Abstract

BackgroundPsoriatic arthritis (PsA) is a disease characterized by chronic pain and it is often associated with the presence of fibromyalgia (FMS) with an estimated prevalence of 18%. Several studies demonstrated the central role of neuropathic pain in FMS. However, patients with inflammatory diseases such as PsA frequently complain of complex pain symptoms, with neuropathic characteristics. Therefore, in PsA we can recognize both an inflammatory pain and a neuropathic pain that can be exacerbated both by the concomitant fibromyalgia or depending only on the PsA itself. In fact, In the context of PsA, the presence of neuropathic pain features has been documented in 28% of patients. This could be a reason why the low remission rate in these patients. Finally, Studies on murin models revealed a possible role of IL17, key cytokine of PsA pathogenesis, in mechanism of neuropathic pain.ObjectivesTo evaluate the role of anti-TNF and antiIL-17 in neuropathic pain in PsA patients treated with the first biological drug (bDMARDS).MethodsA cross-sectional evaluation was conducted on 38 PsA patients classified by Classification criteria for Psoriatic Arthritis (CASPAR), referred to the PsA outpatient clinic of “University of Campania Luigi Vanvitelli”. Thirty patients were treated with anti-TNF (mean age 53 years, 17F, 13M), 8 were treated with anti-IL17 (mean age 50 years, 5F, 3M), for almost 6 months. For each patient, an assessment of disease activity using DAPSA and physical function was carried out. The presence of comorbid fibromyalgia syndrome (FMS) was evaluated according to ACR 2016 criteria. We investigated neuropathic pain features through the PainDETECT Questionnaire (PDQ).ResultsNine patients treated with anti TNF were in DAPSA remission; 18 patients had low disease activity, 3 had High disease activity, FMS was detected in 11 of 30 patients, no one in DAPSA remission for PsA. Characteristics of neuropathic pain (PDQ ≥ 19) were found in 13 (43.3%) patients overall; unlikely neuropathic pain (PDQ < 12) in 16 (53.3%) patients. In the first group 7 patients had FMS, in the second group 3 had FMS. So, our analysis revealed the presence of neuropathic pain in 6 patients (54,5%) with PsA treated with antiTNF with no FMS; all of them were in low disease activity. The same analysis was conducted on anti IL17 treated population: 4 patients were in DAPSA remission, 2 patients in low disease activity, 2 patients in high, disease activity. FMS was diagnosed in 3 patients, 1 of them was in DAPSA remission for PsA. PDQ>19 was found only in 1 patient, who had FMS in comorbidity; the others had no neuropathic pain. So, we had no PsA patient treated with antiIL17, that manifested symptoms of neuropathic pain.ConclusionThe contribute of IL-17 in developing of neuropathic pain suggests the possible role of anti IL17 as therapy; our results support this tesis suggesting a possible role of anti IL17 in treatment of neuropathic pain. A limit to our work is given by the low sample size for which further studies are necessary to confirm this data.

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