ObjectiveWe performed a scoping review of the relevant literature on home‐based telehealth in rheumatology to understand its appropriate application in rheumatology practice.MethodsWe searched the Cochrane Library, PubMed, Web of Science, and scientific meeting abstracts to identify articles that specifically addressed telehealth suitability, barriers to telehealth, patient‐reported outcomes (PROs) collected in telehealth settings, and telehealth satisfaction. From the initial search of 4,882 studies, 23 reports were included. In addition, 10 abstracts were also eligible for analysis, resulting in a total of 33 articles: 2 randomized clinical trials, 9 prospective cohort studies, and 22 retrospective studies.ResultsWe found that triage appointments or predictive models could be helpful in selecting patients for telehealth and that telehealth interventions were appropriate for follow‐up of patients with systemic lupus erythematosus and inflammatory arthritis, but that conducting new patient visits over telehealth was not ideal. Barriers to telehealth include patient factors (age, technology access) and need for physician/process factors (eg, physical examinations). PROs collected in regular practice can be incorporated into telehealth. Several small, single‐center studies suggest that telehealth does not lead to negative outcomes compared with in‐person visits, and overall, patients report high patient satisfaction with telehealth. In several scenarios, home‐based telehealth was equivalent to in‐person visits with regard to patient outcomes and satisfaction.ConclusionThe widespread potential of telehealth to manage and deliver care for people with rheumatic disease is significant. As such, further research in the form of randomized controlled trials can help contribute to growing evidence that shapes telehealth implementation for patients with rheumatic diseases.

Rheumatoid arthritis (RA) is a chronic, progressive inflammatory disorder that manifests as a symmetric polyarthritis of small and large joints that may lead to joint and periarticular structural damage and the consequences of systemic inflammation. This overview of early RA examines the unmet needs and challenges in RA, how to best diagnose RA, and pitfalls in early diagnosis and treatment. The rules for referral to a rheumatologist are reviewed. Primary care physicians are at the front line of early diagnosis and need to start disease-modifying therapy as soon as a diagnosis of RA is established.

Rheumatoid arthritis (RA) is a chronic, progressive inflammatory disorder that manifests as a symmetric polyarthritis of small and large joints that may lead to joint and periarticular structural damage and the consequences of systemic inflammation. This overview of early RA examines the unmet needs and challenges in RA, how to best diagnose RA, and pitfalls in early diagnosis and treatment. The rules for referral to a rheumatologist are reviewed. Primary care physicians are at the front line of early diagnosis and need to start disease-modifying therapy as soon as a diagnosis of RA is established.

This chapter highlights polyarthritis. The co-occurrence of fever and arthritis educes a broad set of diagnostic considerations, especially infection. Yet, most forms of infectious arthritis typically involve one to three joints (monarthritis to oligoarthritis). The presence of a greater number of joints involved (polyarthritis) with fever evokes a more unusual and challenging range of diagnostic possibilities. Knowledge of prevalent forms of polyarthritis capable of fever can facilitate an early, accurate diagnosis and appropriate therapy. Polyarthritis is defined as inflammatory pain with swelling affecting four or more joints. The distribution, chronology of joint inflammation, and host factors help refine the diagnostic possibilities. The presence of fever is unique as most polyarticular conditions do not manifest substantial or sustained fever. Nevertheless, fever or pyrexia is further evidence of an inflammatory, infectious, or autoimmune disorder.

Background: In the phase 3 double-blind SELECT-CHOICE study of patients (pts) with prior inadequate response (IR) or intolerance to biologic disease-modifying antirheumatic drugs (bDMARDs), upadacitinib (UPA) showed superiority to abatacept (ABA) in change from baseline in 28-joint Disease Activity Score using C-reactive protein (DAS28[CRP]) and in the proportion of pts achieving DAS28(CRP) <2.6 at Week 12. Objectives: To describe clinical responses in pts receiving UPA or ABA by number and mechanism of action of prior bDMARDs. Methods: 612 pts were randomized to once-daily UPA 15 mg or monthly intravenous ABA (<60 kg, 500 mg; 60–100 kg, 750 mg; >100 kg, 1000 mg). All pts continued background therapy with stable conventional synthetic DMARDs. From Week 12, pts who did not achieve ≥20% improvement in both tender and swollen joint counts vs baseline at 2 consecutive visits had background medication(s) adjusted or added. In this post hoc analysis, pts were grouped by the number and/or type of bDMARD received prior to enrollment: 1) lack of efficacy (LoE) to ≥1 tumor necrosis factor (TNF) inhibitor; 2) LoE to ≥1 interleukin-6 (IL-6) inhibitor; 3) intolerance to prior bDMARDs; 4) number of prior bDMARDs (1, 2, or ≥3). Mean change from baseline in DAS28(CRP) and DAS28(CRP) <2.6 and other clinical endpoints were evaluated at Weeks 12/24. Results: Most pts had LoE to ≥1 TNF inhibitor (536, 87.6%); 96 (15.7%) had LoE to an IL-6 inhibitor; 79 (12.9%) had intolerance to prior bDMARDs; 408 (66.7%), 134 (21.9%), and 64 (10.5%) had received 1, 2, or ≥3 prior bDMARDs, respectively. Mean change from baseline in DAS28(CRP) was generally greater with UPA vs ABA across the different pt subgroups at Weeks 12/24 (Figure 1). Across endpoints, regardless of prior bDMARD therapy (except in those who failed ≥3 prior bDMARDs), UPA and ABA demonstrated similar responses at Week 12 compared with those observed for the overall treatment groups, even with more stringent criteria such as ACR70 and Clinical Disease Activity Index (CDAI) ≤2.8 (Table 1. below) Responses at Week 24 followed a similar trend to those at Week 12 for DAS28(CRP) <2.6 and other endpoints (Table 1). The safety profile across subgroups was consistent with each respective treatment in the overall study population (data not shown). Table 1. Efficacy endpoints by prior bDMARD subgroup (Week 12 [top] and Week 24 [bottom]) a ACR20 ACR50 ACR70 DAS28(CRP ) ≤3.2 DAS28(CRP) <2.6 CDAI ≤10 CDAI ≤2.8 HAQ-DI MCID b LoE to ≥1 TNF inhibitor UPA 15 mg n=263 75.3 77.9 44.9 59.7 22.8 38.8 49.0 61.2 30.4 46.8 40.7 58.6 9.1 22.8 75.5 74.3 ABA n=273 64.5 72.9 33.7 48.4 13.2 24.9 27.5 46.5 12.5 29.7 33.7 49.8 2.2 12.5 65.2 66.3 LoE to ≥1 IL-6 inhibitor UPA 15 mg n=48 70.8 85.4 37.5 66.7 20.8 29.2 45.8 66.7 25.0 41.7 41.7 58.3 6.3 16.7 78.3 78.3 ABA n=48 77.1 79.2 41.7 56.3 22.9 27.1 25.0 43.8 14.6 29.2 27.1 52.1 2.1 10.4 75.0 75.0 Intolerance to prior bDMARDs UPA 15 mg n=47 83.0 76.6 53.2 57.4 17.0 27.7 53.2 57.4 31.9 29.8 44.7 44.7 8.5 14.9 80.0 73.3 ABA n=32 62.5 71.9 28.1 50.0 0.0 31.3 21.9 56.3 6.3 31.3 21.9 56.3 3.1 9.4 61.3 67.7 1 prior bDMARD UPA 15 mg n=206 77.2 81.1 51.9 63.1 21.8 38.8 52.4 66.0 32.5 47.6 41.7 61.2 9.2 20.9 79.6 76.6 ABA n=202 67.3 77.7 35.1 53.5 15.8 33.7 29.2 51.5 12.4 35.6 36.1 55.9 3.0 16.3 66.7 71.7 2 prior bDMARDs UPA 15 mg n=64 78.1 76.6 34.4 56.3 23.4 39.1 51.6 62.5 26.6 50.0 45.3 54.7 4.7 23.4 73.8 70.5 ABA n=70 64.3 64.3 28.6 42.9 4.3 11.4 27.1 41.4 11.4 24.3 28.6 44.3 1.4 8.6 55.7 55.7 ≥3 prior bDMARDs UPA 15 mg n=29 55.2 65.5 24.1 44.8 17.2 24.1 27.6 41.4 20.7 27.6 27.6 48.3 10.3 17.2 58.6 72.4 ABA n=35 65.7 71.4 40.0 40.0 20.0 17.1 28.6 37.1 20.0 20.0 37.1 40.0 2.9 8.6 77.1 74.3 a Missing information was imputed using NRI. b HAQ-DI MCID=reduction from baseline of ≥0.22 ACR20/50/70, 20/50/70% improvement in ACR criteria; HAQ-DI, Health Assessment Questionnaire-Disability Index Conclusion: Although sample sizes were small for some subgroups, treatment with UPA led to greater clinical responses vs ABA at Week 12, including in pts with LoE to TNF or IL-6 inhibitors, and those with IR or intolerance to 1, 2, or ≥3 prior bDMARDs. Acknowledgements: AbbVie funded this study; contributed to its design; participated in data collection, analysis, and interpretation of the data; and participated in the writing, review, and approval of the abstract. No honoraria or payments were made for authorship. Medical writing support was provided by Grant Kirkpatrick, MSc of 2 the Nth (Cheshire, UK), and was funded by AbbVie. Disclosure of Interests: Andrea Rubbert-Roth Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Chugai, Eli Lilly, Gilead, Janssen, Novartis, Roche, and Sanofi, Ricardo Xavier Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Eli Lilly, Janssen, Novartis, Pfizer, and UCB, Boulos Haraoui Consultant of: AbbVie, Amgen, Eli Lilly, Gilead, MSD, Pfizer, Sandoz, and UCB, Herbert S.B. Baraf Consultant of: Gilead, Janssen, and UCB, Grant/research support from: AbbVie, Eli Lilly, Genentech, Gilead, and Janssen, Maureen Rischmueller Consultant of: AbbVie, Bristol-Myers Squibb, CSL Behring, Eli Lilly, Gilead, Janssen, Pfizer, Sanofi, and UCB, Grant/research support from: AbbVie, Amgen, Bristol-Myers Squibb, Eli Lilly, Janssen, Novartis, Pfizer, Sanofi, and UCB, Naomi Martin Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, Yanna Song Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, Jessica Suboticki Shareholder of: May own stock or options in AbbVie, Employee of: AbbVie, John Cush Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, and Novartis.

OBJECTIVES:This study aims to assess rheumatologists' perceptions, utilization patterns, and attitudes towards the modified New York (mNY) criteria for ankylosing spondylitis (AS) and Assessment of SpondyloArthritis International Society (ASAS) criteria for axial spondyloarthritis (axSpA). METHODS:Members of the national rheumatology societies in five countries (United States of America (USA), Canada, India, Turkey, and Brazil) were invited to participate in a survey containing questions regarding rheumatologists' familiarity, and use of AS and axSpA classification criteria in daily practice, perceived specificity of spondyloarthritis features in making the diagnosis, patterns of imaging tests performed in daily practice, and their opinion about the need for modification of current classification criteria. The responses were analyzed by gender, age, years in practice, as well as by country of practice. Descriptive statistics, t test, and chi-square test were used for comparison of groups. RESULTS:Approximately 6% rheumatologists (478 out of 8021 professional association members) from five countries completed the survey. The country-specific response rates were Brazil 4%, USA 4.3%, India 11%, Canada 14%, and Turkey 29%, though the overall contributions from individual countries were USA 47%, India 14.9%, Brazil 13.8%, Turkey 12.8%, and Canada 8.8%. The mean age of respondents was 50 years (± 11.8), 31% were females and 90% spent majority (> 75%) of their time in clinical practice. The mNY and ASAS criteria were regularly used in clinical practice by 44 and 66% of responders, respectively. Those reporting "always" using ASAS criteria were more likely to be women (p = 0.006), and within 5 years of completing rheumatology training. Vast majority (74%) regarded Inflammatory Back Pain (IBP) as a specific feature for axSpA. Majority (50 and 60%, respectively) regarded uveitis and dactylitis as "very specific" features helping them make the diagnosis of axSpA, whereas heel enthesitis, peripheral inflammatory arthritis, and response to NSAIDs were considered "somewhat specific" by 50% of the responders. Less than half (47%) of the responders used the mNY grading for X-ray of SI joints. In the case of normal X-ray of SI joint, the use of MRI was more frequent than CT scan (83.6 vs. 10.9%) in assessing for sacroiliitis. If sacroiliitis was not seen on X-rays, the likelihood of ordering MRI was significantly higher among rheumatologists completing training within < 15 years versus > 25 years prior (90 vs. 75%, p = 0.007). Overall, 70% thought that ASAS criteria were adequately specific for clinical trials. However, 42% respondents still felt a need to modify ASAS classification criteria for axSpA. Also, 46% respondents felt that mNY criteria should be modified. CONCLUSIONS:In the absence of diagnostic criteria, majority of rheumatologists are using the classification criteria for diagnosis of axSpA. Though axSpA classification criteria are perceived to be specific for clinical trials, 40% rheumatologists feel the need to modify these criteria. Key Points • This study informs how rheumatologists in five countries spread over four different continents diagnose axSpA in clinical practice. • Since majority rheumatologists among survey respondents across the countries use ASAS criteria for diagnosis of axSpA, more specific criteria may be required to avoid overdiagnosis. • MRI is commonly used to rule out sacroiliitis in case of normal X-ray of sacroiliac joints.

Background: Patients (pts) with rheumatoid arthritis (RA) are at an increased risk for the development of venous thromboembolism (VTE, including pulmonary embolism [PE] and deep vein thrombosis [DVT]) vs the general population (~2-fold increase). 1 Beyond RA, additional risk factors have been described, with prior history of VTE and obesity posing particular risk. VTE events have been observed in pts receiving JAK inhibitors, including upadacitinib (UPA). Objectives: To describe the incidence of VTE in pts with RA receiving UPA relative to active comparators in the phase 3 clinical trial program and to evaluate potential risk factors. Methods: Adjudicated events of treatment-emergent VTE were determined in pts receiving UPA in an integrated analysis (data cut-off, 30 Jun 2019) of five randomized phase 3 trials (SELECT-EARLY, SELECT-MONOTHERAPY, SELECT-NEXT, SELECT-COMPARE, and SELECT-BEYOND), of which 4 evaluated both the UPA 15 mg and 30 mg QD doses and 1 (SELECT-COMPARE) evaluated only UPA 15. Incidence of VTE was also determined in pts receiving adalimumab (ADA) + methotrexate (MTX) in SELECT-COMPARE and MTX monotherapy in SELECT-EARLY. Events are attributed to treatment received at time of event and are summarized per events/100 patient yrs. VTE risk factors were assessed using univariate Cox regression models. Results: A total of 35 VTE events were observed across treatment groups. The exposure-adjusted treatment-emergent event rates (E/100 PYs, 95% CI) of VTE were 0.5 (0.3, 0.7) for UPA 15, 0.3 (0.1, 0.7) for UPA 30, 0.5 (0.1, 1.3) for ADA + MTX, and 0.4 (0.1, 1.6) for MTX, with no pattern to event onset across treatments. Events of PE, DVT, or both PE and DVT were reported across treatment groups ( Table ). Pts who experienced VTE, across all treatment groups, on average, were older than pts who did not (62/59/58/61 yrs vs 54/55/54/53 yrs for UPA 15, UPA 30, ADA + MTX, and MTX, respectively). The mean body mass index (BMI) of pts with VTE tended to be higher (34–40 for pts with VTE vs 28-29 kg/m 2 for those without). Across UPA treatment groups, 135/2629 (UPA 15) and 62/1204 (UPA 30) pts had a prior history of VTE; of these pts, 5 (3.7%) and 2 (3.2%) experienced VTE on UPA 15 and UPA 30, respectively. Univariate Cox regression models identified BMI and prior history of VTE as factors associated with VTE in the UPA 15 and 30 mg groups ( Figure ). Age and NSAID use were shown to be associated with VTE risk among pts in the UPA 15 but not 30 mg group. Table. Events of VTE Observed Across Treatment Groups UPA 15 mg QD a N=2629 (4565.8 PYs) UPA 30 mg QD b N=1204 (2309.7 PYs) ADA + MTX c N=579 (768.6 PYs) MTX Monotherapy d N=314 (456.0 PYs) Events, n 21 8 4 2 Patients, n 20 7 4 2 PE only 11 1 3 1 DVT only 5 2 1 0 PE + DVT 4 4 0 1 a From SELECT-EARLY, -MONOTHERAPY, -NEXT, -COMPARE, and -BEYOND. b From SELECT-EARLY, -MONOTHERAPY, -NEXT, and -BEYOND. c From SELECT-COMPARE. d From SELECT-EARLY. VTE, venous thromboembolism; PE, pulmonary embolism; DVT, deep vein thrombosis. Conclusion: VTE event rates appeared balanced across UPA doses and active comparator groups in pts with RA. Risk factors for VTE events identified through univariate analyses in pts who received UPA included prior history of VTE and BMI, two factors previously known to be associated with VTE risk. One limitation is the small sample size, limiting the analysis to univariate. Continued follow-up of pts receiving UPA is ongoing to further contextualize the risk of VTE in the clinical trial program. References: [1]Kim SC, et al. Arthritis Care Res 2013;65:1600-7. Disclosure of Interests: Ernest Choy Grant/research support from: Amgen, Bio-Cancer, Chugai Pharma, Ferring Pharmaceuticals, Novimmune, Pfizer, Roche, UCB, Consultant of: AbbVie, Amgen, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Chelsea Therapeutics, Chugai Pharma, Daiichi Sankyo, Eli Lilly, Ferring Pharmaceuticals, GlaxoSmithKline, Hospita, Ionis, Janssen, Jazz Pharmaceuticals, MedImmune, Merck Sharp & Dohme, Merrimack Pharmaceutical, Napp, Novartis, Novimmune, ObsEva, Pfizer, R-Pharm, Regeneron Pharmaceuticals, Inc., Roche, SynAct Pharma, Sanofi Genzyme, Tonix, UCB, Speakers bureau: Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Chugai Pharma, Eli Lilly, Hospira, Merck Sharp & Dohme, Novartis, Pfizer, Regeneron Pharmaceuticals, Inc., Roche, Sanofi-Aventis, UCB, Iain McInnes Grant/research support from: Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Janssen, and UCB, Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Gilead, Janssen, Novartis, Pfizer, and UCB, John Cush Grant/research support from: AbbVie, Astra Zeneca, Aurinia, Bristol-Myers Squibb, Genentech, Novartis, Pfizer, Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Boehringer-Ingelheim, Genentech, Gilead, Eli Lilly, Novartis and UCB, Jacob Aelion Grant/research support from: AbbVie, Ardea Biosciences, AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Galapagos, GlaxoSmithKline, Janssen, Eli Lilly, Merck, Mesoblast, Novartis, Novo Nordisk, Pfizer, Roche, Sanofi-Aventis, Takeda, and UCB Pharma, Consultant of: AbbVie, Boehringer Ingelheim, Celgene, and Eli Lilly, William Rigby Grant/research support from: Bristol-Myers Squibb, Consultant of: AbbVie, Bristol-Myers Squibb, Genentech, Pfizer, Yanna Song Shareholder of: AbbVie Inc., Employee of: AbbVie Inc., Sebastian Meerwein Shareholder of: AbbVie Inc., Employee of: AbbVie Inc., Jianzhong Liu Shareholder of: AbbVie Inc., Employee of: AbbVie Inc., Nasser Khan Shareholder of: AbbVie Inc., Employee of: AbbVie Inc., Jessica Suboticki Shareholder of: AbbVie Inc., Employee of: AbbVie Inc., Alexander Cohen Consultant of: AbbVie, Apalgon, Aspen, BMS, Pfizer, Bayer, Daiichi Sankyo, Boehringer Ingelheim, Boston Scientific, Janssen, Portola

Objectives. 3-hydroxy-3-methylglutaryl coenzyme-A (HMG Co-A) reductase inhibitors (statins) are standard treatment for hyperlipidaemia. In addition to lipid-lowering abilities, statins exhibit multiple anti-inflammatory effects. The objectives of this study were to determine whether treatment of patients with RA with lovastatin decreased CRP or reduced disease activity. Methods. We conducted a randomized double-blind placebo-controlled 12 week trial of lovastatin vs placebo in 64 RA patients with mild clinical disease activity but an elevated CRP. The primary efficacy end point was the reduction in mean log CRP. Secondary end points included disease activity, RF and anti-CCP antibody titres. Mechanistic end points included levels of serum cytokines. Safety was assessed; hepatic and muscle toxicities were of particular interest. Results. Baseline features were similar between groups. No significant difference in mean log CRP reduction between the two groups was observed, and disease activity did not change from baseline in either treatment group. Mechanistic analyses did not reveal significant changes in any biomarkers. A post hoc analysis of subjects not using biologic therapy demonstrated a significantly greater proportion achieving 20% reduction in CRP from baseline in the lovastatin group compared with placebo (P-value = 0.007). No difference was observed in subjects receiving biologics. Lovastatin was well tolerated with no serious safety concerns. Conclusion. This study showed no anti-inflammatory or clinical effects on RA disease activity after 12 weeks of treatment with lovastatin. Lovastatin had a modest effect on CRP in subjects not using biologics, suggesting statins may be anti-inflammatory in selected patients.

Objective. The Pregnancy and Lactation Autoimmune Network (PLAN) registry was established to evaluate the concerns of women with autoimmune or inflammatory rheumatic diseases (AIRD) pertaining to pregnancy and lactation. Methods. The registry was started as a survey of patients with AIRD at a single rheumatology specialty center in November 2016 and included questions regarding fertility, pregnancy, miscarriages, and lactation before and after diagnosis. Results. The study included 154 subjects from the PLAN registry. More than half (52%) of respondents indicated that their diagnosis negatively changed their views on pregnancy and nearly a third (30%) decided not to have children after AIRD diagnosis. Most (66%) women were concerned that medication use during the childbearing process would affect the baby. One-third (34%) indicated their views on breastfeeding negatively changed as a result of their disease diagnosis. The rates and duration of breastfeeding did not differ significantly for babies born before or after the mothers’ diagnosis (p = 0.50 and p = 0.21, respectively). Eighteen women in our study avoided breastfeeding or stopped breastfeeding earlier than planned to start a medication (including etanercept, adalimumab, hydroxychloroquine, and certolizumab) they believed to be contraindicated during lactation. The PLAN registry included 19 women who breastfed 22 babies while being exposed to a disease-modifying antirheumatic drug or biologic. None of these 19 women reported a delay in their children’s developmental milestones or higher infection rates. Conclusion. This study highlights an unmet need in patients with AIRD of childbearing potential for data and education regarding pregnancy and lactation.

Background Upadacitinib (UPA), a JAK1-selective inhibitor, demonstrated efficacy in the SELECT-BEYOND study in patients (pts) with moderate to severe rheumatoid arthritis (RA) on a stable dose of csDMARDs who had inadequate response (IR) or intolerance to bDMARDs,. Objectives In this analysis we evaluated clinical responses among pts receiving UPA and placebo (PBO) based on the number and mechanism of action (MOA) of prior bDMARDs. Methods 498 pts were randomized to UPA 15mg or UPA 30mg once daily (QD) or PBO for 12 weeks (wks), after which pts on PBO received UPA 15 or 30mg QD from Wk 12 onwards.1 Pts were subgrouped by the number and/or MOA of bDMARD(s) received prior to enrollment: 1) lack of efficacy (LoE) to ≥1 anti-TNF, 2) LoE to an anti-IL-6, and 3) the number of prior bDMARDs (1 vs 2 vs ≥3). ACR20/50/70 responses, DAS28-CRP low disease activity (LDA, ≤3.2), CDAI LDA (≤10), and CDAI remission (≤2.8) were evaluated at Wk 12. The frequency and percentage of treatment-emergent adverse events (TEAE) in each subgroup was assessed over the first 12 wks. Missing values of the efficacy endpoints were imputed using non-responder imputation (NRI). Nominal P-values are reported without multiplicity adjustment. Results Overall baseline disease duration was ∼13 years. The majority of pts had LoE to ≥1 anti-TNF (449, 90%); 88 (18%) had LoE to an anti-IL-6; 235 (47%), 137(28%), and 125 (25%) had been treated with 1, 2, or ≥3 prior bDMARDs, respectively.1 At Wk 12, clinical responses were numerically, and often statistically, better for pts receiving either dose of UPA vs PBO, irrespective of their prior bDMARD exposure and the number of prior bDMARDs received. As most pts had LoE to ≥1 anti-TNF, responses in this group were comparable to the overall study population (Table 1). Pts with LoE to an anti-IL-6 receiving UPA 15 or 30 mg QD experienced improvements vs PBO, particularly in achieving LDA and remission, although responses in these pts were generally lower compared to the overall study population. As expected, there was a trend towards lower responses as the number of prior bDMARDs increased (Table 2). Responses at Wk 24 were generally consistent with those at Wk 12 (data not shown). TEAEs across the subgroups were consistent with the overall study population (data not shown). Conclusion At Wk 12, treatment with UPA at either 15 or 30 mg QD led to significantly better clinical responses vs PBO in this treatment-refractory population, including in pts with LoE to an anti-TNF or an anti-IL-6, and those who had IR/intolerance to 1, 2 or ≥3 prior bDMARDs, with consistent safety profiles as to the overall study population. Acknowledgement AbbVie, Inc was the study sponsor, contributed to study design, data collection, analysis & interpretation, and to writing, reviewing, and approval of final version. Medical writing support was provided by Naina Barretto, PhD, of AbbVie, Inc. Disclosure of Interests Michael Weinblatt Shareholder of: Lycera, Scipher, Vorso, Inmedix, Grant/research support from: Amgen, BMS, Crescendo Bioscience, Sanofi/Regeneron, Consultant for: AbbVie, Amgen, Crescendo Bioscience, Gilead, GSK, Lycera, Merck, Novartis, Pfizer, Roche, Samsung, SetPoint, BMS, Corrona, Eli Lilly and Company, Glen Thomson Grant/research support from: AbbVie, Consultant for: Amgen, Kun Chen Shareholder of: Abbvie, Employee of: Abbvie, Sebastian Meerwein Shareholder of: AbbVie, Employee of: AbbVie Deutschland GmbH & Co. KG, Casey Schlacher Shareholder of: AbbVie, Employee of: AbbVie, John Cush Consultant for: AbbVie, Celgene, Novartis, AstraZeneca and Genentech; AbbVie, UCB, Novartis, BMS, Amgen, Genentech, Celgene, Lilly, and Horizon

Objective. Anti-tumor necrosis factor (anti-TNF) medications are effective in controlling chronic inflammatory diseases, but information about their use and safety in pregnancy is limited. Consequently, anti-TNF agents are often discontinued early in gestation. Certolizumab pegol (CZP), a PEGylated, Fc-free anti-TNF agent approved for the treatment of rheumatic diseases and/or Crohn's disease, has minimal to no active placental transfer. This analysis was undertaken to evaluate pregnancy outcomes in women receiving CZP, especially those exposed during early pregnancy. Methods. Prospective and retrospective data on maternal CZP exposure were extracted from the UCB Pharma safety database through March 6, 2017. Analysis was limited to prospective reports to avoid potential bias associated with retrospective submissions. The numbers of live births, miscarriages, elective abortions, stillbirths, and major congenital malformations were ascertained. Results. Of 1,137 prospectively reported pregnancies with maternal exposure to CZP, 528 (including 10 twin pregnancies) had 538 known outcomes: 459 live births (85.3%), 47 miscarriages (8.7%), 27 elective abortions (5.0%), and 5 stillbirths (0.9%). There were 8 major congenital malformations (1.7%) among the 459 infants. First trimester exposure occurred in 367 (81.2%) of 452 pregnancies resulting in 459 live births. Exposure during all 3 trimesters occurred in 201 (44.5%) of 452 pregnancies. Conclusion. This analysis represents the largest cohort of pregnant women exposed to an anti-TNF agent for management of chronic inflammatory diseases. Analysis of pregnancy outcomes does not indicate a teratogenic effect of CZP, compared to the general population, nor an increased risk of fetal death. The data are reassuring for women of childbearing age considering treatment with CZP.

Megan E. B. Clowse MD, Angela E. Scheuerle MD, Christina Chambers MD, PhD, MPH, Anita Afzali MD, MPH, FACG, Alexa B. Kimball MD, MPH, John J. Cush MD, Maureen Cooney PhD, MPH, Laura Shaughnessy PhD, Mark Vanderkelen MD, Frauke Förger MD Duke University Medical Center, Durham, NC, USA; University of Texas Southwestern Medical Center, Dallas, TX, USA; University of California, La Jolla, CA, USA; The Ohio State University Wexner Medical Center, Columbus, OH, USA; Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA; Baylor Scott & White Research Institute, Dallas, TX, USA; UCB Pharma, Raleigh, NC, USA; UCB Pharma, Braine-l’Alleud, Belgium; Inselspital, University of Bern, Bern, Switzerland