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The Khorana score is a validated tool to identify cancer patients at higher risk of venous thromboembolism (VTE).

The Khorana score is a validated tool to identify cancer patients at higher risk of venous thromboembolism (VTE). We compared its predictive performance to that of the clinical PROTECHT and the polygenic 5‐SNP scores in patients who participated in the Dutch CPCT‐02 study. Data on VTE and its risk factors were retrospectively collected for 2729 patients with advanced stage solid tumors planned for systemic cancer treatment. Patients were followed for 6 months. Overall discriminatory performance of the scores was evaluated by time‐dependent c‐indices. The scores were additionally evaluated dichotomously in competing risk models. A total of 160 (5.9%) patients developed VTE during follow‐up. Time‐dependent c‐indices at 6 months for the Khorana, PROTECHT, and 5‐SNP scores were 0.57 (95% confidence interval [CI]: 0.55–0.60), 0.60 (95% CI: 0.57–0.62), and 0.54 (95% CI: 0.51–0.57), respectively. The dichotomous scores classified 9.6%, 16.8%, and 9.5% as high‐risk, respectively. VTE risk was about 2‐fold higher among high‐risk patients than low‐risk patients for the Khorana (subdistribution hazard ratio [SHR] 1.9, 95% CI: 1.3–3.0), PROTECHT (SHR 2.1, 95% CI: 1.5–3.0), and 5‐SNP scores (SHR 1.7, 95% CI: 1.03–2.8). The sensitivity at 6 months was 16.6% (95% CI: 10.5–22.7), 28.9% (95% CI: 21.5–36.3), and 14.9% (95% CI: 8.5‐21.2), respectively. Performance of the PROTECHT or 5‐SNP score was not superior to that of the Khorana score. The majority of cancer patients who developed VTE during 6‐month follow‐up were not identified by these scores. Future directions for studies on cancer‐associated VTE prediction may include combined clinical‐genetic scores.

COVID-19 is associated with a high incidence of thrombotic complications, which can be explained by the complex and unique interplay between coronaviruses and endothelial cells, the local and systemic inflammatory response, and the coagulation system. Empirically, an intensified dose of thrombosis prophylaxis is being used in patients admitted to hospital with COVID-19 and several guidelines on this topic have been published, although the insufficiency of high quality and direct evidence has led to weak recommendations. In this Viewpoint we summarise the pathophysiology of COVID-19 coagulopathy in the context of patients who are ambulant, admitted to hospital, and critically ill or non-critically ill, and those post-discharge from hospital. We also review data from randomised controlled trials in the past year of antithrombotic therapy in patients who are critically ill. These data provide the first high-quality evidence on optimal use of antithrombotic therapy in patients with COVID-19. Pharmacological thromboprophylaxis is not routinely recommended for patients who are ambulant and post-discharge. A first ever trial in non-critically ill patients who were admitted to hospital has shown that a therapeutic dose of low-molecular-weight heparin might improve clinical outcomes in this population. In critically ill patients, this same treatment does not improve outcomes and prophylactic dose anticoagulant thromboprophylaxis is recommended. In the upcoming months we expect numerous data from the ongoing antithrombotic COVID-19 studies to guide clinicians at different stages of the disease.

Coronavirus disease 2019 (COVID‐19) can lead to systemic coagulation activation and thrombotic complications.

Anticoagulant therapy might reduce the number of miscarriages and adverse pregnancy outcomes in women with recurrent pregnancy loss and inherited thrombophilia. We aimed to assess use of low-molecular-weight heparin (LMWH) versus standard care in this population.