title: [New therapeutic targets in psoriatic arthritis].
abstract: 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.
authors.affiliation: Servicio de Reumatología, Hospital Clínico Universitario Salamanca, Salamanca, España. montillamorales.carlos@gmail.com
authors.forename: Carlos
authors.initials: C
authors.lastname: Montilla Morales
authors.forename: Susana
authors.initials: S
authors.lastname: Gómez-Castro
authors.forename: Mariola
authors.initials: M
authors.lastname: Sánchez
authors.forename: Ruth
authors.initials: R
authors.lastname: López
authors.forename: Cristina
authors.initials: C
authors.lastname: Hidalgo
authors.forename: Javier
authors.initials: J
authors.lastname: Del Pino-Montes
mesh_terms: D000631:Aminopyridines; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D018951:Antigens, CD20 / Q000187:drug effects; D018501:Antirheumatic Agents / Q000627:therapeutic use; D015535:Arthritis, Psoriatic / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D016723:Bone Remodeling / Q000187:drug effects; D017326:Clinical Trials, Phase III as Topic; D000242:Cyclic AMP / Q000502:physiology; D016207:Cytokines / Q000037:antagonists & inhibitors; D000069448:Denosumab; D018450:Disease Progression; D004351:Drug Resistance; D006801:Humans; D007249:Inflammation; D053590:Interleukin 1 Receptor Antagonist Protein / Q000627:therapeutic use; D007375:Interleukin-1; D053612:Janus Kinases / Q000037:antagonists & inhibitors; D008213:Lymphocyte Activation / Q000187:drug effects; D008212:Lymphocyte Depletion; D058990:Molecular Targeted Therapy; D009025:Morpholines; D010078:Oxazines / Q000627:therapeutic use; D058988:Phosphodiesterase 4 Inhibitors; D011725:Pyridines / Q000627:therapeutic use; D011743:Pyrimidines; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology; D013792:Thalidomide / Q000031:analogs & derivatives / Q000627:therapeutic use; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000631:Aminopyridines; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018951:Antigens, CD20; D018501:Antirheumatic Agents; D016207:Cytokines; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D009025:Morpholines; D010078:Oxazines; D058988:Phosphodiesterase 4 Inhibitors; D011725:Pyridines; D011743:Pyrimidines; D014409:Tumor Necrosis Factor-alpha; D000069448:Denosumab; D013792:Thalidomide; D000242:Cyclic AMP; D053612:Janus Kinases; C523665:fostamatinib; C505730:apremilast