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Therapeutics


Benefits of oral systemic drugs in psoriatic arthritis


The main goal when treating psoriatic arthritis is remission, or at least a state of prolonged minimal disease activity, in order to maximise long-term health-related quality of life and social participation. Oral drugs used in its treatment are summarised


Rubén Queiro Silva MD PhD Rheumatology Division Hospital Universitario Central de Asturias (HUCA) Oviedo, Spain


Psoriasis is an immune-mediated chronic skin condition characterised in its most common form by erythematous, scaly patches or plaques resulting from hyperproliferation of epidermal keratinocytes in the skin. It is estimated that almost 1–3 % of the general population is affected by psoriasis.1,2


An


important component of the psoriatic phenotype is psoriatic arthritis (PsA), a chronic inflammatory condition affecting axial and peripheral joints, as well as entheses.1,2


Recent estimations suggest


that up to 40% of psoriatic patients have signs and symptoms of PsA, and many of them are unaware of this diagnosis.3


PsA


is characterised by several degrees of synovitis, enthesitis, dactylitis and spondylitis that normally overlap and change over time.2


Nowadays it is


possible to diagnose and classify patients as having PsA without the need of current psoriasis, or with rheumatoid factor (RF) positivity, due to the generalisation of the ClASsification of Psoriatic ARthritis (CASPAR) criteria.4


PsA can lead to severe joint damage and disability that are comparable with those that occur in rheumatoid arthritis.2 By contrast, PsA and psoriasis share an increased mortality risk compared with the general population.5


This is mainly due to


not only a higher prevalence of classic cardiovascular risk factors, but also to an


"Psoriatic arthritis is characterised by several degrees of synovitis. enthesitis, dactylitis and spondylitis that normally overlap and change with time"


inflammatory cytokines, several of which signal through the Janus kinase (JAK) family of receptor-associated tyrosine kinases.7


Once activated, JAKs recruit and activate signal transducer and activator of transcription (STAT), which in turn drive gene transcription for several inflammatory mediators.7


By contrast,


cAMP levels are regulated by phosphodiesterases (PDEs), intracellular enzymes that convert cAMP to AMP. In immune cells, PDE4 is the predominantly active PDE. The conversion of cAMP to AMP leads to increased pro-inflammatory


cyclic adenosine monophosphate (cAMP), a naturally occurring secondary messenger, helps maintain homeostasis by modulating the network of pro- inflammatory and anti-inflammatory mediators.8


diagnosis of PsA as these criteria have been shown to be highly effective in distinguishing PsA from other inflammatory arthritides.4


However, early


recognition of PsA by dermatologists and GPs is still an unresolved matter. Comprehensive treatment of PsA involves assessment of each of the clinical domains of the disease, including peripheral and axial arthritis, enthesitis, dactylitis, psoriasis, nail disease and cardiovascular comorbidities. Clinicians treating PsA should evaluate the severity of disease in each of these domains and how these domains impact on physical function and quality of life, in order to assess the relative severity of the domain that in turn guides treatment choices.9 Comprehensive management of PsA


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accelerated atherogenesis linked to the inflammatory nature of both conditions.5


Aetiopathogenesis


PsA pathogenesis is characterised by a multigenetic aetiology, and by inflammatory mechanisms that may be triggered by environmental factors (infections, trauma, tobacco, obesity). Disease pathogenesis is also influenced by age at disease onset.6


PsA synovium and lesional skin are targets of interplay for many pro-


mediator production and decreased anti-inflammatory mediator production.8 These findings have allowed the development of new oral molecules in the treatment of psoriatic disease.


Principles governing the treatment of PsA


The diagnosis of PsA remains challenging, as the disease has a heterogeneous clinical phenotype in terms of joint involvement.2


The development of the CASPAR criteria has facilitated the


3


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