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Background Patients diagnosed with rheumatoid arthritis (RA) before pregnancy may experience a postpartum flare. This event may occur independently of the patient treatment, according to recent guidelines.1 Objectives The aim of this study was to identify possible risk factors of postpartum RA flares. Methods We analysed pregnant RA patients treated with b DMARDs pre-conception/during pregnancy which delivered children. Data analysis was performed in a combined maner : prospectively and retrospectively. Data collection was focused on 5 distinct periods of time: pre-conception, 1 st, 2nd, 3rd pregnancy trimesters, postpartum period before 12 weeks and after 12 weeks. Following parameters were analysed: demographic data (type of pregnancy- planned/unplanned), immunology (RF and ACPA positivity), disease activity score DAS-CRP,2 type of medication and duration. Subfertility status and postpartum flares were registered. The retrospective analysis was represented by interview collected data. Flare was defined as early ( 12 weeks) Results Among 96 pregnant patients, 54 (56%) patients delivered 57 children. Out of 54 patients, 17 (31.5%) were analysed prospectively and 37, 68.5% retrospectively. The patients were exposed to 3 types of b DMARDs: TNF blockers,9 Rituximab5 and Tocilizumab.1Rituximab was stopped before pregnancy in 4 out of 5 patients (1 continued therapy during the 1 st trimester- unplanned pregnancy) and all presented a postpartum flare. Out of 9 patients with TNF blocker therapy, 2 of them stopped the drug before pregnancy and the other 7 used the medication until pregnancy test positivity or until the end of the 2nd trimester. In this group, 6 of 9 patients presented a postpartum flare. One patient was treated with Tocilizumab before pregnancy and experienced an early flare. table 1 presents the analysis of a set of collected parameters. Overall, the majority of the patients (77.8%) experienced a postpartum flare. An early postpartum flare was identified in 53.7% and late one in 24.1%, with a mean value of 11.59±9.45 weeks. The prospective group experienced more frequently an early flare in comparison to group 2 (0.244 (95% CI 0.62–0.965) but without statistic significance. A positive correlation was found between active disease during the 2nd and 3rd trimester and postpartum early flare occurrence (p=0.044). No correlation was found between postpartum flare, fertility status or therapy type and duration. Conclusions RA pregnant patients treated with b DMARDs experience a postpartum flare in the majority of the cases. Persistent active disease during the second and third trimester was identified as a risk factor for postpartum disease flare. Larger prospective studies are neede in order to make a better analysis of all evaluated parameters. References [1] Julia flint et all. BSR and BHPR guideline on prescribing drugs in pregnancy and breastfeeding. Rheumatology2016;55(9). [2] Yael A de Man, Johanna MW Hazes, Fleur E van de Geijn, Catharina Krommenhoek, Radboud JEM Dolhain. Measuring disease activity and functionality during pregnancy in patients with rheumatoid arthritis. Arthritis & Rheumatism57:716–722. doi:10.1002/art.22773 Disclosure of Interest None declared

Background Defined as de novo or exacerbation of pathologies that usually responds to biologic agents, paradoxical reactions encompass for a wide spectrum of manifestations (cutaneous, intestinal, ocular) reported during biological therapy (TNF and non-TNF medications) regardless of the underlying rheumatic or non-rheumatic disorder. Objectives To assess drug levels (DL) and anti-drug antibodies (ADA) in patients with paradoxical reactions (de novo or exacerbation of psoriasis, uveitis, Crohn’s disease) induced by biological drugs (bDMARS) in Rheumatoid Arthritis (RA), Ankylosing Spondylitis (AS) and Psoriatic Arthritis (PsA). Methods We performed a retrospective observational study in cohorts of consecutive RA (267), PSA (65) and AS (145) undergoing TNF (i-TNF) or non-TNF biologics according to the local recommendations for initiation and monitoring, attending a single academic rheumatology department. All patients were assessed at every 24 weeks months for disease activity and outcomes; supplementary, drug immunogenicity (ADA and DL) was systematically evaluated in patients developing paradoxical adverse events. DL and ADA were measured with an ELISA assay and antibody binding test, respectively. Serum drug levels were considered positive for infliximab if >0.035 µg/mL, for adalimumab >0.024 µg/mL, for etanercept >0.035 µg/mL, rituximab >0.75 µg/mL, while the cut-offs for ADA positivity to infliximab was established at 5AU/ml, for adalimumab at 10AU/mL, etanercept at 142 AU/mL, rituximab 140 AU/mL (ELISA, Progenika) Results 42 patients with paradoxical psoriasis (30 with de novo lesions, 18 with palmo-plantar pustulosis, 12 with exacerbation of pre-existent lesions), 12 with paradoxical uveitis (5 with a new onset uveitis) and 3 with paradoxical Crohn’s were included in the final analysis. Paradoxical events related to abatacept, certolizumab (one de novo psoriasis per agent) or golimumab (2 new onset uveitis, one flare of Chron’s disease) were excluded from the final analysis as no immunogenicity lab tests were provided. Drug induced paradoxical events were described not only with all TNF inhibitors but also with rituximab. DL was in normal range in all these patients; in addition, ADA were either negative, or, if present, had no impact on drug concentration. Furthermore, we found no significant differences in drug levels of TNF inhibitors for RA, PsA and AS. Moreover, no statistical significant differences were observed in the detection of ADA between the three groups. Conclusions Patients who develop either true or borderline paradoxical AE have adequate drug levels, with normal ADA concentrations. Disclosure of Interest None declared