Psoriatic Arthritis

Table of Contents

1. Overview and Definition
2. Epidemiology
3. Subtypes of Psoriatic Arthritis
4. Causes and Genetic Factors — HLA Associations
5. Symptoms and Joints Affected
6. Diagnostic Criteria and Tests
7. Treatment — DMARDs, Biologics, JAK Inhibitors
8. Natural and Nutritional Approaches
9. Disease Course and Prognosis
10. Complications
11. Prevention and Lifestyle
12. Key Research Papers
13. Connections
14. Featured Videos

Overview and Definition

Psoriatic arthritis sits within the spondyloarthropathy family — a group of inflammatory joint diseases sharing certain genetic markers, a tendency to affect the spine and sacroiliac joints, and a negative rheumatoid factor test. Unlike osteoarthritis (wear-and-tear) or rheumatoid arthritis (a primarily synovial autoimmune disease), PsA attacks joints, entheses (tendon insertion points), skin, and nails simultaneously, driven by dysregulated immune signaling.

The core immunological story involves T-helper 17 (Th17) cells and the cytokines they release — principally interleukin-17 (IL-17) and interleukin-23 (IL-23). These cytokines fuel both the dermal inflammation that causes psoriatic plaques and the synovial and entheseal inflammation responsible for joint destruction. This shared biology explains why the same biologic drug classes (IL-17 inhibitors, IL-23 inhibitors) can treat both the skin and joint components of the disease simultaneously.

Moll and Wright's 1973 paper is the classic early clinical description of PsA as a disease separate from rheumatoid arthritis (PubMed PMID: 4581554). Their classification criteria were among the seven sets compared when the CASPAR criteria were developed in 2006, with a sensitivity of 0.91 in that comparison (PubMed PMID: 16871531).

Epidemiology

Psoriasis prevalence varies by region: a 2020 systematic analysis estimated it at 0.14% in east Asia, 1.50% in North America, 1.92% in western Europe and 1.99% in Australasia (PubMed PMID: 32467098). Among people with psoriasis, the 2019 meta-analysis found a pooled PsA proportion of 19.7%, and its authors summarized this as about 1 in 4 (PubMed PMID: 29928910). In a US population-based cohort followed over 30 years, fewer than 10% of people with newly diagnosed psoriasis developed clinically recognized PsA (cumulative incidence 5.1% at 20 years) (PubMed PMID: 19177544). Estimates of PsA prevalence in the general population vary between studies; a 2005 review gave a range of 0.3% to 1% (PubMed PMID: 15708927).

PsA usually begins in adulthood. In a Dublin early-arthritis clinic cohort of 129 PsA patients, mean age at onset of psoriasis was 29.8 years and mean age at onset of arthritis 40.4 years (PubMed PMID: 14523223). In the population-based cohort above, scalp lesions (hazard ratio 3.89), nail dystrophy (2.93) and intergluteal or perianal lesions (2.35) were the psoriasis features linked with a higher risk of developing PsA (PubMed PMID: 19177544).

A 2005 review drawing on the University of Toronto PsA program (Gladman and colleagues) described PsA as typically starting as a mild, oligoarticular disease that becomes polyarticular over time, is severe in at least 20% of patients, and reduces health-related quality of life (PubMed PMID: 15708927).

Subtypes of Psoriatic Arthritis

Moll and Wright originally described five clinical patterns of PsA. These subtypes are not mutually exclusive — a patient may start with one pattern and develop another over time — but they remain a useful clinical framework:

1. Oligoarticular asymmetric arthritis — The typical presenting pattern early in the disease, affecting four or fewer joints in an asymmetric pattern (e.g., left knee and right ankle). Often relatively mild but can progress.
2. Symmetric polyarthritis (RA-like) — Involves five or more joints in a roughly symmetric pattern, resembling rheumatoid arthritis clinically but remaining RF-negative.
3. Distal interphalangeal (DIP) predominant — Primarily targets the DIP joints (the outermost finger and toe joints). Closely associated with nail involvement (pitting, onycholysis) because the nail matrix and the DIP joint enthesis share the same anatomical territory.
4. Axial spondylitis (spondyloarthropathy pattern) — Predominantly affects the spine and sacroiliac joints, resembling ankylosing spondylitis. Associated with HLA-B27 when radiological sacroiliitis is present (Search PubMed). Can cause inflammatory back pain and progressive spinal stiffness.
5. Arthritis mutilans — The rarest and most destructive subtype, characterized by osteolysis (bone resorption) at the small joints of the hands and feet, leading to the "telescoping" of digits ("opera-glass hand" deformity). It causes severe functional disability.

Causes and Genetic Factors — HLA Associations

PsA results from a complex interplay of genetic predisposition, immune dysregulation, and environmental triggers. No single gene causes the disease; rather, multiple genetic variants collectively lower the threshold for immune activation at the skin and joint.

Key HLA Associations

• HLA-Cw6 — The primary HLA association of psoriasis itself (Search PubMed).
• HLA-B27 — Associated with PsA, both with its peripheral arthritis and with spinal disease when radiological sacroiliitis is present; spinal disease without radiological sacroiliitis is probably not associated with HLA-B27 (Search PubMed).
• HLA-B38 and HLA-B39 — Possibly associated with PsA, but results differ considerably between series and a 1994 review found no firm conclusion possible (Search PubMed).
• HLA-DR4 — A possible, not conclusive, association with the symmetric seronegative pattern of peripheral PsA; genes outside the MHC are also likely to contribute (Search PubMed).

Immune Pathways

The IL-17/IL-23 axis is central to PsA pathogenesis. IL-23 (produced by dendritic cells and macrophages) drives differentiation and survival of Th17 cells, which in turn produce IL-17A and IL-17F. These cytokines stimulate keratinocytes to proliferate (driving psoriatic plaques) and activate fibroblasts and osteoclasts in the joint, causing synovitis and bone erosion. TNF-alpha also plays a critical amplifying role at the joint level. This mechanistic understanding has directly guided drug development: blocking TNF, IL-17, IL-23, or downstream JAK-STAT signaling all produce clinical benefit.

Environmental Triggers

Environmental factors are thought to act together with genetic factors (Search PubMed). Obesity is the best-measured of them: in a UK cohort of 75,395 people with psoriasis, the relative risk of developing PsA was 1.22 with a body mass index of 30–34.9 and 1.48 with a BMI of 35 or more, compared with a BMI under 25 (PubMed PMID: 22586165).

Symptoms and Joints Affected

PsA presents heterogeneously. Many patients begin with mild joint symptoms that are ignored or attributed to normal wear, only receiving a diagnosis years later. The most characteristic features include:

Hallmark Features

• Dactylitis ("sausage digits") — Diffuse swelling of an entire finger or toe, caused by a combination of joint effusion, synovial inflammation, and tendon sheath swelling. Reported in an average of 25% of PsA patients across 35 studies in a 2020 meta-analysis, which also found that dactylitis increases radiographic progression (Search PubMed).
• Enthesitis — Inflammation at tendon and ligament insertion sites. Common locations include the Achilles tendon insertion at the heel, the plantar fascia insertion (causing heel pain), the patellar tendon insertion, and the epicondyles of the elbow. Enthesitis is a hallmark that distinguishes PsA (and spondyloarthropathies generally) from rheumatoid arthritis; the same meta-analysis found an average prevalence of 30% (Search PubMed).
• Nail involvement — Present in 60% of PsA patients across 26 studies in the 2020 meta-analysis, though definitions were often unclear (Search PubMed); in the Dublin early-arthritis cohort, 67% of patients with psoriasis had nail dystrophy at presentation (PubMed PMID: 14523223). Features include nail pitting (small depressions in the nail surface), onycholysis (separation of the nail from the nail bed), subungual hyperkeratosis (thickening under the nail), and oil-drop discoloration (a translucent yellow-brown spot visible through the nail).

Joint Distribution

Any synovial joint can be affected. Peripheral joints most commonly involved include the DIP joints, the knees, ankles, and wrists. Axial involvement (sacroiliac joints and spine) occurs in a minority of patients (10% had inflammatory spine pain at presentation in the same early cohort, PubMed PMID: 14523223), sometimes causing morning stiffness in the lower back and buttocks that improves with movement — classic inflammatory back pain. Temporomandibular joints and sternoclavicular joints may also be affected, though less commonly.

Associated Skin Disease

Active psoriatic plaques are present in most but not all patients at the time of PsA diagnosis. In some patients the skin disease is mild or in an inconspicuous location (scalp, nails, umbilicus, gluteal cleft) and may be overlooked unless specifically examined. The severity of skin disease does not reliably predict joint severity — patients with minimal skin disease can have severe, erosive arthritis.

Diagnostic Criteria and Tests

There is no single diagnostic test for PsA. Diagnosis is clinical, supported by laboratory findings and imaging. The CASPAR (Classification Criteria for Psoriatic Arthritis) criteria, developed by Taylor and colleagues in 2006 (PubMed PMID: 16871531), are the standard classification tool used in research and increasingly in clinical diagnosis.

CASPAR Criteria

To meet CASPAR criteria, a patient must have inflammatory articular disease (joint, spine, or enthesis) plus at least 3 points from the following items:

1. Current psoriasis (2 points) — OR personal history of psoriasis (1 point) — OR family history of psoriasis (1 point)
2. Nail dystrophy: pitting, onycholysis, hyperkeratosis on current examination (1 point)
3. Negative rheumatoid factor (1 point)
4. Current dactylitis or history of dactylitis recorded by a rheumatologist (1 point)
5. Radiographic evidence of juxta-articular new bone formation in the hand or foot (1 point)

In the development study (588 PsA cases and 536 controls with other inflammatory arthritis, mostly rheumatoid arthritis), the CASPAR criteria had a specificity of 98.7% and a sensitivity of 91.4%; they were more specific but less sensitive than the Vasey and Espinoza criteria (PubMed PMID: 16871531).

Laboratory Tests

• Rheumatoid factor (RF) and anti-CCP antibodies — Usually negative in PsA (seronegative). A positive result in a person with psoriasis raises the question of coexisting RA.
• ESR and CRP — Inflammatory markers elevated in active disease but non-specific.
• HLA-B27 — Useful when axial disease is suspected.
• Uric acid — Sometimes elevated; PsA and gout can coexist, and hyperuricemia is associated with psoriasis.
• Complete blood count, liver function, renal function — Baseline before starting DMARDs or biologics.

Imaging

Plain radiographs may show erosions (particularly at DIP joints), new bone formation (periostitis), and the characteristic "pencil-in-cup" deformity in arthritis mutilans. MRI is more sensitive for detecting early synovitis, enthesitis, and sacroiliitis before structural damage appears. Ultrasound is increasingly used at the bedside to detect subclinical enthesitis and synovitis.

Treatment — DMARDs, Biologics, JAK Inhibitors

The main guidelines describe treatment chosen by disease severity, by the domains involved (peripheral joints, axial disease, skin, enthesitis, dactylitis, nails) and by comorbidities: GRAPPA (Group for Research and Assessment of Psoriasis and Psoriatic Arthritis; 2015 recommendations, updated 2021 — PubMed PMID: 26749174, PubMed PMID: 35761070) and EULAR (2015 recommendations, updated in 2019 and 2023 — PubMed PMID: 26644232, PubMed PMID: 38499325). The 2015 EULAR recommendations placed conventional synthetic DMARDs (csDMARDs) as initial therapy after NSAIDs and local therapy, followed if necessary by a biologic (usually a TNF inhibitor first) or a targeted synthetic DMARD (PubMed PMID: 26644232). In the 2023 EULAR update, a biologic is started if the target is not reached with a conventional DMARD, without preference among modes of action, and JAK inhibitors are proposed mainly after a biologic has failed (PubMed PMID: 38499325). The drug classes below are not a fixed sequence.

NSAIDs and Physical Therapy

NSAIDs (naproxen, indomethacin, diclofenac) reduce pain and stiffness. The 2023 EULAR update states that NSAIDs should be used as monotherapy only for mild PsA and in the short term, and that oral glucocorticoids are not recommended (PubMed PMID: 38499325). EULAR's 2018 physical-activity recommendations for inflammatory arthritis describe physical activity as an integral part of standard care throughout the course of the disease (PubMed PMID: 29997112).

Conventional and Oral Small-Molecule DMARDs

• Methotrexate (MTX) — The csDMARD the 2023 EULAR update prefers for peripheral arthritis, with rapid initiation recommended (PubMed PMID: 38499325). A 2018 systematic review judged the trial evidence for conventional DMARDs in PsA not conclusive, while noting arguments that support methotrexate (PubMed PMID: 28089501).
• Sulfasalazine — Another conventional DMARD used for peripheral joint disease.
• Leflunomide — Another conventional DMARD used for peripheral joint disease.
• Apremilast — An oral phosphodiesterase-4 (PDE4) inhibitor, a targeted synthetic DMARD. The 2015 EULAR recommendations positioned it for use when biologics are inappropriate (PubMed PMID: 26644232).

TNF Inhibitors

TNF inhibitors include etanercept, adalimumab, infliximab, certolizumab pegol, and golimumab. The 2015 EULAR recommendations named a TNF inhibitor as the usual first biologic (PubMed PMID: 26644232); the 2023 update no longer prefers one mode of action (PubMed PMID: 38499325). Adalimumab is the active comparator in the head-to-head trials below, with ACR20 responses of 52% to 65% in those trials (PubMed PMID: 29045212, PubMed PMID: 32386593, PubMed PMID: 33789011).

IL-17 Inhibitors

Secukinumab and ixekizumab are anti-IL-17A monoclonal antibodies. In the head-to-head EXCEED trial (853 patients, 52 weeks), secukinumab did not meet its primary endpoint of superiority over adalimumab for ACR20 response (67% vs 62%, p=0.0719), although more patients stayed on secukinumab (PubMed PMID: 32386593); in the prespecified subgroup with moderate-to-severe psoriasis, complete skin clearance (PASI 100) was reached by 39.1% vs 23.8% (PubMed PMID: 33913511). The 2023 EULAR update states that relevant skin psoriasis should orient the choice towards drugs targeting IL-23 (p40 or p19), IL-17A or IL-17A/F (PubMed PMID: 38499325). In a trial in Crohn's disease, IL-17A blockade with secukinumab was ineffective and adverse events were more frequent than with placebo (PubMed PMID: 22595313), which is why inflammatory bowel disease weighs against this class.

IL-23 Inhibitors

Guselkumab, risankizumab, and tildrakizumab target the p19 subunit of IL-23 (specific IL-23 inhibition without affecting IL-12). In the DISCOVER-2 trial (741 biologic-naive patients), 64% of patients on guselkumab every 4 or every 8 weeks reached an ACR20 response at week 24, against 33% on placebo (PubMed PMID: 32178766).

JAK Inhibitors

JAK inhibitors (Janus kinase inhibitors) are oral targeted synthetic DMARDs that block intracellular signaling downstream of multiple cytokine receptors. In the OPAL Broaden trial (patients with an inadequate response to csDMARDs), month-3 ACR20 responses were 50% with tofacitinib 5 mg twice daily and 61% with 10 mg, against 33% with placebo and 52% with adalimumab; adverse events were more frequent with tofacitinib than with placebo (PubMed PMID: 29045212). In the SELECT-PsA 1 trial (1,704 patients with an inadequate response to non-biologic DMARDs), week-12 ACR20 responses were 70.6% with upadacitinib 15 mg, 78.5% with 30 mg, 36.2% with placebo and 65.0% with adalimumab; both doses were noninferior to adalimumab, and the 30 mg dose, but not the 15 mg dose, was superior (PubMed PMID: 33789011). In ORAL Surveillance, a safety trial in rheumatoid arthritis patients aged 50 or over with at least one cardiovascular risk factor, major adverse cardiovascular events (hazard ratio 1.33) and cancers (1.48) were more frequent with tofacitinib than with a TNF inhibitor, and noninferiority was not shown (PubMed PMID: 35081280). The 2023 EULAR update proposes JAK inhibitors primarily after biologic failure, taking relevant risk factors into account, or when biologics are not an appropriate choice (PubMed PMID: 38499325).

Axial Disease

In ankylosing spondylitis, the IL-23 inhibitor risankizumab showed no meaningful improvement over placebo in a phase 2 trial (PubMed PMID: 29945918), so the evidence for IL-23 inhibition in predominantly axial disease is weaker. The 2023 EULAR update proposes a separate algorithm for predominantly axial or entheseal disease (PubMed PMID: 38499325).

Natural and Nutritional Approaches

The diet and lifestyle studies below are observational studies and small randomized trials, far fewer than the drug trials.

Anti-Inflammatory Diet and Mediterranean Diet

The Mediterranean diet is rich in olive oil, vegetables, legumes, whole grains, fatty fish, and nuts. In a cross-sectional study of 211 PsA patients, higher adherence to it was associated with lower disease activity (DAPSA), and disease activity rose with body mass index (PubMed PMID: 31605152). A cross-sectional design shows an association, not cause and effect.

Omega-3 Fatty Acids

EPA and DHA are the marine omega-3 fatty acids found in fatty fish. In a 24-week randomized trial in 145 PsA patients, 3 g/day of marine n-3 fatty acids lowered disease activity scores, but not significantly more than the olive-oil control; use of NSAIDs and paracetamol and leukotriene B4 formation fell significantly compared with control (PubMed PMID: 28303758).

Vitamin D

A 2023 meta-analysis found lower vitamin D levels in PsA patients than in healthy controls (mean difference −6.42), but higher levels than in people with psoriasis alone; its authors concluded that further studies are needed to understand the role of vitamin D in the development and treatment of PsA (PubMed PMID: 37062151).

Weight Management

Higher body weight is linked with PsA risk (see Environmental Triggers above) and, in the Mediterranean-diet study, with higher disease activity (PubMed PMID: 31605152). In a prospective study of 138 overweight or obese PsA patients starting TNF blockers with a dietary intervention, weight loss of at least 5% at 6 months predicted reaching minimal disease activity; MDA was reached by 23.1%, 44.8% and 59.5% of those losing less than 5%, 5–10% and more than 10% of body weight (PubMed PMID: 23771989).

Curcumin and Other Anti-Inflammatory Supplements

Curcumin (from turmeric) has been studied mainly in psoriasis skin disease; a PubMed search for randomized controlled trials of curcumin in psoriatic arthritis returned none.

Tobacco

In the Danish DANBIO registry (1,388 PsA patients starting a first TNF inhibitor), current smokers had worse patient-reported outcomes at baseline, stayed on treatment for a shorter time and had poorer responses than never-smokers, most clearly in men (PubMed PMID: 25063827).

Disease Course and Prognosis

The course of PsA is highly variable. Some patients experience mild, intermittent disease with prolonged remissions. Others, particularly those with polyarticular, erosive disease, follow a progressive course with accumulating joint damage. In a Dublin early-arthritis cohort treated with conventional DMARDs, 47% of patients had joint erosions in the hands or feet at a median of 24 months, and only 21% were in remission at 2 years (PubMed PMID: 14523223).

Patients who present with polyarticular disease are at risk of disease progression (PubMed PMID: 15708927), and dactylitis increases radiographic progression (Search PubMed). "Treat-to-target" (T2T) means aiming for a defined state such as remission or minimal disease activity (MDA). In the TICOPA trial (206 patients with early PsA), tight control — review every 4 weeks, with treatment escalated whenever MDA criteria were not met — gave higher odds of an ACR20 response at 48 weeks than standard care (odds ratio 1.91), with more serious adverse events in the tight-control group (PubMed PMID: 26433318).

TNF, IL-17 and IL-23 inhibitors and JAK inhibitors have been added to the conventional drugs, and the 2023 EULAR update is built around reaching a treatment target, with drug switches when it is not reached and tapering in sustained remission (PubMed PMID: 38499325).

Mease (2011) reviewed the pathophysiology, assessment tools and management of PsA (PubMed PMID: 21339225); Ritchlin, Colbert and Gladman (2017) published a broader review of pathogenesis, clinical features and treatment (PubMed PMID: 28273019).

Complications

PsA is a systemic disease with extra-articular manifestations and comorbidities beyond the joints:

• Uveitis — Uveitis (inflammation inside the eye) was found in 3.2% of PsA patients on average in the 2020 meta-analysis (Search PubMed).
• Inflammatory bowel disease (IBD) — Crohn's disease or ulcerative colitis was present in 3.3% of PsA patients on average in the 2020 meta-analysis (Search PubMed). The 2023 EULAR update states that IBD and uveitis, if present, should influence drug choice, with monoclonal TNF inhibitors proposed (PubMed PMID: 38499325).
• Cardiovascular disease — A 2017 meta-analysis of 11 observational studies (32,973 PsA patients) found cardiovascular disease 43% more likely than in the general population (pooled odds ratio 1.43), with pooled odds ratios of 1.68 for myocardial infarction, 1.22 for cerebrovascular disease and 1.31 for heart failure (PubMed PMID: 27111228).
• Depression and anxiety — A 2020 meta-analysis found a pooled prevalence of 17% for depression and 19% for anxiety in PsA, with depression more common than in people without PsA (pooled odds ratio 1.68); only 2.4% to 13.5% of patients were reported to be taking antidepressant or anti-anxiety medication (PubMed PMID: 32178850).
• Radiographic joint damage — Erosions and juxta-articular new bone formation (periostitis) cause progressive structural damage. In arthritis mutilans, osteolysis can lead to severe deformity and functional loss.
• Osteoporosis — A 2022 meta-analysis of five cohort studies found PsA associated with vertebral fracture (pooled odds ratio 2.09), with possible publication bias (PubMed PMID: 34496734).

Prevention and Lifestyle

Research on factors linked with the onset and course of PsA includes:

• Psoriasis treatment — In a retrospective cohort of 1,719 people with psoriasis at one university hospital, biologic treatment of the skin was associated with a lower incidence of PsA than topical treatment or no treatment (incidence rate ratio 0.26), but not significantly lower than with conventional DMARDs; in the adjusted model biologic use was protective (hazard ratio 0.19), while male sex, nail involvement and higher body mass index were linked with higher risk (PubMed PMID: 34281904).
• Body weight — Obesity is associated with a higher risk of developing PsA in people with psoriasis (PubMed PMID: 22586165); in overweight patients starting TNF blockers, weight loss of 5% or more was linked with reaching minimal disease activity (PubMed PMID: 23771989).
• Physical activity — The 2018 EULAR physical-activity recommendations, covering rheumatoid arthritis, spondyloarthritis and hip/knee osteoarthritis, describe physical activity as effective, feasible and safe and advocate it as an integral part of standard care throughout the course of these diseases (PubMed PMID: 29997112).
• Smoking — In PsA, current smoking is associated with shorter persistence on, and poorer response to, TNF inhibitors (PubMed PMID: 25063827).
• Mental health — Depression and anxiety are common in PsA, and few patients in the pooled studies were reported to be taking antidepressant or anti-anxiety medication (PubMed PMID: 32178850).
• Monitoring and treat-to-target — In established PsA, treat-to-target means regular review against a defined target (for example Minimal Disease Activity criteria or a DAPSA score) and escalation of therapy when the target is not met; this strategy was tested in the TICOPA trial (PubMed PMID: 26433318). The GRAPPA 2021 recommendations address treatment choice for each disease domain (PubMed PMID: 35761070).

Key Research Papers

1. Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H; CASPAR Study Group (2006). Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis & Rheumatism 54(8):2665-73. The multicenter study establishing the CASPAR criteria (specificity 98.7%, sensitivity 91.4%). — PubMed PMID: 16871531
2. Gladman DD, Antoni C, Mease P, Clegg DO, Nash P (2005). Psoriatic arthritis: epidemiology, clinical features, course, and outcome. Annals of the Rheumatic Diseases 64 Suppl 2:ii14-7. Review from the University of Toronto PsA program on natural history and prognosis. — PubMed PMID: 15708927
3. Moll JM, Wright V (1973). Psoriatic arthritis. Seminars in Arthritis and Rheumatism 3(1):55-78. The classic paper describing five clinical patterns of PsA as an entity distinct from rheumatoid arthritis. — PubMed PMID: 4581554
4. Ritchlin CT, Colbert RA, Gladman DD (2017). Psoriatic Arthritis. New England Journal of Medicine 376(10):957-970. Review of pathogenesis, clinical manifestations, and treatment. — PubMed PMID: 28273019
5. Coates LC, Kavanaugh A, Mease PJ, Soriano ER, Acosta-Felquer ML, Armstrong AW, et al. (2016). Group for Research and Assessment of Psoriasis and Psoriatic Arthritis 2015 Treatment Recommendations for Psoriatic Arthritis. Arthritis & Rheumatology 68(5):1060-71. Domain-based treatment recommendations covering peripheral arthritis, axial disease, enthesitis, dactylitis, skin, and nails. — PubMed PMID: 26749174
6. Gossec L, Smolen JS, Ramiro S, de Wit M, Cutolo M, Dougados M, et al. (2016). European League Against Rheumatism (EULAR) recommendations for the management of psoriatic arthritis with pharmacological therapies: 2015 update. Annals of the Rheumatic Diseases 75(3):499-510. European consensus recommendations for pharmacological management (since updated in 2019 and 2023). — PubMed PMID: 26644232
7. McInnes IB, Behrens F, Mease PJ, Kavanaugh A, Ritchlin C, Nash P, et al.; EXCEED Study Group (2020). Secukinumab versus adalimumab for treatment of active psoriatic arthritis (EXCEED): a double-blind, parallel-group, randomised, active-controlled, phase 3b trial. Lancet 395(10235):1496-1505. Head-to-head trial; the primary endpoint (superiority for ACR20 at week 52) was not met. — PubMed PMID: 32386593
8. McInnes IB, Anderson JK, Magrey M, Merola JF, Liu Y, Kishimoto M, et al. (2021). Trial of Upadacitinib and Adalimumab for Psoriatic Arthritis. New England Journal of Medicine 384(13):1227-1239. The SELECT-PsA 1 phase 3 trial: both doses superior to placebo and noninferior to adalimumab; only the 30 mg dose superior to adalimumab. — PubMed PMID: 33789011
9. Mease PJ (2011). Psoriatic arthritis: update on pathophysiology, assessment and management. Annals of the Rheumatic Diseases 70 Suppl 1:i77-84. Update on disease mechanisms and the assessment tools used in clinical trials and practice. — PubMed PMID: 21339225
10. Mease PJ, Rahman P, Gottlieb AB, Kollmeier AP, Hsia EC, Xu XL, et al.; DISCOVER-2 Study Group (2020). Guselkumab in biologic-naive patients with active psoriatic arthritis (DISCOVER-2): a double-blind, randomised, placebo-controlled phase 3 trial. Lancet 395(10230):1126-1136. ACR20 at week 24 in 64% on guselkumab vs 33% on placebo. — PubMed PMID: 32178766
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15. Coates LC, Soriano ER, Corp N, Bertheussen H, Callis Duffin K, Campanholo CB, et al. (2022). Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA): updated treatment recommendations for psoriatic arthritis 2021. Nature Reviews Rheumatology 18(8):465-479. — PubMed PMID: 35761070
16. Gossec L, Kerschbaumer A, Ferreira RJO, Aletaha D, Baraliakos X, Bertheussen H, et al. (2024). EULAR recommendations for the management of psoriatic arthritis with pharmacological therapies: 2023 update. Annals of the Rheumatic Diseases 83(6):706-719. — PubMed PMID: 38499325
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Connections

• Rheumatology
• Psoriasis — the skin disease that usually precedes PsA; a 2019 meta-analysis found PsA in about 1 in 5 to 1 in 4 people with psoriasis
• Rheumatoid Arthritis — seronegative PsA is often confused with seropositive RA; distinguishing the two determines which biologics to use
• Arthritis — umbrella category covering all inflammatory and degenerative joint diseases
• Ankylosing Spondylitis — axial PsA and AS share HLA-B27 association and respond to similar biologics; both classified as axial spondyloarthropathies
• Lupus — systemic autoimmune disease; can coexist with psoriasis; shares cardiovascular risk elevation
• Gout — can coexist with PsA; hyperuricemia is elevated in psoriasis; both cause acute joint flares
• Osteoarthritis — degenerative joint disease that can be confused with or coexist with psoriatic DIP arthritis
• Sjögren's Syndrome — another seronegative autoimmune condition affecting mucous membranes; can overlap with psoriatic spectrum
• Osteoporosis — complication of chronic inflammation and immobility in PsA; bone mineral density monitoring recommended
• Raynaud's Disease — vascular complication occasionally seen in connective tissue and inflammatory arthritis patients
• Ehlers-Danlos Syndrome — connective tissue disorder causing joint hypermobility; important to distinguish enthesitis pain from hypermobility-related tendon pain
• Vitamin D — a 2023 meta-analysis found lower vitamin D levels in PsA than in healthy controls
• Zinc — trace mineral; see its page for the research on immune function

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