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Background: Patients with inflammatory bowel disease (IBD) may be at increased risk of having venous thromboembolism. Methods: Medical records from 1253 IBD patients attending hospital care during the years 1987-97 were studied. These patients were recruited from a population of 340,000 inhabitants. Patients with verified venous thrombosis were characterized clinically, and blood samples were examined for coagulopathy including analyses of antithrombin, plasminogen, protein C, protein S, factor V, and prothrombin mutations. As control groups we used 99 patients with verified venous thrombosis and no history of IBD and 288 volunteers with no history of thrombosis. Results: The incidence of venous thrombosis was 1.5/1000 IBD patients per year, which is comparable to the background population. The mean age was significantly lower in IBD patients than in non-IBD patients (53 versus 64 years, P = 0.0225). We found one patient with antithrombin deficiency but none with protein C, protein S, or plasminogen deficiency. Factor V mutation was as prevalent in IBD patients with thrombosis as in thrombotic non-IBD patients (27% versus 28%) and 3.0 times (95% confidence interval, 0.8-11.9) more frequent in IBD patients with thrombosis than in healthy controls. Prothrombin mutation was not detected in IBD patients with venous thrombosis. Conclusion: We found no increased incidence of venous thrombosis in IBD patients compared with a background population. However, IBD patients had venous thrombosis earlier in life than non-IBD patients. Although factor V mutation may contribute to thrombosis, IBD acts as a trigger through mechanisms that still remain unexplained.

On both sides of the ocean.

Objective To analyze the clinical features and clinical significance of patients with inflammatory bowel disease (IBD) complicated by thrombosis. Methods From March 14th, 2001 to February sixth 2017, at Nanjing General Hospital of Nanjing Military Command, 27 IBD patients with thrombosis diagnosed by clinical symptoms, endoscopy, imaging and pathology were enrolled. During the same period, 81 gender and age matched IBD patients without thrombosis were included in the control group. The basic data, information of IBD diagnosis and treatment and thrombotic events of patients were collected and analyzed. T-test and Chi-square test were performed for statistical analysis. Binary logistics regression was used for risk factors analysis. Results The mean age of diagnosis of IBD patients with thrombosis was (44.8±15.8) years, which was higher than that of the IBD patients of control group ((36.0±14.4) years), and the difference was statistically significant (t=2.69, P=0.008). Among 27 IBD patients with thrombosis, arterial thrombosis was 51.9%(14/27), deep venous thrombosis of the lower extremity veins was 29.6%(8/27), portal venous system involved was 11.1% (3/27), pulmonary embolism was 3.7%(1/27) and disseminated intravascular coagulation accounted for 7.4%(2/27). Nine patients (33.3%, 9/27) underwent surgery six months before the diagnosis of thrombosis. The results of binary logistic regression indicated that the age of diagnosis and vascular catheterization were independent risk factors for thrombosis in IBD patients (odds ratio (OR)=1.04, 95%confidence interval (CI)1.01 to 1.07, P=0.01; OR=5.64, 95%CI 1.39 to 22.96, P=0.02). After medicine treatment or surgery, 81.5%(22/27) of the patients improved, 9.1%(2/22) were worse and 13.6%(3/22) died. Conclusion Screening and prevention of thrombosis should be paid attention in IBD patients with a history of vascular catheterization, at active phase and older age when diagnosed. Key words: Inflammatory bowel diseases; Venous thrombosis; Risk factors

Introduction: Flares of inflammatory bowel disease (IBD) have been associated with venous thromboembolism, and recent studies suggest an association between IBD and myocardial infarction. The association between IBD flares and cerebral thrombotic disease is less clear. We therefore sought to evaluate the risk of cerebral venous and arterial stroke during IBD flares. Hypothesis: IBD flares are associated with an increased risk of a cerebral thrombotic event. Methods: We used data on all admissions at nonfederal acute care hospitals in California, Florida, and New York to identify patients with a primary ICD-9-CM diagnosis code for ulcerative colitis or Crohn’s disease between 2005 and 2012. Patients with a documented abdominal surgery during the index hospitalization were excluded. An IBD flare was defined as a period of 120 days from the start of the index IBD-related hospitalization. Our outcomes were ischemic stroke and cerebral venous sinus thrombosis. We used a self-controlled case series design in which we compared the risk of a thrombotic event in the 120 days after hospitalization versus the risk during the 120 days prior to hospitalization. Results: We identified 31,993 patients with IBD, of whom 98 (0.31%) developed ischemic stroke. As compared with the control period preceding the index hospitalization, the risk of stroke was significantly elevated during the 120 days after IBD-related hospitalization (incidence rate ratio [IRR] 2.0; 95% confidence interval [CI] 1.3-3.0). In subgroup analyses, this elevated risk was apparent only in the 16,280 patients older than the median age of 44 years (IRR 1.9; 95% CI, 1.27-2.95), and not in the 15,713 patients younger than 44 years of age, among whom we identified only one stroke. We found only one patient with a documented venous sinus thrombosis and thus could not estimate the risk associated with an IBD flare. Conclusion: We found an association between IBD-related hospitalization and the risk of ischemic stroke in older patients. These results build on recent studies suggesting an association between IBD and the risk of arterial thrombotic events. Further research is needed to better define the association between IBD and cerebrovascular events, especially rare events such as cerebral sinus thrombosis.

Background The population of elderly-onset (diagnosis >=65 years old) inflammatory bowel disease (IBD) is growing worldwide. Management of this population poses challenges, given the overall increased morbidity at the elderly age. Data related to complications in this population are limited. We performed a population-based study of elderly IBD patients to characterize complications compared with non -IBD matched individuals. Methods As part of the validated epidemiological cohort of the Israeli IBD Research Nucleus (epi-IIRN), we included all elderly-onset IBD patients (age at diagnosis >65 years) from the four Israeli health funds diagnosed from 1.1.2005 until 30.06.2020, covering 98% of the Israeli population. Each IBD case was matched at diagnosis to 3 non-IBD individuals by year of birth, sex, geographic district, and health fund. Comparison of incidence of pneumonia, osteoporotic fractures, bacteremia/septicemia and venous thromboembolism events were made. Time to complication was compared using the Kaplan-Meier survival analysis, stratified by IBD subtype, sex and any exposure of >3 months to immunosuppressive IBD medications. Cox proportional hazard models were sought to explore complications risk adjusted by comorbidities (chronic obstructive pulmonary disease, ischemic heart disease and other diseases). Results A total of 2,163 elderly-onset IBD patients were identified (46% males; 48% with Crohn’s disease, median (IQR) age at inclusion 71 [68, 76] years, exposure to >3 months of systemic CS 25%, thiopurines 10%, methotrexate 3.3%, anti-TNF 10.2%, Vedolizumab 5.7%, Ustekinumab 1.7%) and compared to 6,489 matched non-IBD controls. Median (IQR) follow-up time was 74 (40, 118) months. Incidence rates of pneumonia, fractures, bacteremia and venous thromboembolism are shown in table 1. On univariate analysis event-free survival analyses were similar in IBD and controls in pneumonia (p=0.72), osteoporotic fractures (p=0.79), bacteremia (p=0.085) and venous thromboembolism (p=0.14) Figure 1. Survival analysis remained similar when stratified by sex, IBD subtype and drug exposure. Using the comorbidity adjusted Cox model, the overall HR of pneumonia was 1.04 (95% CI 0.835-1.294), for osteoporotic fractures was 1.026 (95% CI 0.815-1.293); of bacteremia 2.161 (95% CI 0.865-5.397) and of venous thromboembolism 0.579 (95% CI 0.272-1.23). Conclusion In this population-based nation-wide study elderly onset IBD was not associated with increased risk of pneumonia, bacteremia, venous thromboembolism, and osteoporotic fractures compared with matched non-IBD elderly individuals. Studies in other populations are still needed to assess complications risk in diverse populations.

PO-684-02 LOWER RATE OF MAJOR BLEEDING IN HIGH-RISK PATIENTS UNDERGOING LEFT ATRIAL APPENDAGE OCCLUSION: A PROPENSITY MATCHED COMPARISON WITH DIRECT ORAL ANTICOAGULATION

The factor V Leiden mutation increases the risk of venous thrombosis in patients with inflammatory bowel disease

Risk stratification algorithms (RSAs) can reduce antibiotic duration (AD) and length of stay (LOS) for early-onset sepsis (EOS). Because of higher EOS and antibiotic resistance rates and limited laboratory capacity, RSA implementation may benefit low- and middle-income countries (LMIC). Our objective was to compare the impact of 4 RSAs on AD and LOS in an LMIC nursery. Neonates <5 days of age admitted for presumed sepsis to a Kenyan referral hospital in 2019 (n = 262) were evaluated by using 4 RSAs, including the current local sepsis protocol ("local RSA"), a simplified local protocol ("simple RSA"), an existing categorical RSA that uses infant clinical examination and maternal risk factors (CE-M RSA) clinical assessment, and the World Health Organization's Integrated Management of Childhood Illness guideline. For each RSA, a neonate was classified as at high, moderate, or low EOS risk. We used к coefficients to evaluate the agreement between RSAs and McNemar's test for the direction of disagreement. We used the Wilcoxon rank test for differences in observed and predicted median AD and LOS. Local and simple RSAs overestimated EOS risk compared with CE-M RSA and the Integrated Management of Childhood Illness guideline. Compared with the observed value, CE-M RSA shortened AD by 2 days and simple RSA lengthened AD by 2 days. LOS was shortened by 4 days by using CE-M RSA and by 2 days by using the local RSA. The local RSA overestimated EOS risk compared with CE-M RSA. If implemented fully, the local RSA may reduce LOS. Future studies will evaluate the prospective use of RSAs in LMICs with other interventions such as observation off antibiotics, biomarkers, and bundled implementation.

Background Inflammatory bowel disease (IBD) patients may have a higher risk of gastrointestinal bleeding during anticoagulant treatment due to mucosal erosions. Millions of patients worldwide receive classic oral anticoagulants or direct-acting anticoagulants (DOACs).The main indication is stroke prophylaxis in atrial fibrillation (AF), with an increasing prevalence in older age groups (8.5% of the Spanish population over 60 years old).Anticoagulants (especially DOACs) safety data are limited in IBD. Our objective was to evaluate the bleeding risk in IBD concerning these treatments. Methods A single-center retrospective study was conducted, collecting clinical characteristics, laboratory parameters and bleeding events. Bleeding risk was compared in two cohorts of IBD patients over 60 years old, treated with anticoagulants or not matched by age, sex, and type of IBD at a ratio of 2 controls for each anticoagulated case. We classified the severity of bleeding events as major or not according to the International Society on Thrombosis and Haemostasis criteria. Major bleeding is defined as fatal or symptomatic bleeding in a critical organ, with a decrease of 2 g/dL in hemoglobin or transfusion of 2 or more units. Chi-square test and Student's t-test were used to compare qualitative or quantitative variables respectively Results 186 subjects were analyzed (62 anticoagulated, 124 were not): 110 had ulcerative colitis (UC) and 76 Crohn's disease (CD). Baseline characteristics are described in Table 1. Of the 62 anticoagulated patients, 69% were on DOACs (26 apixaban,7 edoxaban,6 rivaroxaban,4 dabigatran)26% on classic oral anticoagulants and 5% on low molecular weight heparin. The main indication was AF (66%), followed by thrombosis (26%) and stroke (8%). No statistically significant differences were found in sex, age, location, behavior (CD), or extent of the disease, which was expected since controls were matched for these factors. There were 17 hemorrhagic events (9.1%) and 58,8% were major. The main bleeding cause was gastrointestinal (64.7%) followed by urinary (23.5%). Bleeding was significantly higher with anticoagulation (17.7 vs 4.8%, p=0.004) and specifically with NOACs (20.9 vs 4.8%; p=0.001). Analyzing only the bleeding cases, no statistically significant differences were found in the incidence of major bleeding, need for admission, iron therapy or transfusion with classic anticoagulants or NOACs, nor in hemoglobin or inflammatory parameters (Table 2). All cause mortality was higher in anticoagulated patients (19.4 vs 6.5%; p= 0.007); one case was 2º to digestive bleeding Conclusion IBD patients may have a higher risk of gastrointestinal bleeding during anticoagulant treatment (specifically DOACs), so they may require closer monitoring References -S. Schulman, C. Kearon. Subcommittee on Control of Anticoagulation of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis. Definition of major bleeding in clinical investigations of antihemostatic medicinal products in non-surgical patients. J Thromb Haemost., 3 (2005), pp. 692-694 http://dx.doi.org/10.1111/j.1538-7836.2005.01204.x | Medline -Cea-Calvo L, Redón J, Lozano JV, et al. Prevalencia de fibrilación auricular en la población española de 60 o más años de edad. Estudio PREV-ICTUS. Rev Esp Cardiol. 2007; 60: 616-24 -Gu ZC, Wei AH, Zhang C, Wang XH, Zhang L, Shen L, Li Z, Pan MM, Liu XY, Pu J, Lin HW. Risk of Major Gastrointestinal Bleeding With New vs Conventional Oral Anticoagulants: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. 2020 Apr;18(4):792-799.e61. doi: 10.1016/j.cgh.2019.05.056. Epub 2019 Jun 11. PMID: 31195162. -Viola A, Chiappetta MF, Scolaro M, Bignoli F, Versace A, Fries W. Direct oral anticoagulants increase the risk of anaemia and hospitalization in IBD patients with active intestinal disease. Dig Liver Dis. 2020 Dec;52(12):1525-1526. doi: 10.1016/j.dld.2020.08.033. Epub 2020 Sep 6. PMID: 32900651.

Cytokines and chemokines play an important role in inflammatory bowel disease (IBD) pathogenesis, as demonstrated by the efficacy of cytokine-targeted immunomodulatory therapy in treating IBD. The precise etiology of IBD is unknown, but disease pathogenesis clearly involves genetic, immunologic, and environmental factors. The current hypothesis for IBD etiology suggests that the disease is initiated and perpetuated by a dysregulated immune response to an unknown environmental antigen in a genetically susceptible host. A working hypothesis for the pathogenesis of Crohn's disease, the most debilitating form of IBD, is depicted in Fig. 1. In order to maintain gut homeostasis, the normal mucosal immune system must maintain a delicate balance between a network of proinflammatory and/ or inductive cytokines and anti-inflammatory and/or regulatory cytokines. During bacterial invasion the proinflammatory and inductive type I T-helper cell (Thl)-polarizing cytokines exert pleiotropic effects upon release from antigen-presenting cells (macrophages, dendritic ceUs, etc.) in the intestinal mucosa. Proinflammatory cytokines (i.e. interleukin [IL]-1, IL-6, and tumor necrosis factor [TNF]) activate immune cells in the lamina propria and stimulate intestinal epithelial cells (lEC) and macrophages to produce chemokines which, when secreted, estabUsh a chemotactic gradient across the intestinal mucosa, promoting leukocyte recruitment and extravasation across the intestinal endothelium. Meanwhile, Thlpolarizing cytokines (i.e. IL-12, IL-18, TNF) released from antigen-presenting cells (primarily macrophages) induce activation of naive intraepithelial and lamina propria T lymphocytes and Thl differentiation. These activated Thl cells release Thl cytokines (i.e. IL-2, interferon gamma [IFN-y], and lymphotoxin [LT]), which further perpetuate inflammatory and delayed hypersensitivity immune responses in the gut. In the normal gut mucosa this proinflammatory/ inductive immune response is kept in balance by a network of anti-inflammatory and regulatory cytokines. Regulatory cytokines (i.e. IL-10, IL-4, IL-5, IL-13, and transforming growth factor beta [TGFp]) are derived from many cellular sources within the intestine, including macrophages as well as type IIThelper (Th2) cells and type I T regulatory (Trl) cells. Along with anti-inflammatory cytokines (i.e. IL-1 receptor antagonist [IL-lra] and IL-11) derived primarily from lEC and macrophages, these Th2 cytokines serve to counterbalance the proinflammatory effects of Thl-mediated immune responses. For unknown reasons, patients with IBD cannot maintain normal gut homeostasis. An understanding of the cytokine network and its role in promoting IBD pathogenesis is a crucial step toward finding a cure for this devastating disease. This chapter provides an overview of the cytokines and chemokines that have been implicated in IBD, with specific focus on what is known about each cytokine in relation to IBD pathogenesis and treatment.

Inflammatory Bowel Disease (IBD) is a spectrum of chronic inflammatory diseases of the intestine that includes subtypes of ulcerative colitis (UC) and Crohn’s Disease (CD) and currently has no cure. While IBD results from a complex interplay between genetic, environmental, and immunological factors, sequencing advances over the last 10–15 years revealed signature changes in gut microbiota that contribute to the pathogenesis of IBD. These findings highlight IBD as a disease target for microbiome-based therapies, with the potential to treat the underlying microbial pathogenesis and provide adjuvant therapy to the emerging spectrum of advanced therapies for IBD. Building on the success of fecal microbiota transplantation (FMT) for Clostridioides difficile infection, therapies targeting gut microbiota have emerged as promising approaches for treating IBD; however, unique aspects of IBD pathogenesis highlight the need for more precision in the approach to microbiome therapeutics that leverage aspects of recipient and donor selection, diet and xenobiotics, and strain-specific interactions to enhance the efficacy and safety of IBD therapy. This review focuses on both pre-clinical and clinical studies that support the premise for microbial therapeutics for IBD and aims to provide a framework for the development of precision microbiome therapeutics to optimize clinical outcomes for patients with IBD.

e15621 Background: Thromboembolism (TE) accounts for significant morbidity and mortality in cancer patients. Rates of TE have been reported from 0.9%-28.0%, depending on the population. Patients with germ cell tumors have a 4.0-8.4% risk of TE following platin chemotherapy. Our patients are high-risk, many with advanced disease receiving high-dose chemotherapy and peripheral blood stem cell rescue. We sought to more completely understand TE events in advanced germ cell tumor patients. Methods: Forty-four consecutive patients visiting our germ cell tumor clinic between 11/05/2012 and 1/22/2013 were selected. Data were collected by retrospective chart review from tumor diagnosis until TE (ranging from TE on diagnosis to 20 years later). A logistic regression model was fitted to determine variables that predispose patients to TE. Results: In our patient series, seven (15.9%) had venous TE and none had arterial events. Five patients (11.4%) had TE within 16 weeks of chemotherapy, and 2 at 10 and 19 years after diagnosis, respectively. Two had bilateral pulmonary emboli (PE) (4.5%), 3 had upper or lower extremity DVTs, or both, and 1 had bilateral PE and DVTs. Five patients with TE had nonseminomatous tumors, 2 had non-testis primaries, 4 had relapsed disease, 2 with late relapse (&gt;7 years), 6 had metastatic disease, 3 had retroperitoneal lymph node dissection, and all 7 received platin chemotherapy. In logistic regression analysis, significant risk factors for TE included relapse (P= .016), bulky retroperitoneal lymphadenopathy (P= .006), alpha-fetoprotein &gt;10,000 (P= .047) beta-HCG &gt; 1,000 (P= .020), chemotherapy (P= .031), platin-refractory disease (P= .055), and poor risk disease compared to good risk disease (P=.020). Conclusions: Germ cell tumor patients have a high risk of venous TE. Those with relapsed disease, bulky retroperitoneal lymphadenopathy, platin chemotherapy, platin-refractory, or poor risk disease are at increased risk. Our estimates are higher than previously reported and in contrast to earlier studies, do not include arterial TE. To confirm our findings, we will extend this study to 100 patients. If confirmed, this pattern of TE events may be a consequence of advanced stage disease in our patients.

Inflammatory bowel disease (IBD) is an idiopathic inflammatory, relapsing and life threatening disorder affecting the gastrointestinal tract (GIT). The most common forms of IBD are Crohn's disease (CD) ulcerative colitis (UC) and colorectal cancer. The incidence or prevalence of IBD are increasing worldwide but is highest in the industrialized and western populations. The pathogenesis of IBD includes the various factors like environmental, immunological and genetic factors. These factors are mainly affected the gastrointestinal tract of the person based on our daily life. It causes the mild, moderate and severe inflammation in the intestine lead to IBD. In current, the diagnosis is most important technique to detect the type of IBD and helps to identify UC and CD. The diagnostic technique involves the endoscopy (capsule endoscopy, computed tomographic enterography, ileocolonoscopy etc), device assisted enteroscopy (a novel technique) and laboratory analysis (erythrocytes sedimentation rate and C-reactive protein). The therapeutic drugs such as aminosalicylates, corticosteroids, antibiotics and immunomodulators are still used to manage IBD in some extent. Thus, IBD remain challenges and need better therapeutic approach for its management.

Background The association between inflammatory bowel disease (IBD) and venous thromboembolism (VTE) is well-studied in the adult population. However, in paediatric-onset IBD (PIBD; &amp;lt; 18 years) data are scarce. Most studies are limited in size, as pointed out by the recently published ESPGHAN-ECCO guidelines for the treatment of paediatric acute severe ulcerative colitis. Several studies have indicated an increased risk of cerebral venous sinus thrombosis (CSVT). Assessing the risk among children and adolescents across clinical characteristics is crucial to guide clinical decisions about prophylactic treatment. Methods We used data from nationwide population-based registers to identify patients diagnosed with PIBD in Denmark (1996-2022) and Sweden (2006-2023). Patients with PIBD were matched on the date of first IBD diagnostic listing with up to 10 reference individuals from the general population by age, sex, and place of residence. Occurrence of VTE was compared in absolute (incidence rate difference, IRD) and relative terms (hazard ratios, HR) with 95% confidence intervals (95%CI). Data from Denmark and Sweden were combined using random effects meta-analyses. Comparisons included VTE overall, by VTE subtypes, sex, age, IBD subtypes, and time since diagnosis; and in the data from Sweden only, by disease activity (steroid prescriptions or addition/change of immunomodulators or advanced therapies, hospitalisation or surgery for IBD) and hospitalisation. Results We included 4,009 (Denmark) + 6,781 (Sweden) patients with PIBD and 39,096 + 64,497 reference individuals. Median follow-up time was 9.6 and 8.9 years, respectively. The incidence rate of VTE among patients with IBD was 1.3 per 1,000 person-years (95%CI: 1.1-1.5), and 0.4 (95%CI: 0.2-0.7) among reference individuals, with an IRD of 0.9 (95%CI: 0.7-1.2) per 1,000 person-years and an HR of 3.3 (95%CI: 1.8-6.3) (Table 1). The HR within the first 2 years of IBD was 18.8 (95%CI: 10.3-34.1). While CSVT and other thrombotic events had the highest HRs among VTE subtypes, the absolute risk of CSVT was low, at 1 per 10,000 person-years. In Sweden, disease activity, and hospitalisation, particularly hospitalisation for IBD, were strongly associated with VTE. Conclusion PIBD was associated with a substantially increased relative risk of VTE compared to the general population, although the absolute risk, including that for CSVT, was very low. Clinicians should carefully consider the risk of VTE in this population, in particular early on in the disease course, and during disease activity and hospitalisation. Conflict of interest: Dr. Bröms, Gabriella: Dr Bröms has served as a speaker for Takeda and Janssen and worked on projects at Karolinska Institute, partly financed by Janssen, Pfizer and UCB, unrelated to this study. Trudu, Beatrice: None. Modin, Frederikke Agerbo: None. Moshtaghi-Svensson, John: None. Burisch, Johan: Dr. Burisch reports grants from AbbVie, Janssen-Cilag, MSD, Takeda, Tillots Pharma, Bristol Myers Squibb, and Novo Nordisk Foundation personal fees from AbbVie, Janssen-Cilag, Celgene, MSD, Pfizer, Takeda, Tillots Pharma, Bristol Myers Squibb, Samsung Bioepis, Pharmacosmos, Ferring, Galapagos, Eli Lilly, Dr Falk Pharma, Celltrion, Zealand Pharma and Orion Pharma. Forss, Anders: Served as speaker/advisory board member for Janssen Cilag AB, Pfizer and Tillotts Pharma. Jansson, Sabine: Dr Jansson has received travel support from Ferring Pharmaceuticals and research grants from Takeda Pharma A/S, and Ferring Pharmaceuticals. Unrelated to the work submitted. Ludvigsson, Jonas: Dr Ludvigsson has received financial support from Merck/MSD for a study on inflammatory bowel disease and fibrosis and for developing a paper reviewing national healthcare registers in China. Dr Ludvigsson also has an ongoing research collaboration on celiac disease with Takeda. Earlier support includes a grant from Janssen for an unrelated study on behalf of the Swedish IBD quality register (SWIBREG). Mårild, Karl: Dr Mårild has received payment for two lectures for Pfizer Osooli, Mehdi: Dr Osooli participated in projects at Karolinska institute partly financed by pharmaceutical companies. All unrelated to this study. de Ridder, Lissy: Non-financial Support: Pfizer Other: Abbvie, Pfizer, Janssen, Eli Lilly, Takeda, Medtronic, Alvotech Wewer, Vibeke: None. SWIBREG Study Group, Swibreg: None Malham, Mikkel: None. Olen, Ola: Dr Olén has led projects at Karolinska Institutet financed by grants from Pfizer, Janssen, Alfasigma, AbbVie, Takeda, Bristol Myers Squibb, and Ferring. OO has served as speaker for lectures organized by Janssen, Pfizer, Takeda, and Bristol Myers Squibb.

Safety of Vitamin K Antagonist Treatment for Splanchnic Vein Thrombosis: A Multicenter Retrospective Cohort Study