Briefly, between 19, 40 study centers throughout the United States screened 373,092 postmenopausal women aged 50-79 years, of whom 68,132 were included in the WHI Hormone Therapy (HT) and Diet Modification (DM) trials (Consort diagram in Figure 1). The recruitment and study design have been described elsewhere. We tested this hypothesis in the Women’s Health Initiative (WHI) Calcium and Vitamin D (CaD) clinical trial. Given experimental and observational human data linking vitamin D deficiency with VTE, we hypothesized that vitamin D supplementation would reduce the risk of VTE. In humans, circulating concentrations of 25-hydroxyvitamin D (25-OHD, which reflect total body vitamin D status) may be inversely associated with concentrations of tissue plasminogen activator antigen (tPA, a marker of fibrinolysis activation) and with the risk of incident VTE. In vivo, vitamin D receptor knockout (VDRKO) mice exhibit an exacerbated thrombus formation in response to liposaccharide injection.

1,25-dihydroxyvitamin D3, the biologically potent form of vitamin D, modulates the expression and activity of thrombomodulin and tissue factor in vitro. Recent laboratory and epidemiological findings suggest that vitamin D metabolism may play a role in haemostasis and influence the risk of VTE. Long-term consequences of deep vein thrombosis (DVT) and pulmonary embolism (PE), including post-thrombotic syndrome and chronic thromboembolic pulmonary hypertension, result in considerable health and economic burdens. Each year in the United States, 600,000-900,000 VTE events are thought to be responsible for 100,000 deaths. The prevention of venous thromboembolism (VTE) is a public health priority.

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