASI<10
==[[Psoriatic arthritis natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
|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
==Diagnosis==
|Loss of function
[[Psoriatic arthritis diagnostic study of choice |Diagnostic study of choice]] | [[Psoriatic arthritis history and symptoms|History and Symptoms]] | [[Psoriatic arthritis physical examination|Physical Examination]] | [[Psoriatic arthritis laboratory tests|Laboratory Findings]] | [[Psoriatic arthritis electrocardiogram|Electrocardiogram]] | [[Rheumatoid arthritis x ray|X ray]] | [[Rheumatoid arthritis echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Psoriatic arthritis CT|CT]] | [[Psoriatic arthritis MRI|MRI Findings]] | [[Psoriatic arthritis other imaging findings|Other Imaging Findings]] | [[Psoriatic arthritis other diagnostic studies|Other Diagnostic Studies]]


>2 sites involvement and failure of response
==Treatment==
|}
[[Psoriatic arthritis medical therapy|Medical Therapy]] |  [[Psoriatic arthritis surgical therapy|Surgical Therapy]]  |  [[Psoriatic arthritis Primary prevention|Primary prevention]] | [[Psoriatic arthritis secondary prevention|Secondary prevention]] | [[Psoriatic arthritis future or investigational therapies|Future or Investigational Therapies]]


==Causes==
==Case Studies==
There are no established [[Etiology|causes]] of psoriatic arthritis. The occurrence of [[Psoriatic arthritis (patient information)|psoriatic arthritis]] is secondary to a combination of [[Gene|genes]], immune mechanisms and exposure to specific external factors or triggers, which increase an individual's risk of developing [[Psoriatic arthritis (patient information)|psoriatic arthritis]]. These [[Risk factor|risk factors]] lead to complex interactions between the [[genetics]], [[immune system]], and the environment.<ref name="pmid26476224">{{cite journal |vauthors=Barnas JL, Ritchlin CT |title=Etiology and Pathogenesis of Psoriatic Arthritis |journal=Rheum. Dis. Clin. North Am. |volume=41 |issue=4 |pages=643–63 |date=November 2015 |pmid=26476224 |doi=10.1016/j.rdc.2015.07.006 |url=}}</ref>
:[[Psoriatic arthritis case study 1|Case #1]]


==Pathophysiology==
==Related Chapters==
The pathogenesis of psoriatic arthritis (PsA) involves the following events:<ref name="pmid12639988">{{cite journal |vauthors=Ritchlin CT, Haas-Smith SA, Li P, Hicks DG, Schwarz EM |title=Mechanisms of TNF-alpha- and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis |journal=J. Clin. Invest. |volume=111 |issue=6 |pages=821–31 |year=2003 |pmid=12639988 |pmc=153764 |doi=10.1172/JCI16069 |url=}}</ref>
* In [[joints]] there is a prominent [[lymphocytic]] infiltrate, limited to the [[dermal papillae]] in [[skin]] and to the underlying [[stroma]].
* [[T lymphocytes]], particularly [[CD4+ cell|CD4 cells]], are the most common [[inflammatory]] [[Cell (biology)|cells]] in the [[skin]] and [[joints]], with a [[CD4]]/[[CD8]] ratio of 2:1.
* High levels of [[Tumor necrosis factor-alpha|tumor necrosis factor alpha]] ([[TNF]]), [[Interleukin 8|IL-8]], [[Interleukin 6|IL-6]], [[IL-1]], [[Interleukin 10|IL-10]], and [[Matrix metalloproteinase|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 [[Tumor necrosis factors|TNF]] leads to a high number of [[Osteoclast|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 [[Osteoclast|osteoclasts]].
* [[Osteoclast|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<ref name="pmid15708931">{{cite journal |vauthors=Helliwell PS, Taylor WJ |title=Classification and diagnostic criteria for psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=64 Suppl 2 |issue= |pages=ii3–8 |date=March 2005 |pmid=15708931 |pmc=1766878 |doi=10.1136/ard.2004.032318 |url=}}</ref><ref name="pmid5562018">{{cite journal |vauthors=McEwen C, DiTata D, Lingg C, Porini A, Good A, Rankin T |title=Ankylosing spondylitis and spondylitis accompanying ulcerative colitis, regional enteritis, psoriasis and Reiter's disease. A comparative study |journal=Arthritis Rheum. |volume=14 |issue=3 |pages=291–318 |date=1971 |pmid=5562018 |doi= |url=}}</ref><ref name="pmid9640127">{{cite journal |vauthors=Helliwell PS, Hickling P, Wright V |title=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? |journal=Ann. Rheum. Dis. |volume=57 |issue=3 |pages=135–40 |date=March 1998 |pmid=9640127 |pmc=1752543 |doi= |url=}}</ref><ref name="pmid4604133">{{cite journal |vauthors=Moll JM, Haslock I, Macrae IF, Wright V |title=Associations between ankylosing spondylitis, psoriatic arthritis, Reiter's disease, the intestinal arthropathies, and Behcet's syndrome |journal=Medicine (Baltimore) |volume=53 |issue=5 |pages=343–64 |date=September 1974 |pmid=4604133 |doi= |url=}}</ref>
**[[Rheumatoid arthritis]]
**[[Reactive arthritis]]
**[[Ankylosing spondylitis]]
**[[Arthritis]] associated with [[inflammatory bowel disease]]
**[[Osteoarthritis]]
**[[Gout]]
**[[Chondrocalcinosis|Pseudogout]]


==Epidemiology and Demographics==
{{Diseases of the musculoskeletal system and connective tissue}}
* The [[prevalence]] of [[Psoriatic arthritis (patient information)|psoriatic arthritis]] in general population  ranges from 60 - 250 cases per 100,000  individuals in United states.<ref name="pmid16198775">{{cite journal |vauthors=Gelfand JM, Gladman DD, Mease PJ, Smith N, Margolis DJ, Nijsten T, Stern RS, Feldman SR, Rolstad T |title=Epidemiology of psoriatic arthritis in the population of the United States |journal=J. Am. Acad. Dermatol. |volume=53 |issue=4 |pages=573 |date=October 2005 |pmid=16198775 |doi=10.1016/j.jaad.2005.03.046 |url=}}</ref>
{{WH}}
* The prevalence  ranges in genreal population  from 50 - 210 cases per 100,000 individuals in Europe.<ref name="pmid20476864">{{cite journal |vauthors=Hanova P, Pavelka K, Holcatova I, Pikhart H |title=Incidence and prevalence of psoriatic arthritis, ankylosing spondylitis, and reactive arthritis in the first descriptive population-based study in the Czech Republic |journal=Scand. J. Rheumatol. |volume=39 |issue=4 |pages=310–7 |date=August 2010 |pmid=20476864 |doi=10.3109/03009740903544212 |url=}}</ref>
{{WS}}
* The [[prevalence]] among [[psoriasis]] patients is 11,000 per 100,000 individuals.
e)|adverse effects]] and associated [[Comorbidity|comorbid conditions]].
* The [[incidence]] of psoriatic arthritis is 3.6-6 per 100,000 individuals.<ref name="pmid20476864">{{cite journal |vauthors=Hanova P, Pavelka K, Holcatova I, Pikhart H |title=Incidence and prevalence of psoriatic arthritis, ankylosing spondylitis, and reactive arthritis in the first descriptive population-based study in the Czech Republic |journal=Scand. J. Rheumatol. |volume=39 |issue=4 |pages=310–7 |date=August 2010 |pmid=20476864 |doi=10.3109/03009740903544212 |url=}}</ref>
===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>
===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>
===Race===
* There is insufficient data to support the racial dominance of [[Psoriatic arthritis (patient information)|psoriatic arthritis]].
 
==Risk Factors==
* '''Genetic factors''':<ref name="pmid19182814">{{cite journal |vauthors=Nograles KE, Brasington RD, Bowcock AM |title=New insights into the pathogenesis and genetics of psoriatic arthritis |journal=Nat Clin Pract Rheumatol |volume=5 |issue=2 |pages=83–91 |date=February 2009 |pmid=19182814 |pmc=2790861 |doi=10.1038/ncprheum0987 |url=}}</ref><ref name="pmid21900282">{{cite journal |vauthors=Eder L, Chandran V, Pellet F, Shanmugarajah S, Rosen CF, Bull SB, Gladman DD |title=Human leucocyte antigen risk alleles for psoriatic arthritis among patients with psoriasis |journal=Ann. Rheum. Dis. |volume=71 |issue=1 |pages=50–5 |date=January 2012 |pmid=21900282 |doi=10.1136/ard.2011.155044 |url=}}</ref><ref name="pmid10321964">{{cite journal |vauthors=Gladman DD, Cheung C, Ng CM, Wade JA |title=HLA-C locus alleles in patients with psoriatic arthritis (PsA) |journal=Hum. Immunol. |volume=60 |issue=3 |pages=259–61 |date=March 1999 |pmid=10321964 |doi= |url=}}</ref>
** 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.<ref name="pmid9558177">{{cite journal |vauthors=Gladman DD, Farewell VT, Kopciuk KA, Cook RJ |title=HLA markers and progression in psoriatic arthritis |journal=J. Rheumatol. |volume=25 |issue=4 |pages=730–3 |date=April 1998 |pmid=9558177 |doi= |url=}}</ref>
** Increased risk for both psoriatic arthritis and psoriasis may be associated with following gene polymorphisms:
***  TNF-alpha polymorphisms<ref name="pmid16284098">{{cite journal |vauthors=Rahman P, Siannis F, Butt C, Farewell V, Peddle L, Pellett F, Gladman D |title=TNFalpha polymorphisms and risk of psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=65 |issue=7 |pages=919–23 |date=July 2006 |pmid=16284098 |pmc=1798211 |doi=10.1136/ard.2005.039164 |url=}}</ref>
*** CARD15 gene on chrosome 16q:  Pleiotropic autoimmune gene. It is the first non-MHC gene that can be associated with psoriatic arthritis.<ref name="pmid12879366">{{cite journal |vauthors=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 |title=CARD15: a pleiotropic autoimmune gene that confers susceptibility to psoriatic arthritis |journal=Am. J. Hum. Genet. |volume=73 |issue=3 |pages=677–81 |date=September 2003 |pmid=12879366 |pmc=1180694 |doi=10.1086/378076 |url=}}</ref>
*** Polymorphisms involving IL-23 receptor and IL-12 beta.<ref name="pmid19035472">{{cite journal |vauthors=Filer C, Ho P, Smith RL, Griffiths C, Young HS, Worthington J, Bruce IN, Barton A |title=Investigation of association of the IL12B and IL23R genes with psoriatic arthritis |journal=Arthritis Rheum. |volume=58 |issue=12 |pages=3705–9 |date=December 2008 |pmid=19035472 |pmc=3001112 |doi=10.1002/art.24128 |url=}}</ref>
*** MHC class I chain-related gene A (MICA)<ref name="pmid10323458">{{cite journal |vauthors=Gonzalez S, Martinez-Borra J, Torre-Alonso JC, Gonzalez-Roces S, Sanchez del Río J, Rodriguez Pérez A, Brautbar C, López-Larrea C |title=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 |journal=Arthritis Rheum. |volume=42 |issue=5 |pages=1010–6 |date=May 1999 |pmid=10323458 |doi=10.1002/1529-0131(199905)42:5<1010::AID-ANR21>3.0.CO;2-H |url=}}</ref>
* '''Immune mechanisms''':<ref name="pmid9058659">{{cite journal |vauthors=Partsch G, Steiner G, Leeb BF, Dunky A, Bröll H, Smolen JS |title=Highly increased levels of tumor necrosis factor-alpha and other proinflammatory cytokines in psoriatic arthritis synovial fluid |journal=J. Rheumatol. |volume=24 |issue=3 |pages=518–23 |date=March 1997 |pmid=9058659 |doi= |url=}}</ref><ref name="pmid16936328">{{cite journal |vauthors=Szodoray P, Alex P, Chappell-Woodward CM, Madland TM, Knowlton N, Dozmorov I, Zeher M, Jarvis JN, Nakken B, Brun JG, Centola M |title=Circulating cytokines in Norwegian patients with psoriatic arthritis determined by a multiplex cytokine array system |journal=Rheumatology (Oxford) |volume=46 |issue=3 |pages=417–25 |date=March 2007 |pmid=16936328 |doi=10.1093/rheumatology/kel306 |url=}}</ref><ref name="pmid26476224">{{cite journal |vauthors=Barnas JL, Ritchlin CT |title=Etiology and Pathogenesis of Psoriatic Arthritis |journal=Rheum. Dis. Clin. North Am. |volume=41 |issue=4 |pages=643–63 |date=November 2015 |pmid=26476224 |doi=10.1016/j.rdc.2015.07.006 |url=}}</ref>
** 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 cell|dendritic cells]], which lead to activation of [[T cell|T lymphocytes]] by presenting an unknown antigen to [[CD4|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 [[Synovium|synovial]] and [[Epidermis (skin)|epidermal]] [[Fibroblast|fibroblasts]].
** Excessively proliferated [[Fibroblast|fibroblasts]] from [[Epidermis (skin)|epiderm]] and [[synovium]] may produce excess [[IL-1]], [[Interleukin 6|IL-6]], and platelet-derived growth factors.
** [[T cell|T lymphocytes]] may express [[HLA-DR]] and [[Interleukin 2|IL-2]] receptor, and receptors to several adhesive molecules and cytokines particularly [[Interleukin 6|IL-6]].
** [[Synovial fluid]] of patients with psoriatic arthritis will show increased levels of [[Tumor necrosis factor-alpha|tumor necrosis factor (TNF)-alpha,]] [[IL-1]], [[Interleukin 6|IL-6]], and [[Interleukin 8|IL-8]].
** Elevated concentrations of serum interleukins including [[Interleukin 10|IL-10]], [[Interleukin 13|IL-13]], interferons particularly [[Interferon-alpha|INF- alpha]],  [[Chemokine|chemokines]] such as [[CCL19]], [[vascular endothelial growth factor]], [[fibroblast growth factor]], and decreased levels of [[Granulocyte colony stimulating factor|granulocyte-colony stimulating factor]] may be found.
 
* '''Environmental factors''':
** [[Physical trauma|Trauma]]: Koebner's phenomenon<ref name="pmid24249146">{{cite journal |vauthors=Hsieh J, Kadavath S, Efthimiou P |title=Can traumatic injury trigger psoriatic arthritis? A review of the literature |journal=Clin. Rheumatol. |volume=33 |issue=5 |pages=601–8 |date=May 2014 |pmid=24249146 |doi=10.1007/s10067-013-2436-7 |url=}}</ref>
** [[Infection|Infections]]:<ref name="pmid29124396">{{cite journal |vauthors=Thrastardottir T, Love TJ |title=Infections and the risk of psoriatic arthritis among psoriasis patients: a systematic review |journal=Rheumatol. Int. |volume= |issue= |pages= |date=November 2017 |pmid=29124396 |doi=10.1007/s00296-017-3873-4 |url=}}</ref><ref name="pmid2041889">{{cite journal |vauthors=Arnett FC, Reveille JD, Duvic M |title=Psoriasis and psoriatic arthritis associated with human immunodeficiency virus infection |journal=Rheum. Dis. Clin. North Am. |volume=17 |issue=1 |pages=59–78 |date=February 1991 |pmid=2041889 |doi= |url=}}</ref>
*** [[Bacteria|Bacterial]] (eg, [[streptococcus]])
*** [[Virus|Viral]] (eg, [[Human Immunodeficiency Virus (HIV)|HIV]])<ref name="pmid10914854">{{cite journal |vauthors=Njobvu P, McGill P |title=Psoriatic arthritis and human immunodeficiency virus infection in Zambia |journal=J. Rheumatol. |volume=27 |issue=7 |pages=1699–702 |date=July 2000 |pmid=10914854 |doi= |url=}}</ref>
** [[Smoking]]: May have inverse relation with psoriatic arthritis among [[psoriasis]] patients.<ref name="pmid21953342">{{cite journal |vauthors=Eder L, Shanmugarajah S, Thavaneswaran A, Chandran V, Rosen CF, Cook RJ, Gladman DD |title=The association between smoking and the development of psoriatic arthritis among psoriasis patients |journal=Ann. Rheum. Dis. |volume=71 |issue=2 |pages=219–24 |date=February 2012 |pmid=21953342 |doi=10.1136/ard.2010.147793 |url=}}</ref>
 
== Natural History, Complications and Prognosis==
*Common complications or [[Comorbidity|comorbid conditions]] associated with psoriatic arthritis include:<ref name="pmid16981296">{{cite journal |vauthors=Han C, Robinson DW, Hackett MV, Paramore LC, Fraeman KH, Bala MV |title=Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis |journal=J. Rheumatol. |volume=33 |issue=11 |pages=2167–72 |date=November 2006 |pmid=16981296 |doi= |url=}}</ref><ref name="pmid24115739">{{cite journal |vauthors=Labitigan M, Bahče-Altuntas A, Kremer JM, Reed G, Greenberg JD, Jordan N, Putterman C, Broder A |title=Higher rates and clustering of abnormal lipids, obesity, and diabetes mellitus in psoriatic arthritis compared with rheumatoid arthritis |journal=Arthritis Care Res (Hoboken) |volume=66 |issue=4 |pages=600–7 |date=April 2014 |pmid=24115739 |pmc=3969762 |doi=10.1002/acr.22185 |url=}}</ref><ref name="pmid26493817">{{cite journal |vauthors=Eder L, Wu Y, Chandran V, Cook R, Gladman DD |title=Incidence and predictors for cardiovascular events in patients with psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=75 |issue=9 |pages=1680–6 |date=September 2016 |pmid=26493817 |doi=10.1136/annrheumdis-2015-207980 |url=}}</ref><ref name="pmid18163513">{{cite journal |vauthors=Rohekar S, Tom BD, Hassa A, Schentag CT, Farewell VT, Gladman DD |title=Prevalence of malignancy in psoriatic arthritis |journal=Arthritis Rheum. |volume=58 |issue=1 |pages=82–7 |date=January 2008 |pmid=18163513 |doi=10.1002/art.23185 |url=}}</ref><ref name="pmid24692521">{{cite journal |vauthors=McDonough E, Ayearst R, Eder L, Chandran V, Rosen CF, Thavaneswaran A, Gladman DD |title=Depression and anxiety in psoriatic disease: prevalence and associated factors |journal=J. Rheumatol. |volume=41 |issue=5 |pages=887–96 |date=May 2014 |pmid=24692521 |doi=10.3899/jrheum.130797 |url=}}</ref><ref name="pmid23326962">{{cite journal |vauthors=Ciacli C, Cojocaru M |title=Systemic osteoporosis--major complication of psoriatic arthritis |journal=Rom J Intern Med |volume=50 |issue=2 |pages=173–8 |date=2012 |pmid=23326962 |doi= |url=}}</ref><ref name="pmid19147616">{{cite journal |vauthors=Curtis JR, Beukelman T, Onofrei A, Cassell S, Greenberg JD, Kavanaugh A, Reed G, Strand V, Kremer JM |title=Elevated liver enzyme tests among patients with rheumatoid arthritis or psoriatic arthritis treated with methotrexate and/or leflunomide |journal=Ann. Rheum. Dis. |volume=69 |issue=1 |pages=43–7 |date=January 2010 |pmid=19147616 |pmc=2794929 |doi=10.1136/ard.2008.101378 |url=}}</ref>
** [[Metabolic syndrome]]
** Progressive [[joint]] destruction and deformity
** [[Hypertension]]
** Increase [[insulin]] resistance and [[diabetes mellitus]]
** [[Dyslipidemia]]
** Increased [[Atherosclerosis|atherosclerotic]] risk
** [[Myocardial infarction in the elderly|Myocardial infarction]]
** [[Congestive heart failure]]
** [[Cardiac arrhythmia|Arrythmias]]
** [[Stroke]]
** [[Inflammatory bowel disease]]
** [[Osteoporosis]]
** [[Depression]]
** Increased risk for [[Cancer|malignancy]] ([[breast]], [[prostate]], and [[lung]])
** [[uveitis]]
** [[Non-alcoholic fatty liver disease|Non alcoholic fatty liver disease]]
** Decreased [[quality of life]]
*[[Prognosis]] is generally good with early [[diagnosis]] and treatment with [[Disease-modifying antirheumatic drug|DMARDs]] and [[TNF inhibitor|TNF inhibitors]]. Overall survival rate also depends on management of [[Comorbidity|comorbid conditions]] along with [[arthritis]] treatment.<ref name="pmid25603589">{{cite journal |vauthors=McLaughlin M, Ostör A |title=Early treatment of psoriatic arthritis improves prognosis |journal=Practitioner |volume=258 |issue=1777 |pages=21–4, 3 |date=December 2014 |pmid=25603589 |doi= |url=}}</ref><ref name="pmid20682670">{{cite journal |vauthors=Buckley C, Cavill C, Taylor G, Kay H, Waldron N, Korendowych E, McHugh N |title=Mortality in psoriatic arthritis - a single-center study from the UK |journal=J. Rheumatol. |volume=37 |issue=10 |pages=2141–4 |date=October 2010 |pmid=20682670 |doi=10.3899/jrheum.100034 |url=}}</ref>
 
== Diagnosis ==
===Diagnostic Criteria===
* The [[diagnosis]] of psoriatic arthritis is easily confirmed when the [[Skin|cutaneous]] manifestations of [[psoriasis]] coexist with [[arthritis]].<ref name="pmid25232529">{{cite journal |vauthors=Liu JT, Yeh HM, Liu SY, Chen KT |title=Psoriatic arthritis: Epidemiology, diagnosis, and treatment |journal=World J Orthop |volume=5 |issue=4 |pages=537–43 |date=September 2014 |pmid=25232529 |pmc=4133459 |doi=10.5312/wjo.v5.i4.537 |url=}}</ref><ref name="pmid13395269">{{cite journal |vauthors=WRIGHT V |title=Psoriasis and arthritis |journal=Ann. Rheum. Dis. |volume=15 |issue=4 |pages=348–56 |date=December 1956 |pmid=13395269 |pmc=1006908 |doi= |url=}}</ref><ref name="pmid15708931">{{cite journal |vauthors=Helliwell PS, Taylor WJ |title=Classification and diagnostic criteria for psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=64 Suppl 2 |issue= |pages=ii3–8 |date=March 2005 |pmid=15708931 |pmc=1766878 |doi=10.1136/ard.2004.032318 |url=}}</ref><ref name="pmid10364901">{{cite journal |vauthors=Punzi L, Pianon M, Rossini P, Schiavon F, Gambari PF |title=Clinical and laboratory manifestations of elderly onset psoriatic arthritis: a comparison with younger onset disease |journal=Ann. Rheum. Dis. |volume=58 |issue=4 |pages=226–9 |date=April 1999 |pmid=10364901 |pmc=1752862 |doi= |url=}}</ref>
* It must be differentiated from other arthritides based on the joint involvement patterns, clinical features, [[imaging]] and [[Medical laboratory|laboratory]] studies.
* The following manifestations may be helpful in diagnosing psoriatic arthritis in an individual in the absence of psoriatic [[skin]] lesions.<ref name="pmid14719207">{{cite journal |vauthors=Scarpa R, Cosentini E, Manguso F, Oriente A, Peluso R, Atteno M, Ayala F, D'Arienzo A, Oriente P |title=Clinical and genetic aspects of psoriatic arthritis "sine psoriasis" |journal=J. Rheumatol. |volume=30 |issue=12 |pages=2638–40 |date=December 2003 |pmid=14719207 |doi= |url=}}</ref>
** [[Family history]] of [[psoriasis]] in first degree relatives
** Asymmetric [[joint]] distribution
** Involvement of distal [[Joint|joints]]
** [[Nail (anatomy)|Nail]] involvement (eg, pitting, nail bed destruction, onycholysis)
** [[Dactylitis]]
** Hidden [[Psoriasis|psoriatic plaques]]
* The CASPAR criteria (ClASsification criteria for Psoriatic ARthritis):<ref name="pmid16871531">{{cite journal |vauthors=Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H |title=Classification criteria for psoriatic arthritis: development of new criteria from a large international study |journal=Arthritis Rheum. |volume=54 |issue=8 |pages=2665–73 |date=August 2006 |pmid=16871531 |doi=10.1002/art.21972 |url=}}</ref>
** The CASPAR study stated that a patient present with inflammatory articular disease (inflammatory peripheral [[arthritis]], [[Enthesopathy|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:
**** Current [[psoriasis]] (2points) or previous history of [[psoriasis]] (1 point) or  family history of psoriasis (1 point)
*** [[dactylitis]] (1 point)
*** [[Nail (anatomy)|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%.
 
===Symptoms===
* Common [[symptom]] may be associated with [[Psoriatic arthritis (patient information)|psoriatic arthritis]] include:<ref name="pmid23493653">{{cite journal |vauthors=Sankowski AJ, Lebkowska UM, Cwikła J, Walecka I, Walecki J |title=Psoriatic arthritis |journal=Pol J Radiol |volume=78 |issue=1 |pages=7–17 |date=January 2013 |pmid=23493653 |pmc=3596149 |doi=10.12659/PJR.883763 |url=}}</ref><ref name="pmid28769135">{{cite journal |vauthors=Krajewska-Włodarczyk M, Owczarczyk-Saczonek A, Placek W |title=Fatigue - an underestimated symptom in psoriatic arthritis |journal=Reumatologia |volume=55 |issue=3 |pages=125–130 |date=2017 |pmid=28769135 |pmc=5534506 |doi=10.5114/reum.2017.68911 |url=}}</ref><ref name="pmid22294201">{{cite journal |vauthors=Dhir V, Aggarwal A |title=Psoriatic arthritis: a critical review |journal=Clin Rev Allergy Immunol |volume=44 |issue=2 |pages=141–8 |date=April 2013 |pmid=22294201 |doi=10.1007/s12016-012-8302-6 |url=}}</ref><ref name="pmid10364901">{{cite journal |vauthors=Punzi L, Pianon M, Rossini P, Schiavon F, Gambari PF |title=Clinical and laboratory manifestations of elderly onset psoriatic arthritis: a comparison with younger onset disease |journal=Ann. Rheum. Dis. |volume=58 |issue=4 |pages=226–9 |date=April 1999 |pmid=10364901 |pmc=1752862 |doi= |url=}}</ref>
** [[Arthralgia|Joint pain]] and [[Swelling (medical)|swelling]]
** [[Joint stiffness]]
** Morning [[Joint stiffness|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]].
** [[Enthesopathy|Enthesitis]]: [[Pain]] can be felt in areas where [[Tendon|tendons]], [[Ligament|ligaments]], and [[synovium]] attach to bones.
*** Common locations include:
**** [[Achilles tendinitis]]
**** [[Plantar fasciitis]]
** [[Dactylitis]]: Sausage-like [[Swelling (medical)|swelling]] of the entire [[finger]] or [[toe]].
** [[Skin]] lesions: Scaly, erythematous [[Papule|papules]] and [[Plaque|plaques]]
** Dystrophic [[Nail (anatomy)|nails]]
** Ocular symptoms include [[Erythema|redness]] and [[Tears|tearing]] due to [[conjunctivitis]], [[blepharitis]], and [[uveitis]].
** [[Fatigue]]
 
=== Physical Examination ===
*[[Patient|Patients]] with [[Psoriatic arthritis (patient information)|psoriatic arthritis]] usually appear normal.
*[[Physical examination]] of a patient with [[Psoriatic arthritis (patient information)|psoriatic arthritis]] may include:
* [[Joint]] involvement:<ref name="pmid4581554">{{cite journal |vauthors=Moll JM, Wright V |title=Psoriatic arthritis |journal=Semin. Arthritis Rheum. |volume=3 |issue=1 |pages=55–78 |date=1973 |pmid=4581554 |doi= |url=}}</ref><ref name="pmid17828344">{{cite journal |vauthors=Scarpa R, Peluso R, Atteno M |title=Clinical presentation of psoriatic arthritis |journal=Reumatismo |volume=59 Suppl 1 |issue= |pages=49–51 |date=2007 |pmid=17828344 |doi= |url=}}</ref>
** [[Joint]] [[tenderness]]
** [[Joint]] [[Edema|swelling]] may or may not be present
** Patterns of [[joint]] involvement in [[Psoriatic arthritis (patient information)|psoriatic arthritis]] may include according to moll and wright :
*** Distal [[arthritis]]: Involving mostly [[Interphalangeal joint|DIP joints]], may be symmetric or asymmetric. It may involve multiple [[Joint|joints]] or only few [[Joint|joints]].
*** Asymmetric [[oligoarthritis]]: Most common pattern can be seen in [[Psoriatic arthritis (patient information)|psoriatic arthritis]]. It is characterized by asymmetric involvement of less than 5 small or large [[Joint|joints]].
*** Symmetric [[polyarthritis]]
*** Arthritis mutilans: Resorption of [[Phalanx bones|phalanges]], [[Metatarsus|metatarsals]] and, [[Metacarpus|metacarpals]].
*** [[Spondylitis]]
*** [[Sacroiliitis]]
** Joint effusion
* [[Achilles tendinitis]]<ref name="pmid12894068">{{cite journal |vauthors=De Simone C, Guerriero C, Giampetruzzi AR, Costantini M, Di Gregorio F, Amerio P, Giampietruzzi AR |title=Achilles tendinitis in psoriasis: clinical and sonographic findings |journal=J. Am. Acad. Dermatol. |volume=49 |issue=2 |pages=217–22 |date=August 2003 |pmid=12894068 |doi= |url=}}</ref>
* [[Dactylitis]]: sausage digit due to swelling of the whole finger or toe.<ref name="pmid15271771">{{cite journal |vauthors=Brockbank JE, Stein M, Schentag CT, Gladman DD |title=Dactylitis in psoriatic arthritis: a marker for disease severity? |journal=Ann. Rheum. Dis. |volume=64 |issue=2 |pages=188–90 |date=February 2005 |pmid=15271771 |pmc=1755375 |doi=10.1136/ard.2003.018184 |url=}}</ref>
* [[Skin]]:<ref name="pmid10941813">{{cite journal |vauthors=Elkayam O, Ophir J, Yaron M, Caspi D |title=Psoriatic arthritis: interrelationships between skin and joint manifestations related to onset, course and distribution |journal=Clin. Rheumatol. |volume=19 |issue=4 |pages=301–5 |date=2000 |pmid=10941813 |doi= |url=}}</ref><ref name="pmid87081">{{cite journal |vauthors=Wright V, Roberts MC, Hill AG |title=Dermatological manifestations in psoriatic arthritis: a follow-up study |journal=Acta Derm. Venereol. |volume=59 |issue=3 |pages=235–40 |date=1979 |pmid=87081 |doi= |url=}}</ref>
** Psoriatic arthritis may occur after the onset of [[psoriasis]] in most of the [[Patient|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 (anatomy)|nail]], intergluteal, and perianal regions.<ref name="pmid19177544">{{cite journal |vauthors=Wilson FC, Icen M, Crowson CS, McEvoy MT, Gabriel SE, Kremers HM |title=Incidence and clinical predictors of psoriatic arthritis in patients with psoriasis: a population-based study |journal=Arthritis Rheum. |volume=61 |issue=2 |pages=233–9 |date=February 2009 |pmid=19177544 |pmc=3061343 |doi=10.1002/art.24172 |url=}}</ref>
*** Scaly, erythematous [[Papule|papules]] and [[Plaque|plaques]]
*** Pustular lesions
*** Guttate lesions
*** Auspitz sign: Small [[bleeding]] points seen upon disruption of a psoriatic scale.
* Nails:<ref name="pmid28769136">{{cite journal |vauthors=Sobolewski P, Walecka I, Dopytalska K |title=Nail involvement in psoriatic arthritis |journal=Reumatologia |volume=55 |issue=3 |pages=131–135 |date=2017 |pmid=28769136 |pmc=5534507 |doi=10.5114/reum.2017.68912 |url=}}</ref><ref name="pmid27251673">{{cite journal |vauthors=Lai TL, Pang HT, Cheuk YY, Yip ML |title=Psoriatic nail involvement and its relationship with distal interphalangeal joint disease |journal=Clin. Rheumatol. |volume=35 |issue=8 |pages=2031–2037 |date=August 2016 |pmid=27251673 |doi=10.1007/s10067-016-3319-5 |url=}}</ref>
** [[Pitted nails|Nail pits]]
** [[Onycholysis]]
** [[hyperkeratosis|Subungual hyperkeratosis]]
** [[Splinter hemorrhage|Splinter hemorrhages]]
** Beau lines
** [[Leukonychia]]
** Oil drop patches
** Nail crumbling
** Nail destruction
* '''Involvement of [[Eye|eyes]]''':<ref name="pmid970993">{{cite journal |vauthors=Lambert JR, Wright V |title=Eye inflammation in psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=35 |issue=4 |pages=354–6 |date=August 1976 |pmid=970993 |pmc=1007395 |doi= |url=}}</ref><ref name="pmid27419848">{{cite journal |vauthors=Abbouda A, Abicca I, Fabiani C, Scappatura N, Peña-García P, Scrivo R, Priori R, Paroli MP |title=Psoriasis and Psoriatic Arthritis-Related Uveitis: Different Ophthalmological Manifestations and Ocular Inflammation Features |journal=Semin Ophthalmol |volume=32 |issue=6 |pages=715–720 |date=2017 |pmid=27419848 |doi=10.3109/08820538.2016.1170161 |url=}}</ref>
** [[conjunctivitis]]
** [[Uveitis]]
** [[Iritis]]
* [[Edema]] of [[Hand|hands]] or feet: Swelling of hands and feet which is asymmetrical with pitting edema may be found in some cases.<ref name="pmid11407082">{{cite journal |vauthors=Cantini F, Salvarani C, Olivieri I, Macchioni L, Niccoli L, Padula A, Falcone C, Boiardi L, Bozza A, Barozzi L, Pavlica P |title=Distal extremity swelling with pitting edema in psoriatic arthritis: a case-control study |journal=Clin. Exp. Rheumatol. |volume=19 |issue=3 |pages=291–6 |date=2001 |pmid=11407082 |doi= |url=}}</ref>
 
=== Laboratory Findings ===
*There are no specific [[Medical laboratory|laboratory]] findings associated with [[Psoriatic arthritis (patient information)|psoriatic arthritis]] and most the tests are non-specific.
*However, there are certain [[Medical laboratory|laboratory]] tests that can check for markers of [[inflammation]] and to exclude other [[Disease|diseases]]. These include:<ref name="pmid17828345">{{cite journal |vauthors=Punzi L, Podswiadek M, Oliviero F, Lonigro A, Modesti V, Ramonda R, Todesco S |title=Laboratory findings in psoriatic arthritis |journal=Reumatismo |volume=59 Suppl 1 |issue= |pages=52–5 |date=2007 |pmid=17828345 |doi= |url=}}</ref>
** [[Complete blood count|CBC]] with differential count
*** [[Leukocytosis]]
*** [[Anemia|Anaemia]]
** Elevated [[Erythrocyte sedimentation rate|ESR]]
** Elevated [[C-reactive protein|CRP]] (C- reactive protein)
** [[Autoantibody|Autoantibodies]]: The following [[Autoantibody|autoantibodies]] may be found in patients with [[Psoriatic arthritis (patient information)|psoriatic arthritis]].<ref name="pmid15834057">{{cite journal |vauthors=Johnson SR, Schentag CT, Gladman DD |title=Autoantibodies in biological agent naive patients with psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=64 |issue=5 |pages=770–2 |date=May 2005 |pmid=15834057 |pmc=1755477 |doi=10.1136/ard.2004.031286 |url=}}</ref>
*** [[Rheumatoid factor]]
*** [[Antinuclear antibodies|ANA]] ([[Antinuclear antibodies]])
*** Anti-citrullinated peptide antibodies (ACPA)
** Genetic markers:<ref name="pmid23916976">{{cite journal |vauthors=Chandran V, Bull SB, Pellett FJ, Ayearst R, Rahman P, Gladman DD |title=Human leukocyte antigen alleles and susceptibility to psoriatic arthritis |journal=Hum. Immunol. |volume=74 |issue=10 |pages=1333–8 |date=October 2013 |pmid=23916976 |doi=10.1016/j.humimm.2013.07.014 |url=}}</ref><ref name="pmid21900282">{{cite journal |vauthors=Eder L, Chandran V, Pellet F, Shanmugarajah S, Rosen CF, Bull SB, Gladman DD |title=Human leucocyte antigen risk alleles for psoriatic arthritis among patients with psoriasis |journal=Ann. Rheum. Dis. |volume=71 |issue=1 |pages=50–5 |date=January 2012 |pmid=21900282 |doi=10.1136/ard.2011.155044 |url=}}</ref>
*** [[HLA-B27]]
*** [[HLA-C]]*06
** [[Synovial fluid]] analysis: Elevated [[White blood cells|WBC]] count suggestive of [[inflammation]].
 
===Imaging Findings===
* [[X-rays|X-ray]] of digits:<ref name="pmid25231177">{{cite journal |vauthors=McGonagle D, Hermann KG, Tan AL |title=Differentiation between osteoarthritis and psoriatic arthritis: implications for pathogenesis and treatment in the biologic therapy era |journal=Rheumatology (Oxford) |volume=54 |issue=1 |pages=29–38 |date=January 2015 |pmid=25231177 |pmc=4269795 |doi=10.1093/rheumatology/keu328 |url=}}</ref><ref name="pmid16126794">{{cite journal |vauthors=Siannis F, Farewell VT, Cook RJ, Schentag CT, Gladman DD |title=Clinical and radiological damage in psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=65 |issue=4 |pages=478–81 |date=April 2006 |pmid=16126794 |pmc=1798082 |doi=10.1136/ard.2005.039826 |url=}}</ref><ref name="pmid23430715">{{cite journal |vauthors=Haddad A, Chandran V |title=Arthritis mutilans |journal=Curr Rheumatol Rep |volume=15 |issue=4 |pages=321 |year=2013 |pmid=23430715 |doi=10.1007/s11926-013-0321-7 |url=}}</ref>
** Bone destructive changes including formation of subchondral cyst and erosions
** Fluffy [[periostitis]]
** [[Ankylosis]]
** [[Phalanx bones|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 [[Interphalangeal articulations of hand|DIP joints]] but also affects [[Interphalangeal articulations of hand|PIP joints]]
** [[Osteolysis]] and [[ankylosis]] both coexists in the same [[Joint|joints]] of [[Hand|hands]] and [[foot]]
** [[Enthesopathy|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
[[File:Psoriatic-arthritis of hands.jpg|centre|thumb|Psoriatic-arthritis of hands showing pencil-in-cup deformity  - By Case courtesy of Dr Jeremy Jones, <a href="https://radiopaedia.org/">Radiopaedia.org</a>. From the case <a href="https://radiopaedia.org/cases/8798">rID: 8798</a>]]
 
* '''[[Magnetic resonance imaging|MRI]]''': MRI may reveal the following findings:<ref name="pmid20966327">{{cite journal |vauthors=Spira D, Kötter I, Henes J, Kümmerle-Deschner J, Schulze M, Boss A, Horger M |title=MRI findings in psoriatic arthritis of the hands |journal=AJR Am J Roentgenol |volume=195 |issue=5 |pages=1187–93 |date=November 2010 |pmid=20966327 |doi=10.2214/AJR.10.4281 |url=}}</ref>
** [[enthesitis]]
** [[Periostitis]]
** Joint erosions
** [[Synovitis]] (articular or flexor tendon sheath)
** [[Ankylosis]]
** [[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>
** 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 [[Bone fracture|fractures]]. <ref name="pmid11196516">{{cite journal |vauthors=Frediani B, Allegri A, Falsetti P, Storri L, Bisogno S, Baldi F, Filipponi P, Marcolongo R |title=Bone mineral density in patients with psoriatic arthritis |journal=J. Rheumatol. |volume=28 |issue=1 |pages=138–43 |date=January 2001 |pmid=11196516 |doi= |url=}}</ref>
 
== 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.<ref name="pmid26644232">{{cite journal |vauthors=Gossec L, Smolen JS, Ramiro S, de Wit M, Cutolo M, Dougados M, Emery P, Landewé R, Oliver S, Aletaha D, Betteridge N, Braun J, Burmester G, Cañete JD, Damjanov N, FitzGerald O, Haglund E, Helliwell P, Kvien TK, Lories R, Luger T, Maccarone M, Marzo-Ortega H, McGonagle D, McInnes IB, Olivieri I, Pavelka K, Schett G, Sieper J, van den Bosch F, Veale DJ, Wollenhaupt J, Zink A, van der Heijde D |title=European League Against Rheumatism (EULAR) recommendations for the management of psoriatic arthritis with pharmacological therapies: 2015 update |journal=Ann. Rheum. Dis. |volume=75 |issue=3 |pages=499–510 |date=March 2016 |pmid=26644232 |doi=10.1136/annrheumdis-2015-208337 |url=}}</ref><ref name="pmid21953336">{{cite journal |vauthors=Gossec L, Smolen JS, Gaujoux-Viala C, Ash Z, Marzo-Ortega H, van der Heijde D, FitzGerald O, Aletaha D, Balint P, Boumpas D, Braun J, Breedveld FC, Burmester G, Cañete JD, de Wit M, Dagfinrud H, de Vlam K, Dougados M, Helliwell P, Kavanaugh A, Kvien TK, Landewé R, Luger T, Maccarone M, McGonagle D, McHugh N, McInnes IB, Ritchlin C, Sieper J, Tak PP, Valesini G, Vencovsky J, Winthrop KL, Zink A, Emery P |title=European League Against Rheumatism recommendations for the management of psoriatic arthritis with pharmacological therapies |journal=Ann. Rheum. Dis. |volume=71 |issue=1 |pages=4–12 |date=January 2012 |pmid=21953336 |doi=10.1136/annrheumdis-2011-200350 |url=}}</ref>
** Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA)<ref name="pmid18952643">{{cite journal |vauthors=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 |title=Treatment recommendations for psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=68 |issue=9 |pages=1387–94 |date=September 2009 |pmid=18952643 |pmc=2719080 |doi=10.1136/ard.2008.094946 |url=}}</ref>
** American College of Rheumatology (ACR)
** National Psoriasis Foundation (NPF)
** American Academy of Dermatology (AAD) Psoriasis Guidelines of Care<ref name="pmid21306785">{{cite journal |vauthors=Menter A, Korman NJ, Elmets CA, Feldman SR, Gelfand JM, Gordon KB, Gottlieb A, Koo JY, Lebwohl M, Leonardi CL, Lim HW, Van Voorhees AS, Beutner KR, Ryan C, Bhushan R |title=Guidelines of care for the management of psoriasis and psoriatic arthritis: section 6. Guidelines of care for the treatment of psoriasis and psoriatic arthritis: case-based presentations and evidence-based conclusions |journal=J. Am. Acad. Dermatol. |volume=65 |issue=1 |pages=137–74 |date=July 2011 |pmid=21306785 |doi=10.1016/j.jaad.2010.11.055 |url=}}</ref>
** British Society of Rheumatology (BSR)<ref name="pmid23887065">{{cite journal |vauthors=Coates LC, Tillett W, Chandler D, Helliwell PS, Korendowych E, Kyle S, McInnes IB, Oliver S, Ormerod A, Smith C, Symmons D, Waldron N, McHugh NJ |title=The 2012 BSR and BHPR guideline for the treatment of psoriatic arthritis with biologics |journal=Rheumatology (Oxford) |volume=52 |issue=10 |pages=1754–7 |date=October 2013 |pmid=23887065 |doi=10.1093/rheumatology/ket187 |url=}}</ref>
* Pharmacologic therapy for [[psoriatic arthritis]] include, [[Non-steroidal anti-inflammatory drug|non-steroidal anti-inflammatory drugs]] ([[Non-steroidal anti-inflammatory drug|NSAID]]<nowiki/>s),  conventional synthetic [[Disease-modifying antirheumatic drug|DMARDs]] (eg, [[methotrexate]], [[sulfasalazine]], [[Cyclosporine|cyclosporin A]], [[leflunomide]]), biologic[[Disease-modifying antirheumatic drug|DMARD]]<nowiki/>s<nowiki/>  including, [[TNF inhibitor|TNF inhibitors]] (eg, [[etanercept]], [[infliximab]], [[adalimumab]], [[golimumab]]), [[Phosphodiesterase inhibitors|phosphodiesterase (PDE) inhibitors]] (eg, [[apremilast]]), interleukin(IL) inhibitors (eg, [[secukinumab]], [[ixekizumab]], [[abatacept]]) and [[Joint|intraarticular]] [[Glucocorticoids|glucocorticoid]] injections.
* '''Peripheral [[arthritis]]''':
** '''Mild disease''': [[Non-steroidal anti-inflammatory drug|Nonsteroidal antiinflammatory drugs]] ([[Non-steroidal anti-inflammatory drug|NSAID]]<nowiki/>s) are the most commonly used drugs for the management of mild active [[psoriatic arthritis]].<ref name="pmid15708943">{{cite journal |vauthors=Nash P, Clegg DO |title=Psoriatic arthritis therapy: NSAIDs and traditional DMARDs |journal=Ann. Rheum. Dis. |volume=64 Suppl 2 |issue= |pages=ii74–7 |date=March 2005 |pmid=15708943 |pmc=1766880 |doi=10.1136/ard.2004.030783 |url=}}</ref><ref name="pmid11296544">{{cite journal |vauthors=Sarzi-Puttini P, Santandrea S, Boccassini L, Panni B, Caruso I |title=The role of NSAIDs in psoriatic arthritis: evidence from a controlled study with nimesulide |journal=Clin. Exp. Rheumatol. |volume=19 |issue=1 Suppl 22 |pages=S17–20 |date=2001 |pmid=11296544 |doi= |url=}}</ref>
*** '''Preferred regimen (1)''': [[Naproxen sodium|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 effect (medicine)|Adverse effects]] of  [[Non-steroidal anti-inflammatory drug|non-steroidal anti-inflammatory drugs]] include increased cardiovascular risk, [[gastritis]], [[Peptic ulcer|ulcers]] and [[Renal insufficiency|low renal clearance]].
** '''Moderate to severe disease''': Conventional synthetic [[Disease-modifying antirheumatic drug|disease-modifying antirheumatic drugs]] ([[Disease-modifying antirheumatic drug|DMARD]]<nowiki/>s) may be considered in [[Patient|patients]] with moderate to severe active peripheral [[arthritis]]. These are also considered in [[Patient|patients]] who are resistant or not responding to [[Non-steroidal anti-inflammatory drug|NSAIDs]], and local [[corticosteroid]] injections.
*** Preferred regimen (1): [[Methotrexate]]<ref name="pmid24219040">{{cite journal |vauthors=Mease P |title=Methotrexate in psoriatic arthritis |journal=Bull Hosp Jt Dis (2013) |volume=71 Suppl 1 |issue= |pages=S41–5 |date=2013 |pmid=24219040 |doi= |url=}}</ref><ref name="pmid7868484">{{cite journal |vauthors=Singh YN, Verma KK, Kumar A, Malaviya AN |title=Methotrexate in psoriatic arthritis |journal=J Assoc Physicians India |volume=42 |issue=11 |pages=860–2 |date=November 1994 |pmid=7868484 |doi= |url=}}</ref>: 15 to 25 mg/week
**** [[Adverse effect (medicine)|Adverse effects]] of [[methotrexate]]: Liver toxicity, [[immunosuppression]], interstitial [[pneumonitis]], increased infection risk.
**** [[Folic Acid|Folic acid]] supplementation should be given to all patients taking [[methotrexate]].
*** Preferred regimen (2): [[Leflunomide]]: 20 mg/day
**** [[Adverse effect (medicine)|Adverse effects]] of [[Leflunomide]]: Liver toxicity, [[diarrhea]], [[rash]], [[alopecia]], [[pneumonitis]].
*** Preferred regimen (3): [[Sulfasalazine]]<ref name="pmid7868484">{{cite journal |vauthors=Singh YN, Verma KK, Kumar A, Malaviya AN |title=Methotrexate in psoriatic arthritis |journal=J Assoc Physicians India |volume=42 |issue=11 |pages=860–2 |date=November 1994 |pmid=7868484 |doi= |url=}}</ref>: 2-3 gms/day
**** [[Adverse effect (medicine)|Adverse effects]] of [[sulfasalazine]]: [[Nausea and vomiting|Nausea]], [[diarrhea]], abdominal pain, [[rash]], and [[neutropenia]].
*** Preferred regimen (4): [[Cyclosporine]] A: 3.5 mg/kg per day<ref name="pmid2396865">{{cite journal |vauthors=Steinsson K, Jónsdóttir I, Valdimarsson H |title=Cyclosporin A in psoriatic arthritis: an open study |journal=Ann. Rheum. Dis. |volume=49 |issue=8 |pages=603–6 |date=August 1990 |pmid=2396865 |pmc=1004173 |doi= |url=}}</ref>
**** [[Adverse effect (medicine)|Adverse effects]] of [[Cyclosporine]] A: [[Hypertension]], [[Renal insufficiency|kidney damage]].
** '''Severe disease''' '''and the presence of adverse prognostic factors''': [[TNF inhibitor|TNF inhibitors]] (eg, [[etanercept]], [[infliximab]], [[adalimumab]], [[golimumab]]), interleukin(IL) inhibitors (eg, [[secukinumab]], [[ixekizumab]], [[abatacept]]).
*** Biologic [[Disease-modifying antirheumatic drug|DMARDs]] are considered for  patients who fail to respond or [[contraindication]] to conventional synthetic [[Disease-modifying antirheumatic drug|DMARDs]]. It is also administered in patients with presence of poor [[prognosis]] factors, even if they have not failed a standard [[Disease-modifying antirheumatic drug|DMARDs]] therapy.
**** '''TNF inhibitors:'''
***** Preferred regimen (1): [[Adalimumab]]<ref name="pmid16200601">{{cite journal |vauthors=Mease PJ, Gladman DD, Ritchlin CT, Ruderman EM, Steinfeld SD, Choy EH, Sharp JT, Ory PA, Perdok RJ, Weinberg MA |title=Adalimumab for the treatment of patients with moderately to severely active psoriatic arthritis: results of a double-blind, randomized, placebo-controlled trial |journal=Arthritis Rheum. |volume=52 |issue=10 |pages=3279–89 |date=October 2005 |pmid=16200601 |doi=10.1002/art.21306 |url=}}</ref>: It is a human anti-[[Tumor necrosis factor-alpha|TNF alpha]] monoclonal [[antibody]].  Dosage: 40 mg can be given s.c every 2 weeks
***** Preferred regimen (2): [[Etanercept]]<ref name="pmid15248226">{{cite journal |vauthors=Mease PJ, Kivitz AJ, Burch FX, Siegel EL, Cohen SB, Ory P, Salonen D, Rubenstein J, Sharp JT, Tsuji W |title=Etanercept treatment of psoriatic arthritis: safety, efficacy, and effect on disease progression |journal=Arthritis Rheum. |volume=50 |issue=7 |pages=2264–72 |date=July 2004 |pmid=15248226 |doi=10.1002/art.20335 |url=}}</ref>: It is a [[Tumor necrosis factors|TNF]] receptor p75-IgG1 fusion [[protein]]. Dosage: 50 mg can be given s.c every week.
***** Preferred regimen (3): [[Infliximab]]<ref name="pmid15677701">{{cite journal |vauthors=Antoni C, Krueger GG, de Vlam K, Birbara C, Beutler A, Guzzo C, Zhou B, Dooley LT, Kavanaugh A |title=Infliximab improves signs and symptoms of psoriatic arthritis: results of the IMPACT 2 trial |journal=Ann. Rheum. Dis. |volume=64 |issue=8 |pages=1150–7 |date=August 2005 |pmid=15677701 |pmc=1755609 |doi=10.1136/ard.2004.032268 |url=}}</ref>:  It is a chimeric [[Monoclonal antibodies|monoclonal antibody]] against [[Tumor necrosis factor-alpha|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]]<ref name="pmid19333944">{{cite journal |vauthors=Kavanaugh A, McInnes I, Mease P, Krueger GG, Gladman D, Gomez-Reino J, Papp K, Zrubek J, Mudivarthy S, Mack M, Visvanathan S, Beutler A |title=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 |journal=Arthritis Rheum. |volume=60 |issue=4 |pages=976–86 |date=April 2009 |pmid=19333944 |doi=10.1002/art.24403 |url=}}</ref>: it is a human IgG1k anti-[[Tumor necrosis factor-alpha|TNF alpha antibody]]. Dosage: 50 mg can be given  s.c and monthly.
***** Preferred regimen (5): [[Certolizumab pegol]]<ref name="pmid23942868">{{cite journal |vauthors=Mease PJ, Fleischmann R, Deodhar AA, Wollenhaupt J, Khraishi M, Kielar D, Woltering F, Stach C, Hoepken B, Arledge T, van der Heijde D |title=Effect of certolizumab pegol on signs and symptoms in patients with psoriatic arthritis: 24-week results of a Phase 3 double-blind randomised placebo-controlled study (RAPID-PsA) |journal=Ann. Rheum. Dis. |volume=73 |issue=1 |pages=48–55 |date=January 2014 |pmid=23942868 |pmc=3888622 |doi=10.1136/annrheumdis-2013-203696 |url=}}</ref>: It is a Fab fragment of anti-[[Tumor necrosis factor-alpha|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 [[Infection|infections]] including  [[Bacteria|bacterial]] and [[opportunistic infection]]. Therefore, before starting treatment with TNF inhibitors screening for [[Tuberculosis|TB]], [[Hepatitis B]], and [[Hepatitis c|C]] should be done.
**** '''IL inhibitor therapy''': This is considered in patients with severe peripheral [[arthritis]], where [[TNF inhibitor|TNF therapy]] is [[Contraindication|contraindicated]] or not responding even after switching to different [[TNF inhibitor]].
***** '''Anti-IL-17 therapies''' :
****** Preferred regimen (1): [[Secukinumab]]<ref name="pmid26135703">{{cite journal |vauthors=McInnes IB, Mease PJ, Kirkham B, Kavanaugh A, Ritchlin CT, Rahman P, van der Heijde D, Landewé R, Conaghan PG, Gottlieb AB, Richards H, Pricop L, Ligozio G, Patekar M, Mpofu S |title=Secukinumab, a human anti-interleukin-17A monoclonal antibody, in patients with psoriatic arthritis (FUTURE 2): a randomised, double-blind, placebo-controlled, phase 3 trial |journal=Lancet |volume=386 |issue=9999 |pages=1137–46 |date=September 2015 |pmid=26135703 |doi=10.1016/S0140-6736(15)61134-5 |url=}}</ref>: It is a [[Monoclonal antibodies|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]]<ref name="pmid27553214">{{cite journal |vauthors=Mease PJ, van der Heijde D, Ritchlin CT, Okada M, Cuchacovich RS, Shuler CL, Lin CY, Braun DK, Lee CH, Gladman DD |title=Ixekizumab, an interleukin-17A specific monoclonal antibody, for the treatment of biologic-naive patients with active psoriatic arthritis: results from the 24-week randomised, double-blind, placebo-controlled and active (adalimumab)-controlled period of the phase III trial SPIRIT-P1 |journal=Ann. Rheum. Dis. |volume=76 |issue=1 |pages=79–87 |date=January 2017 |pmid=27553214 |pmc=5264219 |doi=10.1136/annrheumdis-2016-209709 |url=}}</ref> : Dosage: 160 mg initially, then 80 mg every two or four weeks can be given subcutaneously.
***** '''Anti-IL-12/23 therapy''':
****** Ustekinumab<ref name="pmid23769296">{{cite journal |vauthors=McInnes IB, Kavanaugh A, Gottlieb AB, Puig L, Rahman P, Ritchlin C, Brodmerkel C, Li S, Wang Y, Mendelsohn AM, Doyle MK |title=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 |journal=Lancet |volume=382 |issue=9894 |pages=780–9 |date=August 2013 |pmid=23769296 |doi=10.1016/S0140-6736(13)60594-2 |url=}}</ref>: 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.
**** [[Abatacept]]<ref name="pmid28473423">{{cite journal |vauthors=Mease PJ, Gottlieb AB, van der Heijde D, FitzGerald O, Johnsen A, Nys M, Banerjee S, Gladman DD |title=Efficacy and safety of abatacept, a T-cell modulator, in a randomised, double-blind, placebo-controlled, phase III study in psoriatic arthritis |journal=Ann. Rheum. Dis. |volume=76 |issue=9 |pages=1550–1558 |date=September 2017 |pmid=28473423 |pmc=5561378 |doi=10.1136/annrheumdis-2016-210724 |url=}}</ref>: It is a costimulatory [[T cell|T-cell]] molecule, blocking signal activation of the CD28 receptor on the [[T cell]] inhibiting [[T cell|T-cell]] activation. Dosage: 125 mg can be given subcutaneously once in a week.
* '''Axial disease/ spondylitis''':<ref name="pmid25362712">{{cite journal |vauthors=Nash P, Lubrano E, Cauli A, Taylor WJ, Olivieri I, Gladman DD |title=Updated guidelines for the management of axial disease in psoriatic arthritis |journal=J. Rheumatol. |volume=41 |issue=11 |pages=2286–9 |date=November 2014 |pmid=25362712 |doi=10.3899/jrheum.140877 |url=}}</ref>
** Mild disease: [[Non-steroidal anti-inflammatory drug|Non-steroidal anti-inflammatory drugs]] ([[Non-steroidal anti-inflammatory drug|NSAIDs]]), local [[corticosteroid]] injections, [[patient]] education, [[Physical exercise|exercise]]  and [[Physical therapy|physiotherapy]] may be recommended to treat mild axial involvement.
*** Preferred regimen (1): [[Naproxen sodium|Naproxen]]: 375-500 mg/twice a day
*** Preferred regimen (2): [[Celecoxib]]: 200 mg/twice a day
** Moderate to severe disease: [[TNF inhibitor|TNF inhibitors]]
* [[Skin disease|'''Skin disease''']]:<ref name="pmid24566842">{{cite journal |vauthors=Mease PJ, Armstrong AW |title=Managing patients with psoriatic disease: the diagnosis and pharmacologic treatment of psoriatic arthritis in patients with psoriasis |journal=Drugs |volume=74 |issue=4 |pages=423–41 |date=March 2014 |pmid=24566842 |pmc=3958815 |doi=10.1007/s40265-014-0191-y |url=}}</ref>
** [[Phototherapy]]: First line of treatment  including [[Ultraviolet|UVB]], [[PUVA]].
** Fumeric esters, [[Retinol|retinols]], [[calcipotriol]]
** Conventional [[Disease-modifying antirheumatic drug|DMARDs]] and [[TNF inhibitor|TNF inhibitors]], and [[Retinoic acid|retinoic acid derivatives]] (eg, [[acitretin]]) may be used in combinatination with [[phototherapy]].
* [[Nail changes|'''Nail disease''']]:<ref name="pmid25471223">{{cite journal |vauthors=Crowley JJ, Weinberg JM, Wu JJ, Robertson AD, Van Voorhees AS |title=Treatment of nail psoriasis: best practice recommendations from the Medical Board of the National Psoriasis Foundation |journal=JAMA Dermatol |volume=151 |issue=1 |pages=87–94 |date=January 2015 |pmid=25471223 |doi=10.1001/jamadermatol.2014.2983 |url=}}</ref>
** Topical [[Corticosteroid|corticosteroids]], [[calcipotriol]] creams, [[Disease-modifying antirheumatic drug|DMARDs]] and [[TNF inhibitor|TNF inhibitors]] may be helpful.
 
* '''Enthesitis''':
** Mild disease: [[Non-steroidal anti-inflammatory drug|NSAIDs]], local [[corticosteroid]] injection, [[physical therapy]] may be helpful.
** Moderate to severe disease: [[TNF inhibitor|TNF inhibitors]]
* [[Dactylitis|'''Dactylitis''']]:<ref name="pmid25362714">{{cite journal |vauthors=Rose S, Toloza S, Bautista-Molano W, Helliwell PS |title=Comprehensive treatment of dactylitis in psoriatic arthritis |journal=J. Rheumatol. |volume=41 |issue=11 |pages=2295–300 |date=November 2014 |pmid=25362714 |doi=10.3899/jrheum.140879 |url=}}</ref>
** [[Non-steroidal anti-inflammatory drug|NSAIDs]], steroid injections, conventional [[Disease-modifying antirheumatic drug|DMARDs]] and [[TNF inhibitor|TNF inhibitors]] can be helpful.
** Biologic [[Disease-modifying antirheumatic drug|DMARDs]] can be considered for treatment of [[dactylitis]] if, therapy with [[Non-steroidal anti-inflammatory drug|NSAIDs]], [[Glucocorticoid|steroid]] injections, conventional [[Disease-modifying antirheumatic drug|DMARDs]] fails.
* '''Non pharmacologic therapy''':
** [[Physical exercise|Exercise]]
** [[Weight]] reduction
** [[Physical therapy]]
** [[Occupational therapy]]
** Educating the [[patient]] about [[disease]] course,  [[joint]] protection and [[Comorbidity|comorbid]] conditions.
** [[Orthotics]]
 
=== Surgery ===
*[[Surgery]] may be indicated in patients of psoriatic arthritis with severe [[joint]] damage that limit [[mobility]].<ref name="pmid10782824">{{cite journal |vauthors=Zangger P, Esufali ZH, Gladman DD, Bogoch ER |title=Type and outcome of reconstructive surgery for different patterns of psoriatic arthritis |journal=J. Rheumatol. |volume=27 |issue=4 |pages=967–74 |date=April 2000 |pmid=10782824 |doi= |url=}}</ref>
*Common procedures include hand joint [[surgery]] involving [[Interphalangeal articulations of hand|PIP]] and [[Interphalangeal articulations of hand|DIP]] joints, [[Hip (anatomy)|hip]] or [[knee]] surgery.


=== Prevention ===
[[Category:Arthritis]]
* There are no established preventive measures for [[Psoriatic arthritis (patient information)|psoriatic arthritis]].
[[Category:Autoimmune diseases]]
* Patients are monitored regularly for [[disease]] activity, drug efficacy, [[Adverse effect (medicine)|adverse effects]] and associated [[Comorbidity|comorbid conditions]].
[[Category:Rheumatology]]
 
==References==
{{Reflist|2}}
[[Category: Pick One of 28 Approved]]
 
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Latest revision as of 23:52, 29 July 2020


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]

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