Tab Application Banner
  • Users Online: 116
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
REVIEW ARTICLE
Year : 2020  |  Volume : 15  |  Issue : 5  |  Page : 45-51

Psoriatic arthritis: An up to date overview


Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, England, UK

Date of Web Publication23-May-2020

Correspondence Address:
Dr. Laura Coates
NIHR Clinician Scientist, Botnar Research Centre, Windmill Road, Oxford OX2 8DG, England
UK
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-3698.284751

Rights and Permissions
  Abstract 


Psoriatic arthritis (PsA) is a chronic, systemic inflammatory arthritis with symptoms spanning six domains including peripheral arthritis, enthesitis, dactylitis, axial disease, psoriasis, and nail disease. The classification of disease has been refined over recent years following the development of criteria such as ClASsification of PsA criteria. In addition to classification, treatment options for PsA have continued to expand over recent years, with the development of monoclonal antibody therapies targeting the underlying immunological mediators involved in PsA such as interleukin (IL)-17, tumor necrosis factor-alpha, and IL-23. Therapies have shown that robust treatment in patients, achieving tight disease control, improves outcomes and overall quality of life. This review provides a broad overview of the epidemiology, classification, and treatment of PsA.

Keywords: Diagnosis, outcome measures, prognosis, psoriatic arthritis, spondyloarthritis, treatment


How to cite this article:
Hackett S, Coates L. Psoriatic arthritis: An up to date overview. Indian J Rheumatol 2020;15, Suppl S1:45-51

How to cite this URL:
Hackett S, Coates L. Psoriatic arthritis: An up to date overview. Indian J Rheumatol [serial online] 2020 [cited 2020 Jun 3];15, Suppl S1:45-51. Available from: http://www.indianjrheumatol.com/text.asp?2020/15/5/45/284751




  Introduction Top


Psoriatic arthritis (PsA) is a chronic, often seronegative, inflammatory musculoskeletal condition associated with a broad range of symptomology including enthesitis, dactylitis, spondylitis, psoriatic skin and nail diseases, and arthritis.[1] Psoriasis is characterized by scaly erythematous lesions, normally on the extensor surfaces of the body including, but not limited to, the elbows, knees, umbilicus, and scalp.[2] Despite initially thought of as a benign disease, this notion has significantly changed, with studies showing that 40% of patients have three or more comorbid conditions, with the presence of a comorbidity associated with overall lower quality of life (QoL).[3] In addition, PsA patients also have a vastly reduced QoL even compared to patients with psoriasis alone.[4]

Historically, PsA was initially described as the coincidence of two relatively common conditions: arthritis and psoriasis. Prof. Verna Wright, who suggested that the features of PsA were in keeping with spondyloarthropathy, rather than rheumatoid arthritis (RA), primarily brought about the notion that PsA was a distinct disease entity.[5] In the 1970s, Wright and Moll demonstrated that PsA could be defined by five clinical disease patterns: distal, oligoarticular, polyarticular, primarily axial, and arthritis mutilans.[6]

Conventionally, PsA has been a challenge for clinicians to diagnose, primarily owing to the heterogeneous nature of the disease. However, as the disease has been progressively studied, more stringent criteria have been developed in order to standardize diagnosis.[7]

The prevalence and incidence of PsA varies considerably globally. The PsA prevalence estimates in the United States range from 0.06% to 0.25%, and 0.05% to 0.21% in Europe. The reported incidence in the general population has been reported as 3.6–7.2/100,000.[8]

Treatment and management of PsA has changed considerably over recent decades with the advent of biological therapies. A variety of therapies targeting the immunological basis of PsA have shown robustly to ameliorate not only joint disease progression, but also symptomatic improvement in the inflammation as well as functional ability of PsA patients.[9]

Over the past five decades, there has been much interest in defining PsA with respect to not only its clinical phenotype, but also the pathological mechanisms that underpin the disease. Therefore, this review aims to discuss the clinical assessment and diagnosis of PsA, as well as the current recommendations surrounding treatment of patients.


  Epidemiology Top


Despite significant development in the field of PsA over the past 40 years, the epidemiology of PsA remains a much underresearched area. A recent systematic review identified 28 studies examining the epidemiology of PsA that suggested a worldwide prevalence of 133/100,000 and incidence of 83/100,000.[10]

Studies have shown considerable variability in prevalence, owing to a variety of factors including multiplicity of detection criteria and the populations studied. A study by Wilson et al.[11] demonstrated reported incidence of PsA among psoriasis patients as 7%, 3.1%, and 5.1% over 5, 10, and 20 years, respectively, following diagnosis.[11] A more recent study of 266-pooled studies containing a total of 976,408 psoriasis patients suggested that approximately one in four patients with psoriasis also have PsA.[12]


  Diagnosis and Classification Top


PsA can often be challenging for clinicians to diagnose, owing to the broad similarities with other rheumatological conditions such as RA, osteoarthritis, and gout.[13] Indeed, it is estimated that there is a prevalence of between 10% and 15% of undiagnosed PsA patients in dermatology clinics,[14] with a delay in diagnosis correlating with worse disease outcomes.

In principle, there is no diagnostic test for PsA: patients are diagnosed primarily on clinical signs and symptoms. Symptoms are often heterogeneous with symptoms traditionally described in “domains,” namely peripheral arthritis, enthesitis, dactylitis, axial disease, psoriasis, and nail disease.[15] Patients do not always have symptoms across all the six domains; indeed, they may have symptoms in only a few. In an attempt to standardize classification, a cross-sectional scoring system was developed for PsA patients.

The ClASsification of Psoriatic ARthritis (CASPAR) criteria were developed in 2006 and have been demonstrated extensively to possess both high sensitivity and specificity.[7] In order to meet the CASPAR criteria, patients must have an inflammatory articular disease (joint, spine, or entheseal) and ≥3 points from the criteria outlined in [Table 1].
Table 1: ClASsification of Psoriatic ARthritis criteria for Psoriatic arthritis: *ClASsification of Psoriatic ARthritis criteria have been demonstrated to possess extensive sensitivity and specificity since their proposal in 2006

Click here to view


The CASPAR criteria have been compared with the original diagnostic criteria proposed by Moll and Wright, with studies showing that addition of parameters such as family history of psoriasis, previously not including in the Moll and Wright criteria, allows for the diagnosis of PsA in patients who develop inflammatory articular disease even if the patient is rheumatoid factors positive and has polyarticular symmetrical arthritis.[16] The CASPAR criteria have also been examined in a retrospective context in an existing disease cohort, which showed that the feasibility, specificity, and sensitivity of the CASPAR are maintained, suggesting that they may be also useful in standardizing the existing cohorts for research purposes.[17] In addition, the CASPAR criteria have also been studied in early PsA disease: sensitivity of the criteria is lower than that of established disease, as these patients may not yet have experienced all of the typical features of PsA such as radiographic changes.[18]


  Assessment Top


With respect to disease severity, assessment sits at the crux of determining management and response to treatment. Several tools are at the disposal of rheumatologists to assess composite disease in PsA, many of which have been adapted from other rheumatological scoring systems.

The importance of accurate disease assessment has been highlighted by several studies. First, the importance of full assessment and joint counts is paramount in PsA, with patients often inaccurately assessed using reduced joint counts designed for RA and therefore, unable to predict treatment change.[19] Second, studies such as the TIght Control of Psoriatic Arthritis trial demonstrated the benefit of consistent and frequent disease activity assessment using objective outcomes.[20] However, despite these important findings, the heterogeneity of PsA confounds composite disease measurement: often patients present with involvement of multiple disease domains, meaning that translating such symptoms into a validated “relevant-for-all” measure is challenging. Fueled by expanding research within the PsA field, as well as the inadequacies of the existing disease severity measurements, there have, therefore, been significant development in the creation of scoring systems specific to PsA patients.

Minimal Disease Activity

The Minimal Disease Activity (MDA) is an index developed from patient profiles taken from an observational PsA database.[21] Statistical determination of set “cutoff” points for seven key criteria. The criteria for MDA are defined as achieving five of the seven following criteria: tender joint count ≤1; swollen joint count ≤1; Psoriasis Activity and Severity Index (PASI) ≤1 or body surface area ≤ 3; patient pain visual analog score (VAS) ≤15; patient global disease activity VAS ≤20; Health Assessment Questionnaire (HAQ) ≤0.5; and tender entheseal points ≤1. The scoring system has been externally validated and has been applied as end points in a variety of trials.[22],[23]

Psoriatic arthritis Disease Activity Score

The PsA Disease Activity Score (PASDAS) was developed as a more accurate composite measure of disease activity in PsA. The PASDAS was designed according to domains identified in randomized controlled trials in PsA patients. The authors developed new indices using multilinear regression and compared scores to the existing composite measure including Composite PsA Disease Activity Index, Disease Activity for PsA, and Disease Activity Score for RA (DAS28). The PASDAS was shown to have a better ability at discriminating between higher and lower disease activities.[24] The composite scoring system has been validated, with studies showing that PASDAS has the ability to differentiate between low, moderate, and high disease activities.[25]


  Treatment of Psoriatic Arthritis Top


Rheumatological conditions have historically been treated with disease-modifying antirheumatic drugs (DMARDs), however, their long-term therapeutic effects in PsA are largely based on clinical experience rather than extensive trial-based analysis. A variety of treatment options exist for PsA including nonpharmacological-based treatment such as weight loss, smoking cessation, and exercise. Symptomatic treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroid injections. DMARDs such as methotrexate (MTX) and newer biological-based therapies, such as adalimumab and secukinumab, have also been validated in PsA patients. Owing to a historical lack of treatment evidence in PsA patients, a variety of trials have aimed to rectify this deficit and examine outcomes in patients treated with a variety of therapeutics.

Non-steroidal anti-inflammatory drug

NSAID therapy provides symptomatic relief for patients, although fail to resolve or halt joint destruction or the psoriatic component of PsA.[26] Indeed, controlled studies have failed to show reduction in PASI score or erythrocyte sedimentation rate (ESR).[27]


  Traditional Disease-modifying Antirheumatic Drug Therapies Top


MTX, a potent immunosuppressant, has traditionally been used for the treatment of PsA. Previous studies have suggested that MTX reduces disease severity and is often favored for treatment due to low cost and once–per-week dosing profile.[28] However, despite wide use, a recent Cochrane review suggested that MTX is only slightly more beneficial compared to placebo treatment with respect to disease response (Psoriatic Arthritis Response Criteria [PSARC] score), function, health-related QoL, disease activity measured by DAS28-ESR, radiographic progression, serious adverse events (AEs), and withdrawals due to AEs. The authors were unable to ascertain whether effects were more harmful.[29] Despite these findings, the SEAM-PsA study which examined the efficacy of MTX, etanercept monotherapy, or the combination of MTX and etanercept in PsA patients demonstrated that etanercept monotherapy and combination therapy with etanercept and MTX showed greater efficacy than MTX monotherapy in patients with PsA across multiple domains.[30]

Leflunomide, an immunomodulatory agent exerting its effects through inhibition of dihydroorotate dehydrogenase, has also been historically used to treat PsA. Evidence on the use of leflunomide are conflicting: some small studies have demonstrated improvement in disease severity in 50% of patients treated,[31] while others have demonstrated only a modest improvement in disease scoring. A double-blind, randomized, placebo-controlled trial examined the efficacy of leflunomide in 95 treated patients and 91 placebo-treated patients. At 24 weeks, 58.9% of leflunomide-treated patients were classified as responders, assessed by PsARC, compared to 29.7% of placebo-treated patients.[32] These findings suggest that leflunomide is a safe and effective treatment for PsA.

Sulfasalazine is an anti-folate immunomodulator acting via inhibition of dihydropteroate synthase. Sulfasalazine has been traditionally used for treatment in RA. Although seemingly of limited efficacy in axial disease,[33] studies have shown some therapeutic efficacy in PsA patients: a prospective double-blind, placebo-controlled randomized study of 24-week duration was carried out comparing the efficacy and tolerability of sulfasalazine versus placebo in patients with PsA. However, findings from the trial showed that the only statistically significant different primary outcome at the end point was pain with no significant differences shown between clinical and biological variables.[34]

A recent retrospective study aimed to assess the response to treatment of DMARDs in PsA patients. Measuring ESR, C-reactive protein level, Bath Ankylosing Spondylitis Disease Activity Index, Bath Ankylosing Spondylitis Function Index, wellbeing, and treatment effect, the authors examined scores at baseline and 1-year follow-up in 73 patients. Across the use of the three DMARDs examined – MTX, sulfasalazine, leflunomide – sulfasalazine was noted to provide the greatest improvement in disease scoring at follow-up.[35]

A newer drug, apremilast, has recently been developed for the treatment of PsA through inhibition of phosphodiesterase-4 (PDE) – an enzyme primarily involved in the hydrolysis of the intracellular signaling molecule cyclic adenosine monophosphate. Through inhibition of PDE-4, apremilast induces upregulation of various anti-inflammatory cytokines including interleukin (IL)-10 and decreases the expression of inducible nitric oxide synthase and IL-23.[36] A variety of placebo-controlled randomized controlled trials have demonstrated the efficacy of apremilast in PsA, including the PALACE trials.[37] The latest trial, PALACE-4, examined the use of 20-mg or 30-mg apremilast twice daily against placebo in 527 DMARD-naïve patients.[37] The authors demonstrated that apremilast achieved greater ACR20/ACR50 responses and HAQ-Disability Index improvements, with minimal AEs, compared to placebo, suggesting that apremilast may offer improvements in PsA symptoms.


  Biological Therapies Top


With the advent of biological therapeutics, the treatment landscape for PsA patients has changed considerably over the past two decades. Elucidating the underlying immunological principles has allowed the development of a range of biological therapeutics targeting a broad range of immunological signaling mechanisms. A variety of biological therapies have been examined for the treatment of PsA.

The main crux of PsA biological treatment has been anti-tumor necrosis factor (TNF)-α treatment. Therapeutics that neutralize TNF-α, a potent pro-inflammatory cytokine, have shown their respective efficacies in a range of immune-mediated disorders, including psoriasis,[38] rheumatoid arthritis,[39] and PsA.[40]

The link between PsA and TNF-α has been demonstrated in several studies.[41] The inflammatory nature of PsA is apparent by the abundance of inflammatory cell infiltrates in joints and skin lesions. Indeed, cytokines that are primarily derived from macrophages, dendritic cells, and monocytes such as TNF-α have been shown to be raised in the synovium of PsA patients.[41] The basis of anti-TNF-α therapies has been confirmed in both pathological and clinical settings.

Etanercept, a fusion protein of the TNF receptor and an IgG1 antibody, has demonstrated robust efficacy in PsA patients. The initial randomized, double-blind, placebo-controlled study resulted in 87% of etanercept patients meeting PsARC, compared with 23% of placebo-treated patients.[42] ARC20 was achieved by 73% of etanercept patients in contrast to 13% of placebo controls. From this initial study, larger and more in-depth studies have examined etanercept use and shown that reduction in radiographic disease progression is superior to placebo controls.[43]

In addition to etanercept, the use of other anti-TNF-α therapies, including infliximab, adalimumab, certolizumab, and golimumab, has also proven effects in PsA patients. Infliximab is a chimeric monoclonal antibody against TNF-α that binds to both membrane-bound and soluble TNF-α. The IMPACT 2 study demonstrated the efficacy of infliximab in PsA patients: 200 patients unresponsive to previous treatment were treated with infliximab or placebo. After 14 weeks, 58% of the patients receiving infliximab and 27% of placebo-treated patients achieved PsARC, with therapeutic effects maintained throughout the 24-week study period. The study also demonstrated reduction in dactylitis in infliximab patients compared to placebo (12% vs. 34% at 24 weeks), with no increase in AEs.[44] The Study of Etanercept and Methotrexate in Combination or as Monotherapy in Subjects with Psoriatic Arthritis (SEAM study) was conducted to evaluate the efficacy of MTX monotherapy, etanercept monotherapy, or the combination of MTX and etanercept in early PsA. By examining ACR20 response, the study demonstrated that both etanercept monotherapy and etanercept plus MTX combination therapy were significantly more efficacious than MTX monotherapy in early PsA patients. These findings suggest that etanercept's effects are not enhanced by combination with MTX.[30]

In addition to TNF-α, other principle cytokines play an important regulatory role in PsA, including IL-12, IL-17, and IL-23.[45] To this end, a variety of monoclonal antibody-based therapies have been developed in an attempt to address the underlying immunopathogenesis of PsA.

Ustekinumab is a fully human immunoglobulin G1 κ (IgG1 κ) monoclonal antibody against the common sub-unit p40 of IL-12 and IL-23. IL-12 and IL-23 play pivotal roles in governing Th1 and Th17 inflammatory responses, respectively.[46] Ustekinumab has been extensively validated in psoriasis and, subsequent to its success, has been trialed in PsA patients.[47] Recent findings have shown that ustekinumab yields slightly lower ACR response rates in patients compared to anti-TNF or anti-IL-17 agents.[48] Furthermore, some studies have also shown worsening of symptoms in some PsA patients following commencement of ustekinumab.[49] As a result, guidelines published by the European League Against Rheumatism (EULAR) have advised anti-TNF-α therapy as first-line biological treatment, with patients designated as nonresponders or contraindications to consider ustekinumab therapy (Gossec et al., 2016).[50]

Secukinumab is a human Ig-G1-κ monoclonal antibody, which binds to the IL-17A receptor, reducing IL-17-mediated immune activation.[51] Studies have demonstrated IL-17 levels in the synovial fluid and serum of PsA patients.[52] Furthermore, IL-17 has been demonstrated to play a fundamental role in the resorption of bone and RANKL-mediated osteoclastogenesis.[53] Blockade of IL-17 signaling, therefore, offers a dual approach to PsA: first the reduction of systemic inflammation and second, attenuation of joint destruction.

Initially, secukinumab was assessed in a randomized, double-blind, placebo-controlled trial in PsA patients in 2014.[54] The study demonstrated that 39% of the 42 patients enrolled in the study achieved ACR20 responses after 6 weeks, versus 23% for placebo, with “good” EULAR responses achieved in 21.7% of PsA patients. Although the primary end point was not reached, clinical responses, acute-phase reactant, and QoL improvements were greater with secukinumab than that with placebo-treated patients. A variety of studies have since addressed the clinical effectiveness of secukinumab, namely the FUTURE studies.[55] Most recently, the FUTURE 5 study has examined the effects of administering a loading dose of subcutaneous secukinumab in PsA patients, compared to placebo.[51] The FUTURE 5 demonstrated robust ACR20 response at 16 weeks with both loading doses of secukinumab, as well as patients treated without a loading dose, compared to placebo. Furthermore, radiographic disease progression was significantly inhibited in all secukinumab patients. These latest findings suggest that secukinumab treatment may offer favorable outcomes in treated PsA patients.

Adding further weight to the contribution of Th-17 signaling in the underlying pathogenesis of PsA, ixekinumab, a humanized IgG4 monoclonal antibody directed against IL-17A, has been assessed in two Phase III clinical trials: SPIRIT-P1 and SPIRIT P2. Findings from these studies have demonstrated that ixekinumab has demonstrated significant efficacy compared to placebo in patients with moderate-to-severe PsA that had previously failed NSAIDs, conventional DMARDs, or TNFα inhibitors.[56],[57]

Treatment guidelines for psoriatic arthritis patients: Group for Research and Assessment of Psoriasis and Psoriatic Arthritis

In 2015, the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) and EULAR presented guidelines for the management of PsA, in light of the exponential increase in therapies and assessment tools available for clinicians.[58] Disease domains were discussed and treatment pathways were formulated. The treatment schematic is shown in [Figure 1], as adapted from Coates et al., 2016.[58] The rapid pace of change in therapeutics for PsA has resulted in an update of these treatment recommendations due for presentation in 2020.
Figure 1: Group for Research and Assessment of Psoriasis and Psoriatic Arthritis Guidelines for the management of psoriatic arthritis. In 2015, both the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis and the European League Against Rheumatism presented updated recommendations on the management of psoriatic arthritis[58]

Click here to view



  Conclusion Top


The diagnosis, classification, and management of PsA have changed markedly over recent decades. It is clear that PsA is a multifaceted disease with a significant disease burden including significant comorbidities such as cardiovascular disease, depression, and metabolic complications. In light of the significant health burden posed by PsA, a variety of therapies have been extensively investigated in the treatment of patients, with newer biological agents showing excellent efficacy in achieving tight disease control in patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Mease P. Update on treatment of psoriatic arthritis. Bull NYU Hosp Jt Dis 2012;70:167-71.  Back to cited text no. 1
    
2.
Cunha JS, Qureshi AA, Reginato AM. Management of Psoriasis and Psoriatic Arthritis in a Multidisciplinary Rheumatology/Dermatology Clinic. Fed Pract 2015;32:14S-20S.  Back to cited text no. 2
    
3.
Lee S, Mendelsohn A, Sarnes E. The burden of psoriatic arthritis: a literature review from a global health systems perspective.P T 2010;35:680-9.  Back to cited text no. 3
    
4.
Rosen CF, Mussani F, Chandran V, Eder L, Thavaneswaran A, Gladman DD. Patients with psoriatic arthritis have worse quality of life than those with psoriasis alone. Rheumatology (Oxford) 2012;51:571-6.  Back to cited text no. 4
    
5.
Espinoza LR. The history of psoriatic arthritis (PsA): From moll and wright to pathway-specific therapy. Curr Rheumatol Rep 2018;20:58.  Back to cited text no. 5
    
6.
Moll JM, Wright V. Psoriatic arthritis. Semin Arthritis Rheum 1973;3:55-78.  Back to cited text no. 6
    
7.
Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H, et al. Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis Rheum 2006;54:2665-73.  Back to cited text no. 7
    
8.
Ogdie A, Weiss P. The epidemiology of psoriatic arthritis. Rheum Dis Clin North Am 2015;41:545-68.  Back to cited text no. 8
    
9.
Mease PJ, van der Heijde D, Ritchlin CT, Okada M, Cuchacovich RS, Shuler CL, et al. 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. Ann Rheum Dis 2017;76:79-87.  Back to cited text no. 9
    
10.
Scotti L, Franchi M, Marchesoni A, Corrao G. Prevalence and incidence of psoriatic arthritis: A systematic review and meta-analysis. Semin Arthritis Rheum 2018;48:28-34.  Back to cited text no. 10
    
11.
Wilson FC, Icen M, Crowson CS, McEvoy MT, Gabriel SE, Kremers HM. Incidence and clinical predictors of psoriatic arthritis in patients with psoriasis: a population-based study. Arthritis Rheum 2009;61:233-9.  Back to cited text no. 11
    
12.
Alinaghi F, Calov M, Kristensen LE, Gladman DD, Coates LC, Jullien D, et al. Prevalence of psoriatic arthritis in patients with psoriasis: A systematic review and meta-analysis of observational and clinical studies. J Am Acad Dermatol 2019;80:251-65.  Back to cited text no. 12
    
13.
Merola JF, Espinoza LR, Fleischmann R. Distinguishing rheumatoid arthritis from psoriatic arthritis. RMD Open 2018;4:e000656.  Back to cited text no. 13
    
14.
Villani AP, Rouzaud M, Sevrain M, Barnetche T, Paul C, Richard MA, et al. Prevalence of undiagnosed psoriatic arthritis among psoriasis patients: Systematic review and meta-analysis. J Am Acad Dermatol 2015;73:242-8.  Back to cited text no. 14
    
15.
Tucker LJ, Coates LC, Helliwell PS. Assessing disease activity in psoriatic arthritis: A literature review. Rheumatol Ther 2019;6:23-32.  Back to cited text no. 15
    
16.
Congi L, Roussou E. Clinical application of the CASPAR criteria for psoriatic arthritis compared to other existing criteria. Clin Exp Rheumatol 2010;28:304-10.  Back to cited text no. 16
    
17.
Tillett W, Costa L, Jadon D, Wallis D, Cavill C, McHugh J, et al. The ClASsification for Psoriatic ARthritis (CASPAR) criteria – A retrospective feasibility, sensitivity, and specificity study. J Rheumatol 2012;39:154-6.  Back to cited text no. 17
    
18.
Coates LC, Conaghan PG, Emery P, Green MJ, Ibrahim G, MacIver H, et al. Sensitivity and specificity of the classification of psoriatic arthritis criteria in early psoriatic arthritis. Arthritis Rheum 2012;64:3150-5.  Back to cited text no. 18
    
19.
Coates LC, FitzGerald O, Gladman DD, McHugh N, Mease P, Strand V, et al. Reduced joint counts misclassify patients with oligoarticular psoriatic arthritis and miss significant numbers of patients with active disease. Arthritis Rheum 2013;65:1504-9.  Back to cited text no. 19
    
20.
Coates LC, Moverley AR, McParland L, Brown S, Navarro-Coy N, O'Dwyer JL, et al. Effect of tight control of inflammation in early psoriatic arthritis (TICOPA): A UK multicentre, open-label, randomised controlled trial. Lancet 2015;386:2489-98.  Back to cited text no. 20
    
21.
Coates LC, Fransen J, Helliwell PS. Defining minimal disease activity in psoriatic arthritis: A proposed objective target for treatment. Ann Rheum Dis 2010;69:48-53.  Back to cited text no. 21
    
22.
Mease P, Choy E, Thom H, Kalyvas C, Lopes N, Pricop L, et al. Certolizumab pegol for the treatment of psoriatic arthritis: 4-year outcomes from the RAPID-PsA trial. Ann Rheum Dis 2016;75 Suppl 2:608-9.  Back to cited text no. 22
    
23.
Coates LC, Gladman DD, Nash P, FitzGerald O, Kavanaugh A, Kvien TK, et al. Secukinumab provides sustained PASDAS-defined remission in psoriatic arthritis and improves health-related quality of life in patients achieving remission: 2-year results from the phase III FUTURE 2 study. Arthritis Res Ther 2018;20:272.  Back to cited text no. 23
    
24.
Helliwell PS, FitzGerald O, Fransen J, Gladman DD, Kreuger GG, Callis-Duffin K, et al. The development of candidate composite disease activity and responder indices for psoriatic arthritis (GRACE project). Ann Rheum Dis 2013;72:986-91.  Back to cited text no. 24
    
25.
Perruccio AV, Got M, Li S, Ye Y, Gladman DD, Chandran V. Treating psoriatic arthritis to target: Defining the psoriatic arthritis disease activity score that reflects a state of minimal disease activity. J Rheumatol 2020;47:362-8.  Back to cited text no. 25
    
26.
Nash P, Clegg DO. Psoriatic arthritis therapy: NSAIDs and traditional DMARDs. Ann Rheum Dis 2005;64 Suppl 2:ii74-7.  Back to cited text no. 26
    
27.
Sarzi-Puttini P, Santandrea S, Boccassini L, Panni B, Caruso I. The role of NSAIDs in psoriatic arthritis: Evidence from a controlled study with nimesulide. Clin Exp Rheumatol 2001;19:S17-20.  Back to cited text no. 27
    
28.
Cuchacovich R, Perez-Alamino R, Garcia-Valladares I, Espinoza LR. Steps in the management of psoriatic arthritis: A guide for clinicians. Ther Adv Chronic Dis 2012;3:259-69.  Back to cited text no. 28
    
29.
Wilsdon TD, Whittle SL, Thynne TR, Mangoni AA. Methotrexate for psoriatic arthritis. Cochrane Database Syst Rev 2019;1:CD012722.  Back to cited text no. 29
    
30.
Mease PJ, Gladman DD, Collier DH, Ritchlin CT, Helliwell PS, Liu L, et al. Etanercept and methotrexate as monotherapy or in combination for psoriatic arthritis: Primary results from a randomized, controlled Phase III trial. Arthritis Rheumatol 2019;71:1112-24.  Back to cited text no. 30
    
31.
Asiri A, Thavaneswaran A, Kalman-Lamb G, Chandran V, Gladman DD. The effectiveness of leflunomide in psoriatic arthritis. Clin Exp Rheumatol 2014;32:728-31.  Back to cited text no. 31
    
32.
Kaltwasser JP, Nash P, Gladman D, Rosen CF, Behrens F, Jones P, et al. Efficacy and safety of leflunomide in the treatment of psoriatic arthritis and psoriasis: A multinational, double-blind, randomized, placebo-controlled clinical trial. Arthritis Rheum 2004;50:1939-50.  Back to cited text no. 32
    
33.
Clegg DO, Reda DJ, Abdellatif M. Comparison of sulfasalazine and placebo for the treatment of axial and peripheral articular manifestations of the seronegative spondylarthropathies: A department of veterans affairs cooperative study. Arthritis Rheum 1999;42:2325-9.  Back to cited text no. 33
    
34.
Combe B, Goupille P, Kuntz JL, Tebib J, Lioté F, Bregeon C. Sulphasalazine in psoriatic arthritis: A randomized, multicentre, placebo-controlled study. Br J Rheumatol 1996;35:664-8.  Back to cited text no. 34
    
35.
Roussou E, Bouraoui A. Real-life experience of using conventional disease-modifying anti-rheumatic drugs (DMARDs) in psoriatic arthritis (PsA). Retrospective analysis of the efficacy of methotrexate, sulfasalazine, and leflunomide in PsA in comparison to spondyloarthritides other than PsA and literature review of the use of conventional DMARDs in PsA. Eur J Rheumatol 2017;4:1.  Back to cited text no. 35
    
36.
Schafer P. Apremilast mechanism of action and application to psoriasis and psoriatic arthritis. Biochem Pharmacol 2012;83:1583-90.  Back to cited text no. 36
    
37.
Wells AF, Edwards CJ, Kivitz AJ, Bird P, Nguyen D, Paris M, et al. Apremilast monotherapy in DMARD-naive psoriatic arthritis patients: results of the randomized, placebo-controlled PALACE 4 trial. Rheumatology (Oxford) 2018;57:1253-63.  Back to cited text no. 37
    
38.
Kircik LH, Del Rosso JQ. Anti-TNF agents for the treatment of psoriasis. J Drugs Dermatol 2009;8:546-59.  Back to cited text no. 38
    
39.
Machado MA, Maciel AA, de Lemos LL, Costa JO, Kakehasi AM, Andrade EI, et al. Adalimumab in rheumatoid arthritis treatment: A systematic review and meta-analysis of randomized clinical trials. Rev Bras Reumatol 2013;53:419-30.  Back to cited text no. 39
    
40.
Clunie G, McInnes IB, Barkham N, Marzo-Ortega H, Patel Y, Gough A, et al. Long-term effectiveness of tumour necrosis factor-α inhibitor treatment for psoriatic arthritis in the UK: A multicentre retrospective study. Rheumatol Adv Pract 2018;2:rky042.  Back to cited text no. 40
    
41.
Mease PJ. Tumour necrosis factor (TNF) in psoriatic arthritis: Pathophysiology and treatment with TNF inhibitors. Ann Rheum Dis 2002;61:298-304.  Back to cited text no. 41
    
42.
Mease PJ, Goffe BS, Metz J, VanderStoep A, Finck B, Burge DJ. Etanercept in the treatment of psoriatic arthritis and psoriasis: a randomised trial. Lancet 2000;356:385-90.  Back to cited text no. 42
    
43.
Antoni CE, Kavanaugh A, van der Heijde D, Beutler A, Keenan G, Zhou B, et al. Two-year efficacy and safety of infliximab treatment in patients with active psoriatic arthritis: Findings of the Infliximab Multinational Psoriatic Arthritis Controlled Trial (IMPACT). J Rheumatol 2008;35:869-76.  Back to cited text no. 43
    
44.
Antoni C, Krueger GG, de Vlam K, Birbara C, Beutler A, Guzzo C, et al. Infliximab improves signs and symptoms of psoriatic arthritis: Results of the IMPACT 2 trial. Ann Rheum Dis 2005;64:1150-7.  Back to cited text no. 44
    
45.
Sakkas LI, Zafiriou E, Bogdanos DP. Mini review: New treatments in psoriatic arthritis. focus on the IL-23/17 axis. Front Pharmacol 2019;10:872.  Back to cited text no. 45
    
46.
Dobbin-Sears I, Roberts J, O'Rielly DD, Rahman P. Ustekinumab in psoriatic arthritis and related phenotypes. Ther Adv Chronic Dis 2018;9:191-8.  Back to cited text no. 46
    
47.
McInnes IB, Kavanaugh A, Gottlieb AB, Puig L, Rahman P, Ritchlin C, et al. Efficacy and safety of ustekinumab in patients with active psoriatic arthritis: 1 year results of the phase 3, multicentre, double-blind, placebo-controlled PSUMMIT 1 trial. Lancet 2013;382:780-9.  Back to cited text no. 47
    
48.
Magrey M, Bozyczko M, Wolin D, Mordin M, McLeod L, Davenport E, et al. Evaluation of the feasibility of a web-based survey to assess patient-reported symptom improvement and treatment satisfaction among patients with psoriatic arthritis receiving secukinumab. Clin Drug Investig 2019;39:1205-12.  Back to cited text no. 48
    
49.
Onsun N, Yalcin B, Sallahoglu K, Rezvani A. Worsening of Psoriatic Arthritis After Ustekinumab Treatment. Am J Ther 2018;25:e381-e382.  Back to cited text no. 49
    
50.
Gossec L, Smolen JS, Ramiro S, de Wit M, Cutolo M, Dougados M, et al. European league against rheumatism (EULAR) recommendations for the management of psoriatic arthritis with pharmacological therapies: 2015 update. Ann Rheum Dis 2016;75:499-510.  Back to cited text no. 50
    
51.
Mease P, van der Heijde D, Landewé R, Mpofu S, Rahman P, Tahir H, et al. Secukinumab improves active psoriatic arthritis symptoms and inhibits radiographic progression: Primary results from the randomised, double-blind, phase III FUTURE 5 study. Ann Rheum Dis 2018;77:890-7.  Back to cited text no. 51
    
52.
Blauvelt A, Chiricozzi A. The immunologic role of IL-17 in psoriasis and psoriatic arthritis pathogenesis. Clin Rev Allergy Immunol 2018;55:379-90.  Back to cited text no. 52
    
53.
Yago T, Nanke Y, Ichikawa N, Kobashigawa T, Mogi M, Kamatani N, et al. IL-17 induces osteoclastogenesis from human monocytes alone in the absence of osteoblasts, which is potently inhibited by anti-TNF-alpha antibody: a novel mechanism of osteoclastogenesis by IL-17. J Cell Biochem 2009;108:947-55.  Back to cited text no. 53
    
54.
McInnes IB, Sieper J, Braun J, Emery P, van der Heijde D, Isaacs JD, et al. Efficacy and safety of secukinumab, a fully human anti-interleukin-17A monoclonal antibody, in patients with moderate-to-severe psoriatic arthritis: A 24-week, randomised, double-blind, placebo-controlled, phase II proof-of-concept trial. Ann Rheum Dis 2014;73:349-56.  Back to cited text no. 54
    
55.
McInnes IB, Mease PJ, Kirkham B, Kavanaugh A, Ritchlin CT, Rahman P, et al. Secukinumab, a human anti-interleukin-17A monoclonal antibody, in patients with psoriatic arthritis (FUTURE 2): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet 2015;386:1137-46.  Back to cited text no. 55
    
56.
Mease P, Choy E, Nash P, Kalyvas C, Hunger M, Pricop L, et al. Comparative effectiveness of secukinumab and etanercept in biologic-naïve patients with psoriatic arthritis assessed by matching-adjusted indirect comparison. Eur J Rheumatol 2018;6:113-121. Published 2018 Jul 1. doi:10.5152/eurjrheum.2019.19057.  Back to cited text no. 56
    
57.
Nash P, Kirkham B, Okada M, Rahman P, Combe B, Burmester GR, et al. Ixekizumab for the treatment of patients with active psoriatic arthritis and an inadequate response to tumour necrosis factor inhibitors: Results from the 24-week randomised, double-blind, placebo-controlled period of the SPIRIT-P2 phase 3 trial. Lancet 2017;389:2317-27.  Back to cited text no. 57
    
58.
Coates LC, Kavanaugh A, Mease PJ, Soriano ER, Laura Acosta-Felquer M, Armstrong AW, et al. Group for research and assessment of psoriasis and psoriatic arthritis 2015 treatment recommendations for psoriatic arthritis. Arthritis Rheumatol 2016;68:1060-71.  Back to cited text no. 58
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Epidemiology
Diagnosis and Cl...
Assessment
Treatment of Pso...
Traditional Dise...
Biological Therapies
Conclusion
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed96    
    Printed0    
    Emailed0    
    PDF Downloaded33    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]