Patients with non-small cell lung cancer (NSCLC) are at high risk of venous thromboembolism (VTE), especially during chemotherapy. Even though the contact system is implicated in the pathogenesis of thrombosis, limited data are available on the role of contact system activation in NSCLC-associated VTE.

In a prospective cohort of patients with NSCLC starting chemotherapy, contact system activation and thrombin generation biomarkers were assessed in relation to 6-month VTE occurrence and mortality.

Prechemotherapy plasma samples of 719 newly diagnosed patients with NSCLC were tested for in vivo biomarkers of contact system activation (ie, kallikrein [pKa]:antithrombin [AT; PKa:AT], activated factor [F]XI:AT [FXIa:AT], FXIa:C1-esterase inhibitor C1Inh [FXIa:C1Inh], activated FIX:AT [FIXa:AT]), and thrombin generation (ie, prothrombin fragment 1+2 [F1+2] and thrombin-antithrombin complex [TAT]). Clinical data, VTE, and mortality were recorded prospectively.

The 6-month VTE and mortality cumulative incidences were 11% and 27%, respectively. Basal levels of FXIa:AT complexes, F1+2, and TAT were higher in patients who developed VTE than those in VTE-free patients. Differently, PKa:AT, FIXa:AT, and TAT were lower in survivors than those in nonsurvivors. The multivariable analysis identified FXIa:AT (subdistribution hazard ratio, 1.17; 95% CI, 1.00-1.37) and TAT (subdistribution hazard ratio, 1.28; 95% CI, 1.10-1.50) as VTE-independent risk factors during chemotherapy. A score based on these biomarkers was generated, which was able to discriminate patients at significantly higher rates of VTE and mortality.

Elevated in vivo contact pathway activation and thrombin generation were observed in patients with NSCLC who developed VTE. Furthermore, a score based on both FXIa:AT and TAT levels was developed to identify those patients at higher risk of VTE and mortality.

Mounting evidence indicates that lung adenocarcinoma (LUAD) patients are at elevated risk for venous thromboembolism (VTE), presenting a major clinical challenge. This study utilized public databases to identify crosstalk genes (CGs) between LUAD and VTE, applied machine learning methods to discover shared diagnostic biomarkers, and explored their underlying mechanisms.

Disease-specific genes for VTE were extracted from comprehensive genomic databases (CTD, DisGeNET, GeneCards, OMIM), while transcriptomic profiles of LUAD and VTE cohorts were retrieved from GEO via GEOquery implementation. Molecular crosstalk analysis identified candidate genes through differential expression algorithms and disease-association metrics. Functional annotation employed GO and KEGG analyses to elucidate the biological significance of identified CGs. LASSO regression analysis of VTE and LUAD matrices yielded overlapping diagnostic biomarkers. Immune contexture was characterized via CIBERSORT deconvolution, followed by correlation analyses between hub genes and immune infiltration profiles. Hub genes expression was corroborated through independent cohort validation and serological quantification. Diagnostic utility was evaluated through receiver operating characteristic (ROC) curve and nomogram. Therapeutic potential was assessed via DSigDB-based drug sensitivity profiling.

Through transcriptomic analysis, we identified 381 CGs, which demonstrated significant enrichment in inflammatory cascades, immunological processes, and coagulation pathways. LASSO regression analysis of LUAD and VTE cohorts revealed TIMP1 and TMEM132A as putative shared diagnostic biomarkers. TMEM132A exhibited significant correlation with immune cell infiltration patterns across both diseases, modulating the immune microenvironment. Validation cohorts and serological assessment confirmed elevated TMEM132A expression in LUAD and LUAD combined with VTE phenotypes. The diagnostic accuracy of TMEM132A was substantiated by ROC curves and nomogram analyses. Pharmacological sensitivity analysis indicated that TMEM132A may serve as a potential target for the therapeutic agents birabresib and abemaciclib.

TMEM132A demonstrates diagnostic utility as a predictive biomarker for VTE occurrence in LUAD, suggesting its potential role as a susceptibility gene in this patient cohort.

Fibrinogen has been associated with a variety of malignancies, including colorectal cancer (CRC). However, there is no study on the relationship between fibrinogen and CRC specifically in the Chinese population. The objective of this study was to analyze the relationship between fibrinogen and CRC in the Chinese population. This study included consecutive inpatients undergoing colonoscopies (April 2015‒June 2022). A total of 3,595 individuals, comprising 468 CRCs and 3,127 controls, were included. Logistic regression models and restricted cubic spline analysis were employed to assess the association between fibrinogen and CRC. When fibrinogen levels were divided into quartiles, the ORs for CRC in Q2, Q3, and Q4 compared to Q1 were 2.72 (95% CI: 1.57-4.74), 4.84 (95% CI: 2.84-8.25), and 9.55 (95% CI: 5.55-16.43), respectively. Restricted cubic spline analysis identified a non-linear association between fibrinogen levels and CRC risk with a threshold of 3.794 (95% CI: 3.747-3.841) g/L. Below this threshold, the CRC risk significantly increased (OR 5.944, 95% CI 4.084-8.65, P < 0.001). These findings may offer new insights for the diagnosis and management of CRC.

Atrial fibrillation is the most common cardiac arrhythmia and is a major risk factor for ischemic stroke. Atrial fibrillation and ischemic stroke are major cardiovascular complications in cancer patients, who have a higher burden and worse outcomes than the general population. Clinical risk stratification scores for stroke and bleeding, commonly used in the general population to estimate thromboembolic and bleeding risk, respectively, are less well validated in cancer patients, who have historically been excluded in clinical trials. There is a lack of consensus opinion on how to effectively risk-stratify cancer patients based on the currently available tools and a need for cancer-specific scores that offer a tailored approach to each patient in order to more effectively stratify ischemic stroke and bleeding risk in this cohort of patients. Cancer-mediated physiologic changes and adverse effects of antineoplastic therapy have been implicated as etiologies of the increased risk for both atrial fibrillation and ischemic stroke. Risk stratifying scores such as CHA2DS2-VASc and HAS-BLED, commonly used in the general population, are less well validated in cancer patients. There is a need for cancer-specific scores that can more effectively stratify ischemic stroke and bleeding risk in cancer patients, although given the heterogeneity of cancers, whether a "one score fits all" is uncertain.

The aim of this study was to determine the risk factors associated with deep vein thrombosis (DVT) or pulmonary embolism (PE) within 30 days after multilevel adult spinal deformity (ASD) surgery and to develop risk prediction models.

A retrospective observational study was conducted using the American College of Surgeons National Surgical Quality Improvement Program database from 2010 to 2019. Current Procedural Terminology (CPT) codes 22843 and 22844 were used to query the database and to identify patients who underwent surgical correction of ASD with ≥7 levels of posterior instrumentation. The primary outcomes were the incidences of, and risk factors for, postoperative DVT and PE. Multiple logistic regression was utilized to identify variables associated with an elevated risk of DVT or PE within 30 days after surgery and to develop prediction models for assessing risk.

A total of 7,445 patients (56% female; 73% Caucasian; mean age, 61 years) met the inclusion criteria. Postoperatively, the rate of any venous thromboembolism (VTE; i.e., DVT or PE) was 3.4% (254 patients), the rate of DVT was 2.0% (151 patients), and the rate of PE was 1.7% (127 patients). The following independent predictors of any VTE were identified: weight (odds ratio [OR], 1.054; 95% confidence interval [CI]: 1.027 to 1.081), age per decade of life (OR, 1.106; 95% CI: 1.012 to 1.209), body mass index (BMI; OR, 1.032; 95% CI: 1.015 to 1.049), medicated hypertension (OR, 1.523; 95% CI: 1.168 to 1.987), chronic corticosteroid use (OR, 2.654; 95% CI: 1.848 to 3.812), American Society of Anesthesiologists (ASA) class (OR, 1.768; 95% CI: 1.426 to 2.192), and total operative time (OR, 1.002; 95% CI: 1.002 to 1.003) (p < 0.05 for all). When incorporated into a single model, total operative time, BMI, ASA class, and chronic corticosteroid use were associated with VTE risk.

Four major risk factors were identified as being associated with postoperative VTE risk in patients undergoing surgery for ASD. Corticosteroid use for a chronic medical condition was the strongest predictor of VTE risk, followed by ASA class, BMI, and operative time. Knowledge of these risk factors can aid in preoperative risk assessment, informed consent, and medical decision-making, such as in determining the clinical thresholds for VTE testing and chemoprophylaxis.

Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.

There is active crosstalk between tumor cells and the tumor microenvironment during metastatic progression, a process that is significantly affected by obesity, particularly in breast cancer. Here we analyze the impact of a high fat diet (HFD) on metastasis, focusing on the role of platelets in the formation of premetastatic niches (PMNs). We find that a HFD provokes pre-activation of platelets and endothelial cells, promoting the formation of PMNs in the lung. These niches are characterized by increased vascular leakiness, platelet activation and overexpression of fibronectin in both platelets and endothelial cells. A HFD promotes interactions between platelets, tumor cells and endothelial cells within PMNs, enhancing tumor cell homing and metastasis. Importantly, therapeutic interventions like anti-platelet antibody administration or a dietary switch reduce metastatic cell homing and outgrowth. Moreover, blocking fibronectin reduces the interaction of tumor cells with endothelial cells. Importantly, when coagulation parameters prior to neoadjuvant treatment are considered, triple negative breast cancer (TNBC) female patients with reduced Partial Thromboplastin time (aPTT) had a significantly shorter time to relapse. These findings highlight how diet and platelet activation in pre-metastatic niches affect tumor cell homing and metastasis, suggesting potential therapeutic interventions and prognostic markers for TNBC patients.

There is a well-established relationship between cancer and venous thromboembolism (VTE). Thrombosis in cancer is of major concern as it is a leading cause of mortality, impairs quality of life, and can adversely impact treatment protocols. Despite the role of thrombosis in cancer, no singular source consolidates data on VTE incidence by cancer type worldwide. This systematic review aims to report the incidence of VTE by type of solid cancer worldwide. The current analysis used three databases (MEDLINE, Embase, Cochrane Library) to identify relevant articles. All articles were written in English, assessed solid cancers in adults (≥18; males, females), and reported the incidence of VTE, or information that could be used to calculate incidence. After completing the search and removing duplicates, 3077 articles were assessed. All articles were screened by title and abstract, followed by a full-text review. A total of 124 articles were included in the final evaluation. The cumulative reported incidence of VTE across all types of solid cancer was 9.74 %. The highest reported incidence of VTE was in gastroesophageal cancer (15.43 %), whereas the lowest incidence was in prostate cancer (1.58 %). The two most reported cancers by country within our study cohort were colorectal (n = 23) and lung cancer (n = 23). The reported incidence of VTE in colorectal cancer was highest in Mexico (22.10 %), and lung cancer was highest in Canada (32.91 %). In conclusion, gathering data on global VTE rates in solid cancer identified high-risk cancers and highlighted under-investigated areas that require attention to reduce VTE occurrence in cancer patients.

Children and adolescents with Hodgkin lymphoma (HL) are susceptible to developing venous thromboembolism (VTE) due to several predisposing factors such as cancer itself, central venous catheter use, mediastinal mass, and glucocorticoid therapy, yet reports on the topic are scarce.

To study incidence, risk factors, and treatment of VTE, and the use of thromboprophylaxis, in a retrospective clinical study on pediatric HL.

Children under 18, diagnosed with HL 2005-2019 in Sweden, Denmark, and Finland were included. Data on patient characteristics, treatment, thrombotic events and follow up were collected from patients' medical records.

A total of 490 children were identified and data were assessed for 489. The cumulative 2-year incidence of VTE was 8.1 % (42/489). Older age at diagnosis (p = 0.004), mediastinal involvement (p = 0.024), and HL stage III + IV (p = 0.036) were significant risk factors for VTE. Children over 15 with mediastinal mass and HL stage III or IV had a 1-year cumulative incidence of VTE of 18 % and a nearly three-fold risk of developing VTE compared to all other patients (OR 2.94, 95 % CI 1.47-5.88, p = 0.002). The majority (39/42; 92.9 %) were treated with low-molecular-weight heparin. Four (9.5 %) patients developed post-thrombotic syndrome. Thromboprophylaxis was given to 18/489 (3.7 %) patients with HL, two of whom developed VTE.

VTE is a common complication in adolescents treated for HL with large tumor burden at diagnosis. Prospective studies should focus on identifying patients who would benefit from thromboprophylaxis.

Coagulation status is closely related to the progression of malignant tumors. In the era of neoadjuvant immunochemotherapy (NICT), the prognostic utility of coagulation indicators in patients with locally advanced gastric cancer (LAGC) undergoing new treatments remains to be determined.

To determine whether hypercoagulation is an effective prognostic indicator in patients with LAGC who underwent radical resection after NICT.

A retrospective analysis of clinical data from 104 patients with LAGC, who underwent radical resection after NICT between 2020 and 2023, was performed. D-dimer and fibrinogen concentrations were measured one week before NICT, and again one week before surgery, to analyze the association between these two indicators and their combined indices [non-hypercoagulation (D-dimer and fibrinogen concentrations within the upper limit of normal) vs hypercoagulation (D-dimer or fibrinogen concentrations above the upper limit of normal)] with prognosis. After radical resection, patients were followed-up periodically. The median follow-up duration was 21 months.

Data collected after NICT revealed that the three-year overall survival (OS) and disease-free survival (DFS) rates the non-hypercoagulation group were significantly better than those in the hypercoagulation group [94.4% vs 78.0% (P = 0.019) and 87.0% vs 68.0% (P = 0.027), respectively]. Multivariate analysis indicated that hypercoagulation after NICT was an independent factor for poor postoperative OS [hazard ratio (HR) 4.436, P = 0.023] and DFS (HR 2.551, P = 0.039). Pre-NICT data demonstrated no statistically significant difference in three-year OS between the non-hypercoagulation and hypercoagulation groups (88.3% vs 84.1%, respectively; P = 0.443).

Hypercoagulation after NICT is an effective prognostic indicator in patients with LAGC undergoing radical gastrectomy.

Patients with solid organ cancers are at increased risk of developing cancer-associated thrombosis (CAT), a complication driven by a complex interplay of patient-specific factors, cancer characteristics, and treatment modalities. Data on CAT and its associated risk factors within diverse ethnic groups, such as the Malaysian population, remains limited. This observational, cohort study aimed to address this gap by determining the incidence of CAT and identifying associated risk factors among multi-ethnic Malaysian patients with solid organ cancers.

This study included solid organ cancer patients aged ≥ 18 who attended HCTM and HKL from May 2022 to August 2023. The baseline demographics, and clinical characteristics, were acquired at the cancer diagnosis. Data on cancer treatment, thrombotic events and anticoagulation therapy during the study and its treatment were documented. Multivariable logistic regression analysis was performed to determine the independent factors associated with CAT in solid organ cancer.

A total of 250 solid organ cancer patients were included, with a mean age of 57.7 (13.7) years. This multi-ethnic cohort consisted of mostly Malay patients (55.2%), followed by Chinese (33.2%) and Indian & others (11.6%). The prevalence of CAT at baseline was 4.8%, while the incidence of CAT during follow-up was 12%. Poor performance status and obesity were associated with CAT at baseline. Univariable logistic regression showed platelets ≥ 450 × 109/L and Khorana score ≥ 3 had significantly higher risks of CAT at baseline. Stage IV disease, radiotherapy and chemotherapy, namely platinum-based chemotherapy and antimetabolites were associated with CAT during follow-up. The ROC analysis showed that the KRS significantly predicted CAT (area under the curve, 0.701 (95%CI: 0.594-0.808, p = 0.001).

This study highlights the prevalence of CAT at baseline and the incidence of CAT during follow-up, similar to other studies. Patients' clinical characteristics were associated with CAT at baseline while disease and treatment factors were associated with CAT at follow-up. These findings emphasise the need for targeted thromboprophylaxis in high-risk populations and highlight the importance of risk stratification tools such as the Khorana score for optimal patient management. Future studies involving larger patient cohorts and longer study duration would be beneficial. These findings provide valuable insights to inform clinical decision-making, optimise patient outcomes, and minimise potential risks.

Transcatheter aortic valve replacement (TAVR) is an alternative to surgical aortic valve replacement (SAVR) for high-risk patients with severe aortic stenosis (AS). However, the clinical outcomes and prognostic implications of TAVR in patients with active cancer remain uncertain. This meta-analysis evaluates procedural success, complications, and survival outcomes of TAVR in patients with and without active cancer.

A comprehensive literature search was conducted across PubMed, Scopus, and Web of Science databases. Statistical analysis was performed using a random-effects model. Statistical analyses were conducted using STATA version 18.0.

The results of the meta-analysis showed no significant difference in in-hospital mortality between cancer and non-cancer patients (OR = 1.17; 95% CI: 0.83, 1.65; p = 0.27). Similarly, 30-day mortality did not differ between the two groups (OR = 0.93; 95% CI: 0.72, 1.19; p = 0.49). However, 1-year mortality was significantly higher in cancer patients (OR = 1.93; 95% CI: 1.45, 2.56; p < 0.01). Two-year mortality was also higher in cancer patients (OR = 2.65; 95% CI: 1.79, 3.93; p < 0.01). No significant differences were observed in major bleeding, acute kidney injury, stroke, or permanent pacemaker implantation between the groups.

While TAVR offers comparable in-hospital and short-term survival outcomes for cancer and non-cancer patients, long-term mortality is significantly higher in those with active cancer. These findings suggest that TAVR is a viable option for cancer patients with severe AS but requires careful long-term prognostic considerations. Further studies are needed to optimize management strategies for this complex population.

Coagulation disorders are increasingly recognized as significant complications in patients with solid tumors, affecting morbidity and mortality outcomes. Solid tumors can provoke a hypercoagulable state through the release of pro-coagulant factors, endothelial activation, and inflammation, leading to a heightened risk of coagulation disorders. These coagulation disorders may manifest as venous thromboembolism, arterial thromboembolism, thrombotic microangiopathy, or disseminated intravascular coagulation. These disorders can complicate surgical interventions and impact treatments, including chemotherapy and immunotherapy efficacy, leading to poor outcomes. Understanding the implications of coagulation disorders in solid tumors is essential for optimizing patient management, including identifying high-risk patients, implementing prophylactic measures, elucidating biomarkers for clinical outcomes, and exploring novel therapeutic agents. This review aims to provide insights into the current knowledge surrounding coagulation disorders in solid tumors and their clinical implications.

This study aimed to evaluate the effect of low molecular weight heparin calcium (LMWH-Ca) on the prevention of deep venous thrombosis (DVT) in patients with anterolateral thigh (ALT) flap reconstruction.

In total, 1001 patients with oral cancer who underwent ALT flap reconstruction were recruited. Based on the postoperative use of LMWH-Ca, the patients were divided into case (n = 633) and control groups (n = 368). The incidence of postoperative DVT was compared between groups.

There was no significant difference in DVT incidence between the two groups. Among patients older than 60 years, the incidence of lower limb DVT in the case group (0.813%) was significantly lower than that in the control group (8.108%, p = 0.012).

The postoperative use of LMWH in oral cancer patients with ALT flap transfer does not prevent the development of lower limb DVT. However, patients older than 60 years old benefited from the postoperative use of LMWH-Ca.

The management and treatment of tumor complications pose continuous challenges due to the inherent complexity. However, the advent of drug delivery systems (DDSs) brings promising opportunities to address the tumor complications using innovative technological approaches. This review focuses on common oncological complications, including cancer thrombosis, malignant serous effusion, tumor-associated infections, cancer pain, and treatment-related complications. Emphasis was placed on the application and potential of DDSs in mitigating and treating these tumor complications, and we delved into the underlying mechanisms of common cancer-associated complications, discussed the limitations of conventional treatments, and outlined the current status and potential development of DDSs for various complications in this review. Moreover, we have discussed the existing challenges in DDSs research, underscoring the need for addressing issues related to biocompatibility and targeting of DDSs, optimizing drug delivery routes, and enhancing delivery efficiency and precision. In conclusion, DDSs offer promising avenues for treating cancer complications, offering the potential for the development of more effective and safer drug delivery strategies, thereby improving the quality of life and survival rates of cancer patients.

Glioma is a malignancy with challenging clinical treatment and poor prognosis. Platelets are closely associated with tumor growth, propagation, invasion, and angiogenesis. However, the role of platelet-related genes in glioma treatment and prognosis remains unclear.

A prognostic risk model was established using nine platelet-related prognostic signature genes (CAPG, CLIC1, GLB1, GNG12, KIF20A, PDIA4, SULF2, TAGLN2, and WEE1), and the risk score of samples were calculated. Subsequently, the glioma samples were divided into high- and low-risk groups based on the median values of risk scores. scRNA-seq analysis revealed that the prognostic genes were primarily located in astrocytes and natural killer cells. The immune infiltration proportions of most immune cells differed significantly between high- and low-risk groups. Moreover, we found AZD7762 as a potential candidate for glioma treatment.

Nine platelet-related prognostic genes identified as prognostic signatures for glioma were closely associated with the TME and may aid in directing the clinical treatment and prognosis of gliomas.

This review aims to elucidate the bidirectional relationship between heart failure and cancer by identifying their common and reciprocal risk factors. It seeks to provide a comprehensive understanding of the mechanistic interactions between these two conditions, supported by evidence from preclinical and clinical investigations.

A thorough review of peer-reviewed articles was conducted to identify all possible interactions between cancer and heart failure. Multiple search engines were utilized with queries incorporating terms such as cardio-oncology, heart failure, cancer, risk factors, and mechanistic interactions. Selected studies were analysed to identify shared risk factors and to explore the mechanistic junctions that link the two diseases.

The review identified several common risk factors, including, inflammation, smoking, obesity, clonal haematopoiesis of indeterminate potential, and reduced exercise potential. The pathophysiological mechanisms linking heart failure with cancer include metabolic reprogramming in cancer, cancer-induced thrombosis, cardiac metastasis, paraneoplastic syndrome, cancer-associated cachexia, and anorexia. Additionally, it was found that cancer therapies, such as anthracyclines and radiation, can induce cardiotoxicity, leading to heart failure. The pathophysiological mechanisms that contribute to cancer in heart failure patients were identified as neurohormonal activation, state of hypoxia, secretion of Cardiokines, heart failure medication, innate immune reprograming & cardiac remodelling and coronary atherosclerotic disease.

By highlighting the interconnected nature of heart failure and cancer, this review promotes a cardio-oncologic discourse, encouraging cardiologists and oncologists to consider these diseases as interrelated rather than separate entities. This perspective can lead to the development of novel therapeutic strategies and improve patient management by addressing the dual disease burden. Future research should focus on exploring the translational potential of existing drugs and developing new interventions to target the shared characteristics of heart failure and cancer.

The relationship between thrombosis and cancer is based on evidence that cancer promotes prothrombotic changes in the host hemostatic system. The activation of blood coagulation is closely linked to tumor growth and dissemination.

To evaluate whether quantifications of plasma circulation tumor deoxyribonucleic acid (DNA) and thrombin-antithrombin complex could act as predictors for thrombotic events and death in patients with gastric or colorectal adenocarcinomas, while also evaluating the Karnofsky Performance Status.

Eighty-two patients were included in the study and divided into three groups: controls (n=20), gastric adenocarcinomas (n=21), and colorectal adenocarcinomas (n=41). In order to calculate the Karnofsky index, information was collected to measure the patient's ability to perform common daily tasks. The following serum measurements were conducted: complete blood count, platelet count, extracellular deoxyribonucleic acid, and thrombin-antithrombin complex.

Ten patients (16%) experienced thrombosis during treatment. Patients with thrombin-antithrombin complex levels greater than 0.53 had a five-times higher risk of thrombosis. Lower Karnofsky Performance Status was also a risk factor for the event in this population. Neither thrombin-antithrombin complex nor plasma circulation tumor DNA were predictors of death after multivariate adjustment. Thus, Karnofsky index signaled a better overall survival prognosis for colorectal and gastric adenocarcinoma patients.

Thrombin-antithrombin complex acts as a marker for thrombosis in patients with colorectal and gastric adenocarcinomas. We recommend prophylactic anticoagulation when the Karnofsky value is low and/or the thrombin-antithrombin complex concentration is greater than 0.53 ng/ml.

Tumor imaging represents an ideal environment for collecting novel biomarkers from different technologies, as patients with tumors often undergo multiple imaging studies.With the aging of the Chinese population, the number of elderly patients with gastric cancer is also increasing. In the past, patients with gastric cancer in the elderly have been conservative in whether surgical treatment can be performed, and advanced age is regarded as a relative contraindication to the effect of surgical treatment on gastric cancer patients. To investigate the clinical characteristics of patients with upper gastrointestinal hemorrhage complicated by deep vein thrombosis in elderly patients with gastric cancer. One patient with upper gastrointestinal hemorrhage complicated by deep venous thrombosis, and elderly gastric cancer patients admitted to our hospital on 11 October 2020, were selected. After anti-shock symptomatic support, filter placement, prevention and treatment of thrombosis, gastric cancer eradication, anticoagulation, immune regulation, etc. Treatment and long-term follow-up observation. Long-term follow-up showed that the patient's condition was stable, there was no sign of metastasis or recurrence after radical gastrectomy for gastric cancer, and there were no serious pre- and post-operative complications such as upper gastrointestinal bleeding and deep vein thrombosis, and the prognosis was satisfactory. How to choose the appropriate operation timing and method for elderly gastric cancer patients with upper gastrointestinal bleeding and deep vein thrombosis at the same time to maximize benefits, clinical experience in this area is particularly valuable.

Patients with malignant tumors are prone to present hypercoagulability of blood and form thrombosis, and its pathogenesis is complex involving various factors from clinical and histopathological to genetic influences. Current studies on the potential mechanism of blood hypercoagulability in patients with malignant tumors focus on the following aspects but are not limited: (1) tumor cells release coagulant-promoting substances, (2) tumor cells interact with the fibrinolytic system, (3) tumor cell-mediated platelet activation, (4) tumor-associated complement activation, and (5) genetic factors and clinical factors. Especially, the pathogenesis of blood hypercoagulability is in-depth analyzed covering tumor cells' release of procoagulant substances, the interplay of cancer cells and fibrinolytic system, platelet activation mediated by cancer cells, cancer-associated complement activation, and the action of genetic and clinical factors. We review the pathogenesis of blood hypercoagulability in patients with malignant tumors, which will assist in the research and development of new drugs and providing theoretical support for the formulation of the best treatment plan for patients, to prolong the survival of patients.

This paper present a challenging case of a right ventricular mass in a patient who was at high surgical risk for open removal. The minimally invasive AngioVac device has been used with a successful 50% reduction in mass burden. This report illustrates AngioVac as a safe alternative to invasive surgery.

This study reviews and meta-analysis factors affecting mortality in older adult trauma patients, addressing previously unidentified heterogeneity and risk burden.

Databases (PubMed, Embase, Cochrane and Scopus) were searched for studies from January 1, 2000, to April 30, 2024. Inclusion criteria were patients aged ≥65 years with trauma, assessing survival or death outcomes. Two authors independently screened and extracted data using the PRISMA checklist; disagreements were resolved by a third author.

Eighteen retrospective studies were included (425,355 patients), showing an overall mortality rate of 9.6 ​%. Falls were the predominant cause of injury. Demographic mortality risk factors included advanced age, frailty, male sex, and comorbidities (blood/bleeding disorders, liver disease, cancer, kidney disease, and lung disease). Injury risk factors were identified as contributing to the outcome, including low systolic blood pressure, Glasgow Coma Scale, Injury Severity Score, Revised Trauma Score, and surgical intervention.

Trauma significantly elevates the mortality rate in older adults, with advanced age, gender, comorbidities, injury severity, frailty, and surgical intervention being key factors.

The purpose of this study was to evaluate the discriminatory capability of the Khorana, PROTECHT, CONKO, and COMPASS-CAT scores in ambulatory patients with lung cancer.

This retrospective cohort study included 591 patients with newly diagnosed lung cancer. A symptomatic or incidental VTE occurred in 108 patients.

The Khorana score at a 2-point threshold had a discriminatory capability with an odds ratio (OR) of 1.80 and an AUC of 0.57 for 6 months, and an OR of 1.51 and an AUC of 0.55 for 12 months. The CONKO score at a 2-point threshold had a stronger discriminatory capability for both 6 months and 12 months with ORs of 3.00 and 2.13, and AUCs of 0.63 and 0.59, respectively. Additionally, higher white blood cell counts, higher neutrophil counts, hypoalbuminaemia, and not undergoing lung surgery were related to VTE occurrence (p < 0.05).

The Khorana score with the 2-point threshold was validated in ambulatory patients with lung cancer, with the results indicating a decline in its discriminatory capability over time (at 12 months vs. 6 months from diagnosis). The CONKO score at the original 2-point threshold showed a stronger discriminatory capability but further validation with a larger sample size is recommended. The identified predictors should be further investigated in future research.

Venous thromboembolism (VTE) is a common and potentially life-threatening complication in patients with cancer. Both cancer and its treatments increase the risk of developing VTE. Specific cancer types and individual patient comorbidities increase the risk of developing cancer-associated VTE, and the risk of bleeding is increased with anticoagulation therapies. The aims of this article are to summarize the latest evidence for treating cancer-associated VTE, discuss the practical considerations involved, and share best practices for VTE treatment in patients with cancer. The article pays particular attention to challenging contexts including patients with brain, lung, gastrointestinal, and genitourinary tumors and those with hematological malignancies. Furthermore, the article summarizes specific clinical scenarios that require additional treatment considerations, including extremes of body weight, nausea and gastrointestinal disturbances, compromised renal function, and anemia, and touches upon the relevance of drug-drug interactions. Historically, vitamin K antagonists and low-molecular-weight heparins (LMWHs) have been used as therapy for cancer-associated VTE. The development of direct oral anticoagulants has provided additional treatment options, which, in certain instances, offer advantages over LMWHs. There are numerous factors that need to be considered when treating cancer-associated VTE, and although various treatment guidelines are helpful, they do not reflect each unique scenario that may arise in clinical practice. This article provides a summary of the latest evidence and a practical approach for treating cancer-associated VTE.

The prevalence of venous thromboembolism (VTE) is high in patients with cancer and can often present as the first symptom of malignancy. Cancer-associated VTE is one of the most important risk factors contributing to cancer mortality, making its prevention and treatment critical for patients with lung cancer.

We systematically searched for observational studies that estimated the prevalence of VTE in patients with lung cancer. A comprehensive search of electronic databases, including PubMed, EMBASE and Cochrane Library, was systematically conducted from database inception through January 21, 2022. The qualities of included studies were assessed in three domains, including patient selection, comparison, and results. Random effects meta-analyses of the prevalence of VTE in lung cancer were conducted using the metaprop procedure. Chi-square test and I 2 value were used to evaluate study heterogeneity.

Thirty-five studies involving 742,156 patients were considered eligible for this study. The pooled prevalence of VTE among patients with lung cancer was 5% (95% CI: 0.043-0.056, P = 0.000). The regional prevalence of VTE was 7% (95% CI: 0.06-0.08; I2 = 99.2%) in North America, 8% (95% CI: 0.06-0.10; I2 = 97.6%) in Asia, 6% (95% CI: 0.04-0.09; I2 = 95.9%) in Europe and 11% (95% CI: 0.07-0.15) in Australasia.

The prevalence of lung cancer-related VTE is high and region-specific. These results of this review emphasize the importance of understanding the incidence of lung cancer-related VTE and provide argue for VTE screening of patients with lung cancer.

https://www.crd.york.ac.uk/prospero/, identifier PROSPERO (CRD42022306400).

The deregulation of cell surface heparan sulfate proteoglycans (HSPGs) is a main issue of cancer cells for increasing their malignancy. In these terms, the sulfation pattern of HS, created by an orchestrated activity of enzymes balancing a site-specific sulfation, is of key importance. These enzymes are often deregulated by epigenetic processes in cancer, e.g., being silenced by DNA hypermethylation. Here, we address this issue in human breast cancer cell lines aiming to target epigenetic processes to reactivate HS sulfation, shifting HS into an antithrombotic phenotype for which 3-O-sulfation is particularly important. Treatment of MCF-7 and MDA-MB-231 cells with nontoxic concentrations of 5-azacytidine (azacytidine) and 5-fluoro-2'-deoxycytidine (FdCyd) as DNMT inhibitors or vorinostat for targeting HDAC increased HS3-O-sulfation remarkably, as confirmed by fluorescence microscopy, by upregulating HS3-O-sulfotransferases, detected by quantitative real-time polymerase chain reaction and Western blot. Flow cytometry and microscopic approaches confirm that upon inhibitor treatment, increased HS3-O-sulfation improves cell binding to antithrombin, leading to an antithrombotic activity. Nevertheless, only azacytidine- and vorinostat-treated cells display anticoagulative properties, represented by attenuated thrombin formation, a lower activation of human platelet aggregation, or ATP release. In contrast, FdCyd additionally upregulated tissue factor expression in both cell lines, overshadowing the anticoagulant effects of HS, leading to an overall prothrombotic phenotype. Our data provide evidence for the first time that targeting epigenetic processes in HS sulfation is a valuable means to foster anticoagulative cell properties for decreasing malignancy and metastatic potency. These data warrant further investigations to fine-tune epigenetic targeting and to search for potential biomarkers attributed to these activities.

The ORAL Surveillance trial found a dose-dependent increase in venous thromboembolism (VTE) and pulmonary embolism (PE) events with tofacitinib versus tumor necrosis factor inhibitors (TNFi). We aimed to assess VTE incidence over time and explore risk factors of VTE, including disease activity, in ORAL Surveillance.

Patients with rheumatoid arthritis (RA) aged 50 years or older with at least one additional cardiovascular risk factor received tofacitinib 5 or 10 mg twice daily (BID) or TNFi. Post hoc, cumulative probabilities and incidence rates (patients with first events/100 patient-years) by 6-month intervals were estimated for adjudicated VTE, deep vein thrombosis, and PE. Cox regression models identified risk factors. Clinical Disease Activity Index leading up to the event was explored in patients with VTE.

Cumulative probabilities for VTE and PE were higher with tofacitinib 10 mg BID, but not 5 mg BID, versus TNFi. Incidence rates were consistent across 6-month intervals within treatments. Across treatments, risk factors for VTE included prior VTE, body mass index greater than or equal to 35 kg/m2, older age, and history of chronic lung disease. At the time of the event, most patients with VTE had active disease as defined by Clinical Disease Activity Index.

Incidences of VTE and PE were higher with tofacitinib (10 > 5 mg BID) versus TNFi and were generally consistent over time. Across treatments, VTE risk factors were aligned with previous studies in the general RA population. These data highlight the importance of assessing VTE risk factors, including age, body mass index, and VTE history, when considering initiation of tofacitinib or TNFi in patients with active RA.

Cancer-associated thrombosis is a significant complication in cancer patients, leading to increased morbidity and mortality. The expression of coagulation/fibrinolysis genes, termed the "coagulome", plays a critical role in this process. Using the single-sample gene set enrichment analysis (ssGSEA), we identified seven cancer types with significantly activated coagulation pathways, focusing on lower-grade glioma (LGG) and stomach adenocarcinoma due to their predictive value for overall survival. Through 1000 iterations of the Least Absolute Shrinkage and Selection Operator (LASSO), we selected prognostic genes and constructed effective Cox regression models, particularly for LGG. Incorporating clinical characteristics, we constructed a nomogram for LGG, achieving an impressive area under the curve (AUCs) of 0.79, 0.82, and 0.81 at 1, 3, and 5 years in the test dataset, indicating strong potential for clinical application. Functional enrichment analysis between high-risk and low-risk LGG groups revealed significant enrichment of genes involved in the inflammatory response, interferon-gamma response, and epithelial-mesenchymal transition pathways. Combined with CIBERSORT and single-cell RNA sequencing analysis of LGG, our results demonstrated that the interplay between coagulation and the tumor microenvironment, particularly involving gliomas and myeloid cells, significantly influences tumor progression and patient outcomes.

The clinical translation of the nanoparticle (NP)-based anticancer therapies is still unsatisfactory due to the heterogeneity of the enhanced permeability and retention (EPR) effect. Despite the promising preclinical outcome of the pharmacological EPR enhancers, their systemic toxicity can limit their clinical application. Hyperthermia (HT) presents an efficient tool to augment the EPR by improving tumor blood flow (TBF) and vascular permeability, lowering interstitial fluid pressure (IFP), and disrupting the structure of the extracellular matrix (ECM). Furthermore, the HT-triggered intravascular release approach can overcome the EPR effect. In contrast to pharmacological approaches, HT is safe and can be focused to cancer tissues. Moreover, HT conveys direct anti-cancer effects, which improve the efficacy of the anti-cancer agents encapsulated in NPs. However, the clinical application of HT is challenging due to the heterogeneous distribution of temperature within the tumor, the length of the treatment and the complexity of monitoring.

Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors are widely recognised as being able to induce a potent reduction in low‑density lipoprotein‑cholesterol. An increasing number of studies have suggested that PCSK9 also influences the haemostatic system by altering platelet function and the coagulation cascade. These findings have significant implications for anti‑PCSK9 therapy in patients with specific coagulation conditions, including expanded indications, dose adjustments and drug interactions. The present review summarises the changes in PCSK9 levels in individuals with liver diseases, chronic kidney diseases, diabetes mellitus, cancer and other disease states, and discusses their impact on thrombosis and haemostasis. Furthermore, the structure, effects and regulatory mechanisms of PCSK9 on platelets, coagulation factors, inflammatory cells and endothelial cells during coagulation and haemostasis are described.

Cancer cells induce hypercoagulability in the tumoral microenvironment by expressing Tissue Factor (TF). We aimed to study the impact of the procoagulant signature of cancer cells on the quality and structure of fibrin network. We also studied the impact of fibrin clot shield (FCS) on the efficiency of anticancer agents and the migration of cancer cells.

Pancreatic cancer cells BXPC3 and breast cancer cells MDA-MB231 and MCF7, were cultured in the presence of normal Platelet Poor Plasma (PPP), diluted 10 % in conditioning media. Their potential to induce thrombin generation and their fibrinolytic activity were assessed. The structure of fibrin network was analyzed with Scanning Electron Microscopy (SEM). Cancer cells' mobility with fibrin clot and their interactions with fibrin were observed. Cancer cells were treated with paclitaxel (PTX) or 4-hydroxy-tamoxifen (4OHTam) in the presence or absence of FCS.

Cancer cells, in presence of PPP, induced fibrin network formation. High TF-expressing cancer cells (BXPC3 and MDA-MB23 cells), led to dense fibrin network with fine fibers. Low TF expressing cells MCF7 led to thick fibers. Exogenous TF enhanced the density of fibrin network formed by MCF7 cells. Cancer cells through their inherent profibrinolytic potential migrated within the fiber scaffold. The BXPC3 and MCF7 cells moved in clusters whereas the MDA-MB231 cells moved individually within the fibrin network. FCS decreased the efficiency of PTX and 4OHTam on the viability of cancer cells.

The procoagulant signature of cancer cells is determinant for the quality and structure of fibrin network in the microenvironment. Original SEM images show the architecture of "bird's nest"-like fibrin network being in touch with the cell membranes and surrounding cancer cells. Fibrin network constructed by triggering thrombin generation by cancer cells, provides a scaffold for cell migration. Fibrin clot shields protect cancer cells against PTX and 4OHTam.

Dysregulated hemostasis in cancer patients is associated with various clinical conditions, from thromboembolic complications to disseminated intravascular coagulation. Despite the well-established association between cancer and thromboembolic complications, the mechanisms involved are not completely elucidated. There are several predisposing factors in cancer for increased thrombus generation, such as immobilization and chemotherapy. The term cancer-associated thrombosis (CAT) has been introduced to describe the close bidirectional relationship between cancer and thromboembolic events. Conventional coagulation tests (PT/aPTT) are more accurate in detecting a hypocoagulable rather than a hypercoagulable state; thus, their contribution to CAT management is limited. Traditionally, D-dimer levels have been the most common laboratory study for the evaluation of thrombotic risk. However, D-dimer levels only display a snapshot of the coagulation cascade, and they cannot provide a dynamic evaluation of evolving clot formation. Non-conventional assays, such as viscoelastic methods and microparticle formation are promising tools for the identification of patients at risk for developing CAT. Recent guidelines from the American Society of Clinical Oncology counsel against the estimation of thrombotic risk through a single test and recommend the use of scoring systems that take into account several risk factors. The present review outlines the current insights into the pathophysiological mechanisms of CAT and provides a comprehensive review of the latest advances in the laboratory assessment of CAT and the recent guidelines for the management of patients at risk for developing thromboembolic complications.

Cancer-associated venous thromboembolism (CA-VTE) represents a major cause of morbidity and mortality in patients with cancer. Despite poor outcomes, there is an ongoing knowledge gap in epidemiologic data related to this association.

To compare venous thromboembolism (VTE) characteristics, risk factors, and outcomes between patients with and without active cancer in a racially diverse population.

Our surveillance project occurred at the 3 hospitals in Durham County, North Carolina, from April 2012 through March 2014. Electronic and manual methods were used to identify unique Durham County residents with VTE.

We identified 987 patients with VTE during the surveillance period. Of these, 189 patients had active cancer at the time of their VTE event. Patients with CA-VTE were older (median age: 69 years vs 60 years, P < .0001) and had a lower body mass index (median body mass index: 26.0 kg/m2 vs 28.4 kg/m2, P = .0001) than noncancer patients. The most common cancers in our cohort were gastrointestinal, breast, genitourinary, and lung. The proportion of VTE cases with pulmonary embolism (PE) was greater in the cancer cohort compared with that in the noncancer cohort (58.2% vs 44.0%, P = .0004). Overall survival was lower in the CA-VTE group than in patients without cancer (P < .0001). Black patients with CA-VTE had lower proportion of PE (52.3% vs 67.1%, P = .05) but had decreased survival (P < .0003) in comparison with White patients.

Future studies may be needed to continue to evaluate local and national VTE data to improve VTE prevention strategies and CA-VTE outcomes.

Anesthesiologists are experiencing first-hand the aging population, given older patients more frequently presenting for surgery, often with geriatric syndromes influencing their anesthetic management. The overall incidence and health burden of cancer morbidity and mortality are also rapidly increasing worldwide. This growth in the cancer population, along with the associated risk factors and comorbidities often accompanying a cancer diagnosis, underscores the need for anesthesiologists to become well versed in the preoperative evaluation and management of the adult patient with cancer. This article will focus on the unique challenges and opportunities for the anesthesiologist caring for the adult oncology patient presenting for surgery.

We have developed a micellar formulation of anticancer drugs based on chitosan and heparin grafted with lipoic and oleic acids that can release the cytotoxic cargo (doxorubicin) in response to external stimuli, such as increased glutathione concentration-a hallmark of cancer. Natural polysaccharides (heparin and chitosan) provide the pH sensitivity of the nanocarrier: the release of doxorubicin (Dox) is enhanced in a slightly acidic environment (tumor microenvironment). Fatty acid residues are necessary for the formation of nanoparticles (micelles) and solubilization of cytostatics in a hydrophobic core. Lipoic acid residues provide the formation of a labile S-S cross-linking between polymer chains (the first variant) or covalently attached doxorubicin molecules through glutathione-sensitive S-S bridges (the second variant)-both determine Redox sensitivity of the anticancer drugs carriers stable in blood circulation and disintegrate after intracellular uptake in the tumor cells. The release of doxorubicin from micelles occurs slowly (20%/6 h) in an environment with a pH of 7.4 and the absence of glutathione, while in a slightly acidic environment and in the presence of 10 mM glutathione, the rate increases up to 6 times, with an increase in the effective concentration up to 5 times after 7 h. The permeability of doxorubicin in micellar formulations (covalent S-S cross-linked and not) into Raji, K562, and A875 cancer cells was studied using FTIR, fluorescence spectroscopy and confocal laser scanning microscopy (CLSM). We have shown dramatically improved accumulation, decreased efflux, and increased cytotoxicity compared to doxorubicin control with three tumor cell lines: Raji, K562, and A875. At the same time, cytotoxicity and permeability for non-tumor cells (HEK293T) are significantly lower, increasing the selectivity index against tumor cells by several times.

Venous thromboembolism is an important complication in tumour patients as it occurs frequently in these patients and causes relevant morbidity. The risk of thromboembolic complications in tumour patients is 3-9 times higher than in non-tumour patients and is the second most common cause of death in tumour patients. The risk of thrombosis depends on tumour-induced coagulopathy and on individual factors, type and stage of cancer, time since cancer diagnosis as well as type of systemic cancer therapy. Thromboprophylaxis in tumour patients is effective but can be associated with increased bleeding. Even though there are currently no dedicated recommendations for individual tumour entities, international guidelines recommend prophylactic measures in high-risk patients. A thrombosis risk of >8-10% can be considered an indication for thromboprophylaxis, which is indicated by a Khorana score ≥2, and should be calculated individually using nomograms. In particular, patients with a low risk of bleeding should receive thromboprophylaxis. Risk factors and symptoms of a thromboembolic event should also be intensively discussed with the patient and materials for patient information should be handed out.

Venous thromboembolism (VTE) is a major cause of morbidity and mortality worldwide. Current risk assessment tools, such as the Caprini and Padua scores and Wells criteria, have limitations in their applicability and accuracy. This study aimed to develop machine learning models using structured electronic health record data to predict diagnosis and 1-year risk of VTE.

We trained and validated models on data from 159 001 participants in the Mount Sinai Data Warehouse. We then externally tested them on 401 723 participants in the UK Biobank and 123 039 participants in All of Us. All data sets contain populations of diverse ancestries and clinical histories. We used these data sets to develop small, medium, and large models with increasing features on a range of optimizing portability to maximizing performance. We make trained models publicly available in click-and-run format at https://doi.org/10.17632/tkwzysr4y6.6.

In the holdout and external test sets, respectively, models achieved areas under the receiver operating characteristic curve of 0.80 to 0.83 and 0.72 to 0.82 for VTE diagnosis prediction and 0.76 to 0.78 and 0.64 to 0.69 for 1-year risk prediction, significantly outperforming the Padua score. Models also demonstrated robust performance across different VTE types and patient subsets, including ethnicity, age, and surgical and hospitalization status. Models identified both established and novel clinical features contributing to VTE risk, offering valuable insights into its underlying pathophysiology.

Machine learning models using structured electronic health record data can significantly improve VTE diagnosis and 1-year risk prediction in diverse populations. Model probability scores exist on a continuum, affecting mortality risk in both healthy individuals and VTE cases. Integrating these models into electronic health record systems to generate real-time predictions may enhance VTE risk assessment, early detection, and preventative measures, ultimately reducing the morbidity and mortality associated with VTE.

Cancer patients represent a growing population with drastically difficult care and a lowered quality of life, especially due to the heightened risk of vast complications. Thus, it is well established so far that one of the most prominent complications in individuals with cancer is venous thromboembolism. Since there are various improved methods for screening and diagnosing cancer and its complications, the incidence of cancer-associated thrombosis has been on the rise in recent years. Therefore, the high mortality and morbidity rates among these patients are not a surprise. Consequently, there is an excruciating need for understanding the mechanisms behind this complex process, as well as the imperative for adequate analysis and application of the most suitable steps for cancer-associated thrombosis prevention. There are various and numerous mechanisms offering potential answers to cancer-associated thrombosis, some of which have already been elucidated in various preclinical and clinical scenarios, yet further and more elaborate studies are crucial to understanding and preventing this complex and harsh clinical entity. This article elaborates on the growing incidence, mortality, morbidity, and risk factors of cancer-associated thrombosis while emphasizing the pathophysiological mechanisms in the light of various types of cancer in patients and summarizes the most novel therapy and prevention guidelines recommendations.

Ovarian cancer (OC) and venous thromboembolism (VTE) have a close relationship, in which tumour cells surpass the haemostatic system to drive cancer progression. Long non-coding RNAs (lncRNAs) have been implicated in VTE pathogenesis, yet their roles in cancer-associated thrombosis (CAT) and their prognostic value are unexplored. Understanding how these lncRNAs influence venous thrombogenesis and ovarian tumorigenesis may lead to the identification of valuable biomarkers for VTE and OC management. Thus, this study evaluated the impact of five lncRNAs, namely MALAT1, TUG1, NEAT1, XIST and MEG8, on a cohort of 40 OC patients. Patients who developed VTE after OC diagnosis had worse overall survival compared to their counterparts (log-rank test, p = 0.028). Elevated pre-chemotherapy MEG8 levels in peripheral blood cells (PBCs) predicted VTE after OC diagnosis (Mann-Whitney U test, p = 0.037; Χ2 test, p = 0.033). In opposition, its low levels were linked to a higher risk of OC progression (adjusted hazard ratio (aHR) = 3.00; p = 0.039). Furthermore, low pre-chemotherapy NEAT1 levels in PBCs were associated with a higher risk of death (aHR = 6.25; p = 0.008). As for the remaining lncRNAs, no significant association with VTE incidence, OC progression or related mortality was observed. Future investigation with external validation in larger cohorts is needed to dissect the implications of the evaluated lncRNAs in OC patients.

In this study, the relationship between preoperative plasma D-dimer level and overall survival and recurrence free survival were evaluated in patients with curative resection of pancreatic ductal adenocarcinoma.

Preoperative plasma D-dimer level of 573 patients with pancreatic ductal adenocarcinoma were collected. The univariate and multivariate Cox hazard models were used to identify independent variables associated with overall survival and recurrence free survival in this study. The Kaplan-Meier method was used to evaluate overall survival and recurrence free survival, and the differences between survival curves were analyzed using the Log-rank test. Continuous variables were presented as $\overline{x}\pm s$, parametric analysis was performed using t-test. Categorical variables were analyzed by means of the chi-square or Fisher's exact test.

Based on the analysis for the whole study, the results showed that patients in the elevated plasma D-dimer levels had a tendency to have an elder mean age (58.69 ± 8.32 years vs. 63.05 ± 8.44 years, P < 0.001), larger tumour size ≥4 cm (P = 0.006), advanced T stage (P = 0.024), N stage (P = 0.041), Tumor, Node and Metastasis (TNM) stage (P = 0.029) and postoperative complications (P = 0.042) was more likely occurred. Besides, according to the results of Cox multivariate analysis, elevated preoperative plasma D-dimer level was an independent prognostic factor not only for overall survival (Hazard Ratio (HR):1.430, 95% Confidence Interval (CI) (1.163-1.759), P = 0.001) but also for recurrence free survival (HR:1.236, 95% CI (1.018-1.500), P = 0.032).

In our study, the elevated preoperative plasma D-dimer level may act as an independent prognostic factor for overall survival and recurrence free survival in patients with pancreatic ductal adenocarcinoma after curative resection. Pancreatic ductal adenocarcinoma patients with elevated preoperative plasma D-dimer level had a worse prognosis than those with normal plasma D-dimer level; and the elevated preoperative plasma D-dimer level may imply heavy tumour burden and provide supplementary information regarding disease status.