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Unmet needs

misdiagnosis, a strict collaboration between dermatologists and rheumatologists has been proposed, and several tools for PsA screening for use in dermatology clinics have been developed. Among them, the Psoriatic Arthritis Sceening and Evaluation questionnaires (PASE), the Psoriasis Epidemiology Screening Toll (PEST), and the Toronto Psoriatic Arthritis Screening (ToPAS)9–11 have been compared in a study performed in the UK; interestingly, the data showed low sensitivity in detecting the oligoarticular and axial subsets, and a low specificity as the screening tools have detected also degenerative and other forms of joint or musculoskeletal involvement.12

To better define their

usefulness, these screening questionnaires are currently under formal testing and comparison in an Italian multicentre study, which includes dermatology clinics and their rheumatology unit counterparts (Heracles) based in the same hospital or NHS area, and is still ongoing.

Clinical assessment

PsA is a multifaceted disease, the assessment of which requires attention to peripheral joint involvement, axial disease, dactylitis, and enthesitis, as well as to the skin manifestations because of the variability in clinical phenotype. Domains such as patient assessment of disease activity, pain, fatigue, quality of life, function and the new concept of participation, which can be measured only as patient-reported outcomes (PROMs),13 are likewise important. The assessment of damage is fundamental in order to assess long-term efficacy of treatments and prognosis. In order to summarise all the aspects of this polymorphic disease, a number of composite outcome measures have been proposed, including the PsA disease activity score (PASDAS), GRACE index, PsA Joint Activity Index (PsAJAI) and Composite Psoriatic Arthritis Disease Activity Index (CPDAI).14–16

All these

instruments underline the need for a comprehensive approach in the treatment of PsA, and the appearance of new instruments suggests that the existing ones do not fully satisfy the necessary requirements.


Biomarkers Clinical, laboratory and imaging biomarkers in combination are important in clinical practice in order to help in early diagnosis, early and appropriate treatment, which should be tailored to

patients, and in assessing response to treatment and disease progression or remission.

Clinical features known to predict poor outcome include number of swollen joints, failure of disease-modifying anti- rheumatic agents (DMARDs) treatment and use of steroids, and detection of early erosions. High erythrocyte sedimentation rate is a bad laboratory prognostic factor17 as regards severity and progression of the disease.

Unfortunately, the paucity, or even the

lack, of effective blood tests useful in early diagnosis/prognosis or in guiding the therapeutic interventions is evident compared with biomarkers available in other rheumatic and non-rheumatic conditions. On this basis, GRAPPA has promoted an international, multicentre, BioBank based in Toronto, the aim of which is to collect biological samples and clinical data in order to investigate possible biomarkers to be implemented in the diagnosis, prognosis and long-term follow-up of PsA and psoriasis patients.18

Treatment The first therapeutic interventions in patients with newly diagnosed PsA are non-steroidal anti-inflammatory drugs (NSAIDs), intra-articular steroid injections (generally when a single joint is affected), shortly followed (once the chronicity of the disease is confirmed) by

Table 1: Burden of disease in PsA – areas for further investigation and improvement

Pathogenetic mechanisms • Genetic susceptibility

• Genetic determinants of severity • Triggers

• Inflammatory milieu

• Mechanisms of damage and new bone formation Diagnosis

• Diagnostic and classification criteria • Screening tools

Clinical assessment • Physician

• Patient Reported Outcomes

Biomarkers • Clinical • Blood tests • Imaging

Treatment • Traditional DMARDS • Anti TNF-α antagonists • New biologics

Quality of care • Joint clinics psoriasis and PsA • Patients’ involvement in the decision processes

Economic burden • Costs

• General availability

one or more DMARDs in the peripheral joint disease subsets. In clinical practice, according to international and national guidelines,19,20

the most prescribed

DMARDs are methotrexate (although a recent study by Kingsley and colleagues21 has raised some concerns), sulfasalazine, leflunomide and cyclosporin-A, some of which are effective both in skin and joint manifestations.

In patients with peripheral joint

involvement who fail this first therapeutic approach, and in PsA patients with axial involvement, anti-tumour necrosis factor alpha (TNF-α) compounds have been recommended in order to suppress inflammatory symptoms as well as to stop development of erosive damage and structural changes. In order to avoid joint damage, it is widely advised not to delay the switch from traditional DMARD therapeutic schemes to ‘biologic DMARDs’ in case of failure to obtain a sustained disease remission.19,20


benefit of early intervention in rheumatoid arthritis is widely recognised, and it was logical to assume that a similar rationale would apply for PsA. Recently the ‘Tight Control of Psoriatic Arthritis’ (TICOPA) study, a multicentre, randomised, controlled study, assessed the impact of tight control in early PsA patients. The results suggest that intensive treatment of PsA patients, compared with standard care, significantly improves joint and skin outcomes.22

Every patient with PsA differs in disease phenotype, disease severity and response to treatment. A proportion of patients do not respond or develop side effects to traditional or biologic anti- TNF-α drugs, underlying the possibility of different inflammatory pathways and/or pathogenetic interplays. The emergence of alternative drugs with different mechanisms of action, which provide new effective tools to treat PsA, has been welcomed. Among the new molecules recently proposed for treatment of PsA, apremilast and ustekinumab have been registered by the regulatory authorities and are expected to fill the gap in the therapeutic options because of the novel targets that characterise their mechanisms of action.

Apremilast specifically inhibits the enzymatic activity of PDE4 and therefore influence the expression of several pro- and anti-inflammatory cytokines23 involved in the pathogenesis of PsA. The clinical efficacy and safety profile of apremilast has been studied extensively in

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