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ABSTRACT Background Venous thromboembolic events (VTEs) are the second‐leading cause of death in cancer patients, with an incidence of 5%–17% in lymphoma patients, particularly higher in those with non‐Hodgkin lymphoma (NHL). Existing risk assessment models (RAMs) like the Khorana and ThroLy scores have limitations and are inadequately validated for NHL patients. Coagulation markers such as D‐dimer, thrombin–antithrombin complex (TAT), and thrombomodulin (TM) show a potential predictive value for cancer‐associated VTE but lack extensive research in NHL. Objectives This study aimed to analyze characteristics and predictive risk factors for VTE in newly diagnosed NHL patients and to evaluate and improve the clinical applicability of the Khorana and ThroLy scores. Methods Data were collected from newly diagnosed NHL patients to analyze characteristics and potential predictive risk factors for VTE. The clinical applicability of the Khorana and ThroLy scores was evaluated, and the ThroLy score was improved by adjusting the hemoglobin cutoff and combining it with D‐dimer testing. Sequential testing with TM and TAT levels was also performed. Results VTE developed in 7.09% of NHL patients. Independent risk factors for VTE included clinical Stage III/IV, mediastinal involvement, history of VTE, D‐dimer≥ 1345 μg/dL, and platelet (PLT)≥ 298 × 109, and Hb≥ 110 g/L was an independent protective factor for VTE. The ThroLy score was improved by adjusting the hemoglobin cutoff and combining it with D‐dimer testing. Sequential testing of TM and TAT achieved a sensitivity of 66.7%, specificity of 100%, positive predictive value (PPV) of 100%, and negative predictive value (NPV) of 96.7%. Conclusions VTE is a significant complication in NHL patients. The study highlighted independent risk factors and proposed a modified risk assessment model that effectively predicted VTE risk, potentially optimizing prevention and reducing healthcare costs.

Abstract Objective The causal association between osteoarthritis (OA) and bladder cancer remains unclear. This Mendelian randomization (MR) study was carried out to assess the potential causal effects of any OA, knee OA and hip OA, and bladder cancer. Method Genome‐wide association study (GWAS) summary data for OA and bladder cancer were obtained in GWAS CATALOG, UK Biobank, and FinnGen Consortium. Inverse‐variance weighted (IVW) approach was primarily conducted to evaluate the causal relationships between OA and bladder cancer, and MR‐Egger intercept and Cochran's Q test were mainly used to estimate heterogeneity and pleiotropy. MR‐PRESSO was used to test the presence of horizontal outliers. Leave‐one‐out analysis was utilized to ensure the reliability of the results. Results A higher genetic predisposition to any OA has a causal association with bladder cancer risk, while neither knee OA nor hip OA is causally linked to bladder cancer. MR‐Egger intercept analysis exhibited that any OA and knee OA had no pleiotropic effect on the risk of bladder cancer, and Cochran's Q test showed that any OA, knee OA and hip OA had no heterogeneity on bladder cancer risk. Neither MR PRESSO analysis nor leave‐one‐out analysis revealed any outlier SNPs. Conclusions This MR study exhibited a positive cause‐and‐effect relationship between any type of OA and bladder cancer risk, but not between site‐specific OA, knee OA and hip OA, and bladder cancer. Attention should be paid to the screening and prevention of bladder cancer in OA patients at any site.