Assessment of Jordanian physicians' knowledge about venous thromboembolism risk and management among COVID-19 patients

Objectives: The aim of this study was to assess Jordanian physicians' awareness about venous thromboembolism (VTE) risk among COVID-19 patients and its treatment protocol. Method(s): This was a cross-sectional-based survey that was conducted in Jordan in 2020. During the study period, a convenience sample of physicians working in various Jordanian hospitals were invited to participate in this study. Physicians' knowledge was evaluated and physicians gained one point for each correct answer. Then, a knowledge score out of 23 was calculated for each. Key Findings: In this study, 102 physicians were recruited. Results from this study showed that most of the physicians realize that all COVID-19 patients need VTE risk assessment (n = 69, 67.6%). Regarding VTE prophylaxis, the majority of physicians (n = 91, 89.2%) agreed that low molecular weight heparin (LMWH) is the best prophylactic option for mild-moderate COVID-19 patients with high VTE risk. Regarding severe/critically ill COVID-19 patients, 75.5% of physicians (n = 77) recognized that LMWH is the correct prophylactic option in this case, while 80.4% of them (n = 82) knew that mechanical prevention is the preferred prophylactic option for severe/critically ill COVID-19 patients with high bleeding risk. Moreover, 77.5% of physicians (n = 79) knew that LMWH is the treatment of choice for COVID-19 patients diagnosed with VTE. Finally, linear regression analysis showed that consultants had an overall higher knowledge score about VTE prevention and treatment in COVID-19 patients compared with residents (P = 0.009). Conclusion(s): All physicians knew about VTE risk factors for COVID-19 patients. However, consultants showed better awareness of VTE prophylaxis and treatment compared with residents. We recommend educational workshops be conducted to enhance physicians' knowledge and awareness about VTE thromboprophylaxis and management in COVID-19 patients.Copyright © 2022 The Author(s). Published by Oxford University Press on behalf of the Royal Pharmaceutical Society. All rights reserved.

Pathophysiology of thromboembolism in patients with COVID-19

Introduction and aim. A small number of critically ill patients with coronavirus disease (COVID-19) develop thromboembolism (arterial or venous), both micro- and macrovascular complications such as deep vein thrombosis, pulmonary embolism, and pulmonary arterial thrombosis. The objective of the study is to describe the pathophysiology of venous thromboembolism in patients with COVID-19. Material and methods. In this article a narrative review regarding pathophysiology of thromboembolism in patients with COVID-19. Analysis of the literature. The development of coagulopathy is a consequence of the intense inflammatory response associated with hypercoagulability, platelet activation, and endothelial dysfunction. The pathophysiology that relates pulmonary thromboembolism (PTE) with COVID-19 is associated with a hypercoagulable state. PTE is suspected in hospitalized patients presenting dyspnea, decreased oxygen requirement, hemodynamic instability, and dissociation between hemodynamic and respiratory changes. In COVID-19-associated coagulopathy, initially, patients present with elevated levels of fibrinogen and D-dimer, with minimal changes in prothrombin time and platelet count. The main risk factor for the development of pulmonary embolism is the increase in D-dimer that is associated with the development of PTE. The administration of iodine-based contrast agent to patients with COVID-19 would affect P-creatinine and renal function, where Ultrasound is viewed as cost-effective and highly portable, can be performed at the bedside. Conclusion. Acute respiratory distress syndrome severity in patients with COVID-19 can explain PTE as a consequence of an exaggerated immune response. © 2022 Publishing Office of the University of Rzeszow. All Rights Reserved.

PLACEBO-CONTROLLED EFFICACY AND SAFETY OF UPADACITINIB THROUGH ONE YEAR IN PATIENTS WITH NON-RADIOGRAPHIC AXIAL SPONDYLOARTHRITIS

BackgroundUpadacitinib (UPA), a Janus kinase inhibitor, was effective and well tolerated in patients (pts) with non-radiographic axial spondyloarthritis (nr-axSpA) through 14 weeks (wks) of treatment.[1]ObjectivesThis analysis assessed the efficacy and safety of UPA vs placebo (PBO) through 1 year.MethodsThe SELECT-AXIS 2 nr-axSpA study included a 52-wk randomized, double-blind, PBO-controlled period. Enrolled adults had a clinical diagnosis of active nr-axSpA fulfilling the 2009 ASAS classification criteria, objective signs of inflammation based on MRI sacroiliitis and/or elevated C-reactive protein, and an inadequate response to NSAIDs. One-third of pts had an inadequate response to biologic DMARDs. Pts were randomized 1:1 to UPA 15 mg once daily or PBO. Concomitant medications, including NSAIDs, had to be kept stable through wk 52. The study protocol outlined that pts who did not achieve ASAS20 at any two consecutive study visits between wks 24 to 52 should receive rescue therapy with NSAIDs, corticosteroids, conventional synthetic/biologic DMARDs, or analgesics. Cochran-Mantel-Haenszel (CMH) test with non-responder imputation incorporating multiple imputation (NRI-MI) was used to handle missing data and intercurrent events for binary efficacy endpoints. Mixed-effect model repeated measures (MMRM) was used to assess continuous efficacy endpoints. NRI was used for binary endpoints after rescue and as observed analysis excluding data after rescue for continuous endpoints. Treatment-emergent adverse events (TEAEs) are reported through wk 52.ResultsOf the 314 pts randomized, 259 (82%;UPA, n=130;PBO, n=129) completed wk 52 on study drug. More pts achieved an ASAS40 response with UPA vs PBO from wks 14 to 52 with a 20% treatment difference at wk 52 (63% vs 43%;nominal P <.001;Figure 1). The proportion of pts achieving ASDAS inactive disease with UPA remained higher than PBO at wk 52 (33% vs 11%;nominal P <.0001;Figure 1). Consistent improvements and maintenance of efficacy were also seen across other disease activity measures. Between wks 24 and 52, fewer pts on UPA (9%) than PBO (17%) received rescue therapy. A similar proportion of pts in each treatment group had a TEAE (Table 1). Infections were the most common TEAE;the rates of serious infections and herpes zoster were higher with UPA vs PBO, although no new serious infections were reported from wks 14 to 52. COVID-19 events were balanced between treatment groups. No opportunistic infections, malignancy excluding non-melanoma skin cancer, adjudicated major adverse cardiovascular events, inflammatory bowel disease, or deaths were reported. Two pts (1.3%) on PBO had adjudicated venous thromboembolic events.ConclusionUPA showed consistent improvement and maintenance of efficacy vs PBO through 1 year across multiple disease activity measures. No new safety risks were identified with longer-term UPA exposure. These results continue to support the benefit of UPA in pts with active nr-axSpA.Reference[1]Deodhar A, et al. Lancet. 2022;400(10349):369–379.Table 1.Safety through week 52Event, n (%)PBO (n = 157)UPA 15 mg QD (n = 156)Any AE103 (66%)107 (69%)Serious AE6 (3.8%)6 (3.8%)AE leading to D/C4 (2.5%)6 (3.8%)COVID-19-related AE22 (14%)24 (15%)Deaths00Infection60 (38%)68 (44%) Serious infection1 (0.6%)2 (1.3%) Herpes zoster1 (0.6%)5 (3.2%)Malignancy other than NMSC00NMSC1 (0.6%)0Hepatic disorder7 (4.5%)6 (3.8%)Neutropenia1 (0.6%)8 (5.1%)MACE (adjudicated)00VTE (adjudicated)2 (1.3%)a0Uveitisb3 (1.9%)2 (1.3%)Inflammatory bowel disease00aBoth patients had non-serious events of deep vein thrombosis in the lower limb with risk factors including obesity and prior deep vein thrombosis in one patient and concomitant COVID-19 infection in the other patient.bThree events of uveitis occurred in each treatment group (among n = 3 patients in the PBO group and n = 2 patients in the UPA group);two events in the PBO group and one in the UPA group occurred in patients with a history of uveitis.AcknowledgementsAbbVie funded this study and participated in the study design, res arch, analysis, data collection, interpretation of data, review, and approval of the . All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. Medical writing support was provided by Julia Zolotarjova, MSc, MWC, of AbbVie.Disclosure of InterestsFilip van den Bosch Speakers bureau: AbbVie, Amgen, Galapagos, Janssen, Lilly, Merck, MoonLake, Novartis, Pfizer, and UCB., Consultant of: AbbVie, Amgen, Galapagos, Janssen, Lilly, Merck, MoonLake, Novartis, Pfizer, and UCB., Atul Deodhar Consultant of: AbbVie, Amgen, Aurinia, BMS, Celgene, GSK, Janssen, Lilly, MoonLake, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Bristol Myers Squibb, Celgene, GSK, Lilly, Novartis, Pfizer, and UCB, Denis Poddubnyy Speakers bureau: AbbVie, Biocad, BMS, Galapagos, Gilead, GlaxoSmithKline, Janssen, Lilly, MSD, Medscape, MoonLake, Novartis, Peervoice, Pfizer, Roche, Samsung Bioepis, and UCB, Consultant of: AbbVie, Biocad, BMS, Galapagos, Gilead, GlaxoSmithKline, Janssen, Lilly, MSD, Medscape, MoonLake, Novartis, Peervoice, Pfizer, Roche, Samsung Bioepis, and UCB, Grant/research support from: AbbVie, Lilly, MSD, Novartis, and Pfizer., Walter P Maksymowych Consultant of: AbbVie, BMS, Celgene, Galapagos, Gilead, Janssen, Lilly, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Novartis, Pfizer, and UCB, Employee of: Chief Medical Officer of CARE Arthritis Limited, Désirée van der Heijde Consultant of: AbbVie, Bayer, BMS, Cyxone, Eisai, Galapagos, Gilead, GSK, Janssen, Lilly, Novartis, Pfizer, and UCB, Employee of: Director of Imaging Rheumatology BV, Tae-Hwan Kim Speakers bureau: AbbVie, Celltrion, Kirin, Lilly, and Novartis., Mitsumasa Kishimoto Consultant of: AbbVie, Amgen, Asahi-Kasei Pharma, Astellas, Ayumi Pharma, BMS, Chugai, Daiichi Sankyo, Eisai, Gilead, Janssen, Lilly, Novartis, Ono Pharma, Pfizer, Tanabe-Mitsubishi, and UCB., Xenofon Baraliakos Speakers bureau: AbbVie, BMS, Celgene, Chugai, Merck, Novartis, Pfizer, and UCB, Consultant of: AbbVie, BMS, Chugai, MSD, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie and Novartis, Yuanyuan Duan Shareholder of: AbbVie, Employee of: AbbVie, Kristin D'Silva Shareholder of: AbbVie, Employee of: AbbVie, Peter Wung Shareholder of: AbbVie, Employee of: AbbVie, In-Ho Song Shareholder of: AbbVie, Employee of: AbbVie.

Parameters of coagulation in COVID-19 patients: a correlation with clinical severity

Introduction: COVID-19 infection can be complicated by coagulation derangement and a high risk of thromboembolic episodes. Our study aimedto investigate coagulation parameters in COVID-19 patients and their correlation with clinical severity. Methods: We analyzed coagulation parameters PT, APTT, D-Dimer, and Fibrinogen in 98 RT-PCR-confirmed COVID-19 patients admitted to the Government Institute of Medical Sciences, Gautam Buddha Nagar, Uttar Pradesh, India. Results: This study involved 69 males (70.50%), and 29 (29.5%) were females. The mortality rate was 6.12% (n= 06). Forty-six patients (46.94%) had comorbidities. Thirty-four patients had elevated PT, and 7 had high APTT, whereas D-dimer and fibrinogen levels were raised in 68 and 61 patients, respectively. Among all four parameters, D-Dimer levels were significantly associated with disease severity. Conclusion: Derangement of D-dimer levels is significantly associated with disease severity in COVID-19 infection.

CLINICAL SIGNIFICANCE OF SERUM FERRITIN IN PATIENTS WITH SYSTEMIC SCLEROSIS

BackgroundThe main systemic sclerosis (SSc) manifestations are skin thickening, microangiopathy and ischemic changes in tissues, fibrotic damage to the lungs, heart, kidneys, and digestive system, arthritis, and myopathy. Acute phase reactants (APR) like erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) reflect inflammation activity in various inflammatory conditions. Ferritin is a protein bound to iron;low serum ferritin indicates iron deficiency and/or anemia. Instead, high ferritin levels are associated with inflammatory and non-inflammatory conditions such as dermatomyositis, pulmonary fibrosis, lupus, systemic COVID-19, vasculitis, tissue damage, thromboembolic complications, and metastatic cancer. The possible role of ferritin in SSc as APR is unclear.ObjectivesWe aimed to assess whether ferritin levels can reflect the severity of SSc and predict the outcome.Methods241 files of SSc patients with information on serum ferritin level (ferritin over 300 mg/dL is considered elevated) who visited the Rambam Rheumatology Institute in the years 2004-2021were used for retrospective analysis. Patients' demographic, clinical, laboratory, imaging, and respiratory function data were collected from electronic hospital files. Statistics included Student's T-test, Pearson's chi-squared test, and Kaplan-Meier curve;statistical significance was determined as p<0.05.Results36 patients (FerEl-SSc) had elevated ferritin values;the rest (n=205) represented the second group (FerNor-SSc). Significant differences were seen in gender (male 44.4% - 15.6%), disease duration (4.56 - 7.7 years), modified Rodnan skin score (12.3 - 6.9), as well as in incidence of lung (65.7% - 38.7%), heart (51.4% - 21.1%), and renal (28.6% - 5.9%) involvement. Increased ferritin correlated with elevated ESR, CRP, creatinine, creatine kinase, troponin, and reduced hemoglobin, impaired pulmonary function tests and reduced left ventricular ejection fraction on echocardiography. Patients with elevated ferritin had a significant increase in mortality rates (52.8% and 35.1%) and non-significant reduction in survival.ConclusionOur study demonstrated that ferritin has a potential as a sensitive marker for SSc severity in term of skin thickening, vital organ complications, and mortality. The ferritin test is simple and inexpensive, it can add to the complex SSc assessment and contribute to treatment decision-making in complicated SSc.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

Coagulation Abnormalities in Patients with COVID-19

Coronavirus disease 2019 (COVID-19) is an emerging infectious disease. Bilateral pneumonia, acute respiratory failure, systemic inflammation, endothelial dysfunction, and coagulation activation have been described as key features of severe COVID-19. Fibrinogen and D-dimer are typically increased. Moreover, the risk for venous thromboembolism is markedly increased, especially in patients in the intensive care unit, often despite prophylactic-dose anticoagulation. Pulmonary microvascular thrombosis has also been described and the risk for arterial thrombotic diseases also appears to be increased. Bleeding is less common than thrombosis but can occur. Evaluation for venous thromboembolism may be challenging because symptoms of pulmonary embolism overlap with COVID-19, and imaging studies may not be feasible in all cases. All inpatients should receive thromboprophylaxis unless contraindicated. In hospitalized patients with COVID-19, prophylactic dosing rather than more intensive (intermediate or therapeutic) dosing are suggested. On the other hand, therapeutic dose of anticoagulation is always appropriate to treat deep venous thrombosis or pulmonary embolism, unless contraindicated. This article reviews evaluation and management of coagulation abnormalities in individuals with COVID-19. © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2022.

Major neurological syndromes with COVID-19: lessons to learn

Objective: Covid-19 is a highly infectious viral disease, and our understanding of the impact of this virus on the nervous system is limited. Therefore, we aimed to do a systematic analysis of the neurological manifestations. Methods: We retrospectively studied the clinical, laboratory, and radiological findings of patients with major neurological syndromes (MNS) in Covid-19 over 6 months. Results: We had 39 patients with major neurological syndromes (MNS). The most common MNS was cerebrovascular disease (CVD) (61.53%), in which ischemic stroke (83.33%), cortical sinus thrombosis (12.50%), and haemorrhagic stroke (4.16%) were seen. Among ischemic stroke patients, 50% had a large vessel occlusion, and 66.66% of patients with CVD had a significant residual disability. Cranial neuropathy (15.38%), GBS (10.26%), encephalitis (7.26%), and myelitis (5.12%) were the other MNS. Among the three encephalitis cases, two had CSF-Covid-19 PCR positivity and had severe manifestations and a poor outcome. Associated comorbidities included hypertension (30.76%), diabetes mellitus (12.82%), chronic kidney diseases (7.69%), and polycythaemia vera (2.56%). Lung involvement was seen in 64.1% of patients. Mortality was 17.94% in MNS with Covid-19. Conclusions: The most common major neurological syndrome associated with Covid-19 is CVD with increased frequency of large vessel occlusion causing significant morbidity and mortality. Simultaneous lung and other systemic involvement in MNS results in a deleterious outcome.

Incidence of heparin resistance and heparin failure in patients receiving extracorporeal membrane oxygenation - an exploratory retrospective analysis

Objectives: Unfractionated heparin (UFH) remains the anticoagulation of choice at most centres for patients receiving extracorporeal membrane oxygenation (ECMO). One disadvantage of UFH relies on its individual dosing requirement to achieve target values. In this context heparin resistance has been described, defined as doses exceeding 35,000 IU UFH/d. However, the incidence of heparin resistance and its association with thromboembolic complications despite anticoagulation within target ranges remains unknown. Method(s): This retrospective study included adults receiving venovenous (VV) and venoarterial (VA) ECMO, or extracorporeal CO2-removal (ECCO2R) between 2010 and May 2022. The primary outcome was the incidence of heparin resistance (>35,000 IU of UFH/d). Secondary outcomes were heparin failure (thromboembolic complications despite anticoagulation within target ranges) and survival. A multivariable poisson regression model was fitted to analyse the effect of heparin resistance, COVID-19 and ECMO type on the incidence rate of thromboembolic events. Result(s): Of 197 included patients, 33 (16.8%) had heparin resistance. Patients with COVID-19 (n=51) had a higher rate of heparin resistance compared to nonCOVID-19 patients (37% vs. 9.6%, P<0.001). Thromboembolic complications occurred at a rate of 5.89/100 ECMO days. There was a significant effect of COVID-19 (incidence rate ratio (IRR) 2.12, 95% confidence interval (CI) 1.4 to 3.3, P<0.001) and ECMO type (VA ECMO: IRR 2.35;95% CI 1.43 to 3.87, P<0.001;ECCO2R: IRR 2.63, 95% CI 1.37 to 4.9, P=0.003;reference VV ECMO) on incidence rate of thromboembolic events, but not of heparin resistance (IRR 1.11, 95% CI 0.7 to 1.76, P=0.7). ECMO duration was longer (25d (IQR 11-33) vs. 8d (IQR 4-18), P<0.001) in patients with heparin resistance, but hospital survival did not differ (23 (70%) vs. 91 (57%), P=0.2). Conclusion(s): The study revealed a high incidence of heparin failure in ECMO patients, especially in those with COVID-19. Heparin resistance had no effect on the incidence rate of thromboembolic events, whereas our data suggest an increased risk in patients with COVID19, VA ECMO and ECCO2R.

Enoxaparin Sodium Biosimilar in the Prophylactic Treatment of Veinous Thromboembolism and Thromboembolic Disease: Prophyvar Study

Objectives: Varenox is the first locally manufactured and approved biosimilar in Algeria. It is an enoxaparin sodium (ES) with established good analytical characterization and manufacturing quality control. The aim of the PROPHYVAR study was to generate real-life data in routine practices and to assess the safety and tolerability in the prophylaxis of venous thromboembolism (VTE). Method(s): This is an observational, prospective, multicenter study, conducted between April 2021 and May 2022. The primary safety outcome was the incidence of Adverse Events (AEs) related to the study drug. A sample size of 500 patients was calculated to estimate the proportion of patients with AEs. Assuming that approximately 10% will be lost to follow-up or not evaluable, 550 patients were needed to describe the impact of Varenox use. Result(s): The study was conducted in 25 different sites in Algeria, in 4 therapeutic areas: ICU, orthopedic surgery, obstetrics and nephrology;550 patients were included and received at least one injection of Varenox. The mean age was 47 years, women in majority (62.5%). The patients were overweight or obese (53%), with a history of arterial hypertension (25%), diabetes (7.5%) and renal failure (6.4%). Reasons for hospitalization were mainly fracture (15.5%), pregnancy (8.3%), COVID-19 (7%) or cancer (7%). The majority of patients were treated at prophylactic dose of 0.4ml (80%) or 0.6ml (10%). The median duration of follow-up was 24 days. A total of 38 patients experienced at least one AE (6.9%, CI95=[4.9%;9.4%]). Related AEs were reported in 10 patients (1.8%), mainly in nephrology (N=7 arterio-venous fistula). VTE events were reported in 6 patients (1.1%, CI95=[0.2%;2%]). Conclusion(s): This study suggests that Varenox is safe in the prophylaxis of VTE. To our knowledge this is the first large study describing the use of ES in current medical practice in Algeria.Copyright © 2023

LONG-TERM EFFICACY AND SAFETY OF UPADACITINIB IN PATIENTS WITH PSORIATIC ARTHRITIS: 3-YEAR RESULTS FROM THE PHASE 3 SELECT-PsA 1 STUDY

BackgroundUpadacitinib (UPA) improved symptoms in patients (pts) with psoriatic arthritis (PsA) with prior inadequate response or intolerance to ≥1 non-biologic disease-modifying antirheumatic drug (nbDMARD-IR) through week (wk) 104 or 2 years of treatment in SELECT-PsA 1 [1].ObjectivesTo evaluate efficacy and safety of UPA vs adalimumab (ADA) through wk 152 or 3 years from the ongoing long-term open-label extension of SELECT-PsA 1.MethodsPts were randomized to receive UPA 15 mg (UPA15) or UPA 30 mg (UPA30) once daily, ADA 40 mg (ADA) every other wk, or placebo (PBO). At wk 24, PBO pts switched to UPA15 or UPA30. Following approval of UPA15, the protocol was amended so pts on UPA30 switched to UPA15 (earliest at wk 104). Efficacy was assessed through wk 152, and safety through June 13, 2022.ResultsOf 1704 pts randomized, 911 completed 152 wks of treatment. The proportions of pts achieving.≥20%/50%/70% improvement in American College of Rheumatology criteria (ACR20/50/70), minimal disease activity (MDA), and ≥75%/90%/100% improvement in Psoriasis Area and Severity Index at wk 152 were generally consistent with those at wk 1041. UPA had greater ACR20/50/70 and MDA responses vs ADA, and a greater mean change from baseline (BL) in Health Assessment Questionnaire-Disability Index, pt's assessment of pain, and Bath Ankylosing Spondylitis Disease Activity Index vs ADA. Change from BL in modified total Sharp/van der Heijde score were similar between UPA30 and ADA, and numerically higher with UPA15 (Table 1). The overall UPA safety profile remained unchanged (Figure 1) [1,2]. UPA had numerically higher rates of serious infection (SI), herpes zoster (HZ), anemia, lymphopenia, creatine phosphokinase (CPK) elevation, and non-melanoma skin cancer (NMSC) vs ADA. Increases for SI, HZ, anemia, and CPK elevation with UPA were dose dependent. Rates of major adverse cardiovascular events, venous thromboembolism, and malignancy excluding NMSC were low and generally similar across groups. The most common cause of death was COVID-19.ConclusionEfficacy of UPA in nbDMARD-IR pts with PsA was maintained through 3 years of treatment. No new safety signals were identified.References[1]McInnes IB, et al. Rheumatol Ther 2022;1–18 [Epub ahead of print].[2]McInnes IB, et al. RMD Open 2021;7(3):e001838.Table 1.Efficacy endpoints at wk 152UPA15 (n=429)UPA30a (n=423)ADA (n=429)Proportion of pts (%)NRIAONRIAONRIAOACR20/50/7064.6/52.0/35.9*89.8/71.6/ 48.263.1/54.1*/ 35.787.9/74.4/ 47.861.1/46.6/ 28.786.2/65.2/ 39.8Minimal disease activity37.555.143.5*60.335.950.2PASI75/90/100b50.5/42.5/32.269.2/58.5/ 43.458.1/46.7/3 7.678.6/63.5/ 50.954.0/40.8/ 30.379.6/59.9/ 44.6Resolution of enthesitis by Leeds Enthesitis Indexc50.475.248.973.846.077.0Resolution of dactylitis by Leeds Dactylitis Indexd65.495.266.197.965.497.1Change from BLeMMRMAOMMRMAOMMRMAOHealth Assessment Questionnaire- Disability Index-0.51-0.55-0.53*-0.58-0.45-0.49Pt's assessment of pain (numeric rating scale)-3.3*-3.5-3.3*-3.6-2.8-3.0Bath Ankylosing Spondylitis Disease Activity Indexf-3.09-3.27-3.16-3.54-2.81-2.71Modified total Sharp/van der Heijde score0.210.190.050.040.090.09aFollowing a protocol amendment, all pts on UPA30 switched to UPA15 (earliest switch at wk 104);data are presented by originally randomized group. bPts with psoriasis affecting ≥3% of body surface area at BL. cPts with LEI >0 at BL;resolution LEI=0. dPts with LDI >0 at BL;resolution LDI=0. eData shown as MMRM (least squares mean) and AO (mean). fPts with psoriatic spondylitis at BL. n value ranges: UPA15 (99–429), UPA30 (95–423), ADA (89–429). Nominal *p<0.05 UPA vs ADA.ACR20/50/70, ≥20%/50%/70% improvement in American College of Rheumatology criteria;ADA, adalimumab;AO, as observed;BL, baseline;MMRM, mixed effect model repeated measurement;NRI, non-responder imputation;PASI75/90/100, ≥75%/90%/100% improvement in Psoriasis Area and Severity Index;pt, patient;UPA15/30, upadacitinib 15/30 mg once daily;wk, weekAcknowledgementsAbbVie funded this study and participated in the study design, research, analysis, data collection, interpretation of data, and the review and approval of the publication. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. Medical writing support was provided by Carl Davies, MSc, of 2 the Nth (Cheshire, UK), and was funded by AbbVie.Disclosure of InterestsIain McInnes Grant/research support from: AbbVie, AstraZeneca, Bristol Myers Squibb, Celgene, Eli Lilly, Evelo, Causeway Therapeutics, Gilead, Janssen, Novartis, Pfizer, Sanofi Regeneron, and UCB Pharma, Koji Kato Employee of: AbbVie and may hold stock or options, Marina Magrey Consultant of: BMS, Eli Lilly, Janssen, Novartis, Pfizer, and UCB Pharma, Grant/research support from: AbbVie, Amgen, BMS, and UCB Pharma, Joseph F. Merola Consultant of: AbbVie, Arena, Avotres, Biogen, Bristol Myers Squibb, Celgene, Dermavant, Eli Lilly, EMD Sorono, Janssen, Leo Pharma, Merck, Novartis, Pfizer, Regeneron, Sanofi, Sun Pharma, and UCB Pharma, Mitsumasa Kishimoto Consultant of: AbbVie, Amgen, Asahi-Kasei Pharma, Astellas, Ayumi Pharma, BMS, Celgene, Chugai, Daiichi-Sankyo, Eisai, Eli Lilly, Gilead, Janssen, Kyowa Kirin, Novartis, Ono Pharma, Pfizer, Tanabe-Mitsubishi, and UCB Pharma, Derek Haaland Speakers bureau: AbbVie, Amgen, AstraZeneca, Bristol Myers Squibb, GlaxoSmithKline, Janssen, Novartis, Pfizer, Roche, Sanofi Genzyme, Takeda, Grant/research support from: AbbVie, Adiga Life Sciences, Amgen, Bristol Myers Squibb, Can-Fite Biopharma, Celgene, Eli Lilly, Gilead, GlaxoSmithKline, Janssen, Novartis, Pfizer, Regeneron, Sanofi-Genzyme, UCB;and has received honoraria or other fees from AbbVie, Amgen, AstraZeneca, Bristol Myers Squibb, Eli Lilly, GlaxoSmithKline, Janssen, Merck, Novartis, Pfizer, Roche, Sanofi Genzyme, Takeda, and UCB Pharma, Yihan Li Employee of: AbbVie and may hold stock or options, Yanxi Liu Employee of: AbbVie and may hold stock or options, Jianzhong Liu Employee of: AbbVie and may hold stock or options, Ralph Lippe Employee of: AbbVie and may hold stock or options, Peter Wung Employee of: AbbVie and may hold stock or options.

Outcomes and mortality in a newly implemented ECMO center in Northeast Brazil during pandemic

Objectives: To evaluate the outcomes and risk factors associated with mortality of patients cannulated on ECMO in the context of covid infection during the pandemics in a newly implemented ECMO center Methods: This was a unicentric observational retrospective study performed at Real Hospital Portugues, in Recife, state of Pernambuco, Brazil. All consecutive patients with laboratory confirmed SARS-CoV-2 infection cannulated for VV-ECMO or VA-ECMO for severe ARDS from march 2020 to december 2021 were included retrospectively. Patients recieving ECMO for isolated refratory cardiogenic shock were excluded. Descriptive statistics and association tests were used to analyze characteristics, management and patient outcomes during that period. Result(s): In our cohort of 47 ECMO for covid associated ARDS (CARDS), 39 patients (83%) were admitted by our emergency department. 8 patients (17%) had been transferred from other hospitals as soons as they had been cannulated. 32 patients (68%) were male, median age was 50 years (18-69). Mean body mass index was 31 (21,4-46,3). 37 patients (78%) had at least 1 comorbidity. Major bleeding occurred in 34 (72%) patients. Venous thromboembolism and hemolysis ocurred in 19 (40%) and 13 (23%) patients, respectively. When we compared treatments before ECMO initiation (imunoglobulin, tocilizuman, nitric oxide, neuromuscular blockade and proning), proning was associated with better survival (RR 0,67 IC 0,46-0,97 p 0,029). The mean duration in mechanical ventilation until ECMO cannulation was 9,69 days and mean time in ECMO was 23 days. The 90- day mortality was approximately 72%. Conclusion(s): The only variable associated with a better chance of survival was proning before ECMO. Our mortality (72%) is higher than reported from a recent meta-analysis of 1986 ECMO patients implanted during the first pandemic year(37,1%). However it is similar to a German populational registry of covid patients receiving VV-ECMO (73%). Althought it;s impossible to make causal inferences with such a design and sample sizes, we believe that describing the experience of smaller and newly implemented ECMO centers serves as motivation to improve quality and also to plan for future episodes of pressure on health system.

SAFETY ANALYSIS OF JAKINIBS IN REAL CLINICAL PRACTICE IN A COHORT OF 116 PATIENTS

BackgroundJanus kinase inhibitors (JAKinibs) have demonstrated efficacy in the treatment of rheumatoid arthritis (RA) and spondyloarthritis (SpA), although their safety profile continues to be analysed due to the possible increase in adverse events (AEs) in relation to anti-TNFs (mild and severe infections, haematological alterations, thromboembolism, increase in neoplasms).ObjectivesTo evaluate in real clinical practice the AEs of JAKinibs in a cohort of patients with RA and SpA. In addition, adherence and reasons for discontinuation (1st or 2nd failure, AE) are analysed.MethodsObservational study of 116 patients diagnosed with RA or SpA who received treatment with JAKinibis (tofacitinib, baricitinib, upadacitinib) after failure of treatment with different classical synthetic (FAMEsc) or biological (FAMEb) disease-modifying drugs. The following data were analysed: demographic characteristics of the patients, years of disease progression, 1st or 2nd failures and AE.ResultsMean age was 52 years, with Baricitinib being older (60 years -SD 13.6), higher prevalence of females in all groups, and a disease progression time of about 10 years. Mean number of FAMEsc was 1.6 and mean number of FAMEb was 2,3 to Tofacitinib(Tofa), 2,76 to Baricitinib(Bari) and 4,4 to Upadacitinib(Upa). 71 (63%) patients had active corticosteroid therapy. The median treatment time with Tofa was 8.8 months, Bari 9.5 and Upa 2.4 months.Most frequent AEs with Tofa were urinary tract infections(UTI) (11.9%, 7 cases) and headaches (8.47%, 5 cases). There were 3 cases of herpes zoster (5.1%), one of which was recurrent, and 2 cases respectively of tachycardia and gastrointestinal intolerance (3.4%). With Baricitnib, 2(5%) cases of UTI and 2(5%) of influenza A were reported. Most frequent AEs related to Upadacitinb are gastrointestinal intolerance, labialis and facial herpes, anterior uveitis and recurrent UTI, with 1 case for each adverse event. There were 4 success with Baricitinib treatment: 2 due to severe COVID, 1 influenza A and 1 due to stroke. 17 patients had 1st failure to Tofa(28.81%), 8 to Bari20.0%) and 3 to Upa(18.75%);7(11.86%) and 2(5%) patients had 2nd failure to Tofa and Bari respectively, no with Upa.Mean CRP to Tofa-SD 18.9-was 17.19, 20-SD 22.7- to Bari and 24.2-SD 27.40- to Upa. Mean ESR-SD 15.3- was 25.4, -SD 26.4 and 44.3 -SD 32-, respectively. At 6 months, 36(62%) were continuing on Tofa, 22(56%) on Bari and 4(27%) on Upa. At 12 months, 27(46.6%) were still on Tofa and 12 on Bari(30.8%) and no patients were on upa.Table 1.TofaBariUpaMean age496047Male19%18%20%Female81%82%80%Time course of disease(years)81111Permanence 6 months62%56%27%Permanence 12 months46,6%31%0%Patients with corticotherapy62%64%60%Previous biological drugs2,3 SD 22,8 SD 2,34,4 SD 2,9Patients who discontinued the drug62%59%33%Mean CRP at the end of treatment172024Mean end-of-treatment ESR252644Repeated AEsUTI(7) Headache(5) Shingles(3) Nephritic colic(2) Gastrointestinal intolerance(2) Tachycardia(2)UTI(4) Headache(2)Serious AEsShingles (3)Varicella encephalopathy(1) Stroke(1) Shingles (1)1st failure28,8%20%18,7%2nd failure11,9%5%0%SuccessSARS-Cov2(2) Influenza(1) Stroke(1)Figure 1. Months stay pharmacoConclusionMost frequent adverse events with JAKinibs are mild infections, except gastrointestinal complaints with upadacitinib. Serious adverse events, including 3 deaths from viral infections, were observed, mostly in patients over 65 years. Most frequent cause of discontinuation was treatment failure. We believe that further observational studies are needed to stratify and profile the risk of infection with JAKinibs.References[1]Atzeni F, Popa CD, et al. Safety of JAK inhibitors: focus on cardiovascular and thromboembolic events. Expert Rev Clin Immunol. 2022 Mar;18(3):233-244. Doi: 10.1080/1744666X.2022.2039630 Epub 2022 Feb 17.PMID: 35129033[2]Alves C, Penedones A,et al. The Risk of Infections Associated With JAK Inhibitors in Rheumatoid Arthritis: A Systematic Review and Network Meta-analysis. J Clin Rheumatol. 2022 Mar 1;28(2):e407-e414 PMID:33902098Ackn wledgements:NIL.Disclosure of InterestsNone Declared.

A comprehensive knowledgebase of known and predicted human genetic variants associated with COVID-19 susceptibility and severity

Host genetic susceptibility is a key risk factor for severe illness associated with COVID-19. Despite numerous studies of COVID-19 host genetics, our knowledge of COVID-19-associated variants is still limited, and there is no resource comprising all the published variants and categorizing them based on their confidence level. Also, there are currently no computational tools available to predict novel COVID-19 severity variants. Therefore, we collated 820 host genetic variants reported to affect COVID-19 susceptibility by means of a systematic literature search and confidence evaluation, and obtained 196 high-confidence variants. We then developed the first machine learning classifier of severe COVID-19 variants to perform a genome-wide prediction of COVID-19 severity for 82,468,698 missense variants in the human genome. We further evaluated the classifier's predictions using feature importance analyses to investigate the biological properties of COVID-19 susceptibility variants, which identified conservation scores as the most impactful predictive features. The results of enrichment analyses revealed that genes carrying high-confidence COVID-19 susceptibility variants shared pathways, networks, diseases and biological functions, with the immune system and infectious disease being the most significant categories. Additionally, we investigated the pleiotropic effects of COVID-19-associated variants using phenome-wide association studies (PheWAS) in ~40,000 BioMe BioBank genotyped individuals, revealing pre-existing conditions that could serve to increase the risk of severe COVID-19 such as chronic liver disease and thromboembolism. Lastly, we generated a web-based interface for exploring, downloading and submitting genetic variants associated with COVID-19 susceptibility for use in both research and clinical settings (https://itanlab.shinyapps.io/COVID19webpage/). Taken together, our work provides the most comprehensive COVID-19 host genetics knowledgebase to date for the known and predicted genetic determinants of severe COVID-19, a resource that should further contribute to our understanding of the biology underlying COVID-19 susceptibility and facilitate the identification of individuals at high risk for severe COVID-19.Copyright © 2023 Elsevier Inc.

DERMATO-NEURO SYNDROME PRECIPITATED BY COVID-19 INFECTION IN THE SETTING OF SCLEROMYXEDEMA

BackgroundA black female in her 40s presented with a nonpruritic rash for 10 months consisting of bumps on the face, hands, forearms, and thighs. She had no prior treatment. Past medical history was significant for pulmonary embolism (PE) 6 years prior. She had no personal or family history of autoimmune disease. Physical exam revealed numerous smooth 2-3 mm skin-colored papules over the bilateral forearm dorsa, hands, anterior thighs, and face. Serum protein electrophoresis revealed monoclonal IgG lambda gammopathy. Skin biopsy of her left elbow showed dermal fibroplasia with mucin deposition. IgG was less than 1.5 grams/deciliter;bloodwork was otherwise stable. The diagnosis of scleromyxedema was rendered.ObjectivesThe objective of this clinical case was to evaluate a neurologic sequela of COVID-19 infection in a patient with scleromyxedema.MethodsOne month following diagnosis of scleromyxedema, our patient was diagnosed with COVID-19 five days before admission to the emergency department with altered mental status and aphasia. Rheumatology was consulted due to malignant hypertension and acute kidney injury with question of scleroderma-like renal crisis in the setting of recently diagnosed COVID-19 infection, although she had no other features of systemic sclerosis. The infectious disease team was consulted due to COVID-19-induced inflammatory reaction.ResultsThe patient's creatinine kinase and brain natriuretic peptide were elevated. Creatinine and potassium trended upwards. She developed seizures and became hemodynamically unstable with rapidly declining clinical status. She was transferred to the intensive care unit, where she developed respiratory arrest, shock, hyperkalemia, and acidemia. She received escalating doses of pressors but experienced frequent arrhythmic disturbances and developed asystole. Resuscitation efforts were unsuccessful;she expired within 24 hours of consultation.ConclusionDermato-neuro syndrome (DNS) is a potential complication of scleromyxedema associated with confusion, dysarthria, seizures, and coma. The patient's clinical presentation is consistent with DNS in the setting of scleromyxedema likely precipitated by COVID-19. Intravenous immunoglobulins are first-line treatment for scleromyxedema;however, it is associated with risk of venous thromboembolism. The patient was considered for treatment as an outpatient but deferred due to history of PE. She was reevaluated for treatment upon presentation to the hospital, but given the severity and rapidity of her condition, it was already too late. This is the second reported case of COVID-19 induced DNS in a patient with scleromyxedema. Given the severity, we recommend early initiation of treatment in patients with scleromyxedema and aggressive treatment for those contracting COVID-19.References[1] Haber R, Bachour J, El Gemayel M. Scleromyxedema treatment: a systematic review and update. Int J Dermatol. 2020;59:1191-1201.[2] Flannery MT, Humphrey D. Deep Venous Thrombosis with Pulmonary Embolism Related to IVIg Treatment: A Case Report and Literature Review. Case Rep Med. 2015;971321.[3] Lee YH, Sahu J, O'Brien MS, D'Agati VD, Jimenez SA. Scleroderma Renal Crisis-Like Acute Renal Failure Associated With Mucopolysaccharide Accumulation in Renal Vessels in a Patient With Scleromyxedema. J Clin Rheumatol. 2011;17:318-322.[4] Hoffman-Vold AM, Distler O, Bruni C, et al. Systemic sclerosis in the time of COVID-19. Lancet Rheumatol. 2022;4:e566-575.[5] Fritz M, Tinker D, Wessel AW, et al. SARS-CoV-2: A potential trigger of dermato-neuro syndrome in a patient with scleromyxedema. JAAD Case Rep. 2021;18:99-102.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

Five years of adjuvant chemotherapy in a tertiary oncology centre: outcomes and impact of GCSF on completion of treatment

Background: Patients with non-small cell lung cancer (NSCLC) treated with adjuvant vinorelbine-platinum chemotherapy experience neutropenia, which may lead to early termination of treatment. However, evidence suggests that survival is superior in patients who complete four cycles of chemotherapy [1]. Granulocyte colony stimulating factor (GCSF) prophylaxis is used to prevent neutropenia. During the COVID pandemic, the threshold for initiating prophylaxis was lowered to reduce need for hospital attendance with the concomitant risk of hospital-acquired infection [2]. We evaluated whether GCSF prophylaxis supported completion of chemotherapy in patients treated at St Bartholomew's Hospital. Method(s): Data was retrospectively collected on the 112 patients with NSCLC who received adjuvant vinorelbine-platinum chemotherapy (total 349 cycles) in the period Jan 2017- Jul 2022. GCSF prophylaxis was prescribed at physician discretion. chi2 tests were carried out using SPSS 28. Result(s): A significantly higher proportion of patients who received GCSF prophylaxis completed four cycles of chemotherapy (chi2=5.120, p=0.024). These patients also experienced a lower incidence of grade 3 or 4 neutropenia (chi2=6.801, p=0.009). Over 5 years, 2/112 (1.75%) patients died, both from neutropenic sepsis;neither of these patients received prophylactic GCSF. GCSF prophylaxis was not associated with increase in the incidence of thromboembolic events (chi2=1.462, p=0.442). Conclusion(s): GCSF is safe and effective as primary prophylaxis in NSCLC patients receiving adjuvant chemotherapy. Use of GCSF will reduce proportion of post-operative patients considered too high risk for chemotherapy due to concerns about neutropenia. Disclosure: No significant relationships. [Figure presented]Copyright © 2023 Elsevier B.V.

The use of venovenous extracorporeal membrane oxygenation in COVID-19: An updated systematic review and meta-analysis of clinical outcomes

Objectives: The objective of this study is to assess the clinical benefits and potential risks of using venovenous extracorporeal membrane oxygenation (VV ECMO) as a treatment for COVID-19 patients with severe respiratory failure. Method(s): Relevant studies were identified through searches of electronic databases, including PubMed, EMBASE, and the Cochrane Library, from January 2020 to December 2022. We included observational studies on adult patients who received venovenous (VV) ECMO support for COVID-19-induced ARDS. The primary outcome was in-hospital mortality, 3-month mortality, and complications associated with VV ECMO. Statistical analysis was performed using R version 4.0.3 and the metafor and meta packages. Result(s): The final analysis included 39 studies comprising 10,702 patients. In-hospital mortality for adults receiving ECMO was 34.2% (95% CI: 28.5% - 40.3%;I2 = 93%), while the 3-month mortality rate was 50.2% (95% CI: 44.4% - 56.0%;I2 = 51%). Bleeding requiring transfusion occurred in 33.7% of patients (95% CI, 23.9 - 45.1;I2 = 96%). The pooled estimates for other complications were as follows: overall thromboembolic events 40.9% (95% CI, 24.8 - 59.3;I2 = 97%), stroke 8.7% (95% CI, 5.7 - 13.2;I2 = 72%), deep vein thrombosis 15.4% (95% CI, 9.7 - 23.6;I2 = 80%), pulmonary embolism 15.6% (95% CI, 9.3 - 25.1;I2 = 92%), gastrointestinal haemorrhage 8.1% (95% CI, 5.5 - 11.8;I2 = 56%), and the need for any renal replacement therapy in 38.0% of patients (95% CI, 31.6 - 44.8;I2 = 84%). Bacterial pneumonia occurred in 46.4% of patients (95% CI, 32.5 - 61.0;I2 = 96%). Conclusion(s): Venovenous extracorporeal membrane oxygenation (VV ECMO) may be an effective treatment option for COVID-19 patients with severe respiratory failure. The use of VV ECMO was associated with reduced in-hospital and 3-month mortality. However, bleeding is a common complication that should be closely monitored. Further research is needed to determine the optimal use of VV ECMO in this patient population and to identify factors that may predict a favourable response to treatment.

The pathogenesis of COVID-19: Hypercoagulation and D-dimer in thrombotic complications

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) caused a new coronavirus disease (COVID-19), which is highly contagious and its pathogenesis has not been fully elucidated. In COVID-19, the inflammation and blood coagulation systems are excessively activated. SARS-CoV-2 damages endothelial cells and pneumocytes, which leads to disruption of hemostasis in SARS. Thromboembolism is the main cause of mortality in patients with COVID-19. Clots, including pulmonary embolism (PE) and deep vein thrombosis (DVT), ranging from minor to fatal complications of the SARS-CoV-2 infection are known. Individuals with pre-existing diseases are more susceptible to the development of blood clots and poor outcomes. High levels of circulating cytokines and D-dimer (DD) are influential biomarkers of poor outcomes in COVID-19. The latter occurs as a result of hyperfibrinolysis and hypercoagulation. Plasmin is a key player in fibrinolysis and is involved in the cleavage of many viral envelope proteins, including SARS-CoV. Due to this function penetration of viruses into the host cell occurs. In addition, plasmin is involved in the pathophysiology of acute respiratory distress syndrome (ARDS) in SARS and promotes the secretion of cytokines, such as IL-6 and TNF, from activated macrophages. The focus of existing treatment to alleviate fibrinolysis in patients with COVID-19 is the use of systemic fibrinolytic therapy given thrombotic pathology in severe forms of COVID-19 which may lead to death. However, fibrinolytic therapy may be harmful in the advanced stages of COVID-19, when the status of disseminated intravascular coagulation (DIC) changes from suppressed fibrinolysis to its enhancement during the progression of the disease. This narrative review aims to elucidate the pathogenesis of COVID-19, which will further help in precise diagnosis and treatment. Take-home message: The COVID-19 virus disrupts haemostasis and thromboembolism by over activating the inflammation and blood coagulation systems. High levels of cytokines and D-dimer are indicators of pre-existing diseases and blood clots. Systemic fibrinolytic treatment can reduce severe fibrinolysis in COVID-19, which is caused by plasmin. In the late stages of DIC, when fibrinolysis increases, it may be dangerous. To improve therapy and results, understanding COVID-19 pathogenicity is critical. © 2023 by the authors.

THE IMPACT of PRIOR ANTITHROMBOTIC USE on THROMBOEMBOLIC EVENTS in PATIENTS with CARDIOVASCULAR DISEASE and SEVERE COVID-19 INFECTION

Objective: Our objective in this study is to determine the predictive factors of thromboembolic complications in patients with previous heart disease and severe covid-19 infection and the impact of previous use of antithrombotic drugs on protection against these complications. Method(s): We conducted a single-center retrospective study of 158 patients with heart disease admitted to an intensive care unit for severe SARS-COV-2 infection. To determine the predictive factors, we used a logistic regression analysis. Result(s): Out of 158 patients, 22 were complicated by a thromboembolic event, i.e. 13.9%, mean age of our population was 64.03 (SD = 15.27), with a male predominance of 98 (62%), For the predictive factors of thromboembolic complications, and after multivariate analysis, we find the duration of hospitalization with (OR=0.92 ;95%CI (0.863 - 0.983), p=0.014, previous use of anti-thrombotic drugs as a protective factor with ( OR=0.288, 95%CI (0.091 - 0.911), p=0.034 for anti-platelet agents ) and ( OR=0, 322, 95%CI (0.131 - 0.851), p=0.021) for anti-coagulants (Figure1), and finally thrombocytopenia at admission as a risk factor ( OR=4.58 95%CI (1.2 - 10.627), p=0.021). D-dimer was not detected as a risk factor, and this can be explained by the characteristics of our population. Although the previous use of anti-thrombotic drugs protects against thrombo-embolic complications during severe infection, there was no benefit in terms of mortality (Figure2). Conclusion(s): Prior use of antithrombotic drugs is a protective factor against thromboembolic complications in patients with a history of heart disease but has no effect on mortality.

RISK OF APS AND aPLs POSITIVE PATIENTS FOR THROMBOSIS WITH COVID-19

BackgroundCoagulopathy, thromboembolic events and DIC during COVID-19 infection has been reported. Antiphospholipid antibodies (aPLs), present in 1–5 % of healthy individuals. aPLs are associated with the risk of antiphospholipid syndrome (APS) which is associated with higher risk of thrombosis.ObjectivesWe wanted to see if patients with known APS or aPLs only are at higher risk of a thrombotic event compared to control when developed COVID-19. We retrospectively review EMR for over a year for thrombotic events in patients with COVID and prior history of APS or aPLs only and matched them to control.MethodsPatient characteristics and laboratory testing were summarized according to the following groups: APS, aPLs detected or control. The control were matched according to age and gender for each group. Continuous variable were summarized as median (range) and mean (standard deviation), while categorical variables were reported as frequency (percentage). The binary patient outcome of thrombotic event, hospitalization for COVID, death, and composite event (the combined occurrence of thrombotic events, hospitalization, death) were calculated and interpreted as the multiplicative increase in odds of the given outcome for aPL group compared to control group. Multivariable logistic regression models were adjusted for potential risk factors (immobilization, hypertension, coronary artery disease, diabetes mellitus, and smoking) one at a time due to the rare occurrences of events studied.ResultsIn single variable analysis (unadjusted) the odds of the patient having a thrombotic event was approximately 27 times higher in patients with aPL only compared to Controls (P<0.001). We see similar results in multivariable analyses (adjusted) adjusting for the following variables one at a time: immobilization, hypertension, coronary artery disease, diabetes mellitus, and smoking. In each of the multivariable analyses, the adjusted odds of a thrombotic event was between approximately 24 and 29 times higher in patients with aPL Antibody Only compared to Controls (all P<0.001) indicating that association of aPL Antibody Only with thrombotic event was independent of immobilization, hypertension, coronary artery disease, diabetes, and smoking. There was no statistically significant risk of thrombosis in APS group vs control. Majority of patients with APS were on chronic anticoagulation.ConclusionWe found a statistical significantly difference in patient with aPLs only versus control regarding risk of thrombosis when developed COVID-19. No statistically significant risk was noted in patients with APS. While chronic anticoagulation in APS patients is protective it seemed that patient with aPLs only do carry a high risk of thrombosis if any inciting factors like COVID-19.References[1]C. Huang, Y. Wang, X. Li et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China, Lancet 395 (2020)[2]A. Jayarangaiah, P.T. Kariyanna, X. Chen, A. Jayarangaiah, A. Kumar, COVID-19- Associated coagulopathy: an exacerbated immunothrombosis response, Clin. Appl. Thromb. 26 (2020)[3]Y. Zhang, M. Xiao, S. Zhang et al. Coagulopathy and antiphospholipid antibodies in patients with Covid-19, N. Engl. J. Med. 382 (2020)[4]K.J. Lackner, N. Müller-Calleja, Pathogenesis of antiphospholipid syndrome: recent insights and emerging concepts, Expert Rev. Clin. Immunol. 15 (2019)Acknowledgements:NIL.Disclosure of InterestsNone Declared.