Registries estimate that one third of patients with psoriatic arthritis (PsA) 
are "resistant" to of TNF-alpha blockers. Therefore, the search for new 
approaches to treatment of this disease may be justified. Currently the 
treatment options that have proven effective are associated with inhibition of 
the T cell costimulatory pathway (abatacept and alefacept) and blocking the P40 
fraction of IL-12 and IL-23 (ustekinumab). A novel pathway inhibition, which 
deserves special attention is offered by apremilast. This molecule inhibits 
phosphodiesterase IV, responsible for hydrolyzing cyclic adenosine monophosphate 
to adenosine monophosphate, which causes an increase in cAMP. This metabolite is 
associated with decreased TNF-alpha. It has a modest efficacy (ACR 20 response 
of 43%), and subsequent studies have shown an improvement in visual analog scale 
and the SF36 compared to placebo. Currently there are five clinical trials in 
phase III to assess its effectiveness in parameters of inflammation and 
radiographic progression. The spectrum of possibilities before treatment failure 
with anti-TNF alpha, is augmented by the appearance of several reports that show 
efficacy with the individual use of CD20 inhibitors and IL-1. In patients with 
rheumatoid arthritis (RA) the effectiveness of molecules that inhibit signal 
transduction of cytokines (Anti-JAK) has been proven, so it is possible that in 
the future they may be used in patients with PsA.