Abstract
The monoclonal antibody denosumab reduces bone resorption. Warfarin is an oral anticoagulant used in the prevention and treatment of thrombosis. To date, there have been no studies on the interaction between warfarin and denosumab. The aim of the present study was to assess the maintenance of the Prothrombin Time International Normalized Ratio (INR) in the therapeutic range (TTR) in women under treatment with warfarin and denosumab, in order to evaluate the pharmacological interference of denosumab. No variations of the median TTR were found after undergoing treatment with denosumab: this shows that the intake of denosumab does not require additional checks in anticoagulated patients.
Highlights
Osteoporosis is a systemic disease of multifactorial etiology, characterized by a reduction in bone mass and deterioration of the microarchitecture of the bone tissue, which results in increased fragility and an increased risk of fracture [1]
The amount of bone reabsorbed by osteoclasts is equivalent to the amount of bone formed by osteoblasts, which is due to the interaction between the Receptor activator of nuclear factor-kB (RANK) system and Rank-ligand (RANKL)
The analysis of the therapeutic range (TTR) in the six patients treated with warfarin and denosumab showed an increase from 63% to 70% of the median TTR after the beginning of denosumab treatment and an increase of the 25th percentile from 60% to 68% (Figure 1)
Summary
Osteoporosis is a systemic disease of multifactorial etiology, characterized by a reduction in bone mass and deterioration of the microarchitecture of the bone tissue, which results in increased fragility and an increased risk of fracture [1]. Denosumab has been designed to bind with high affinity and specificity to RANKL, preventing the activation of its RANK receptor and reducing the formation and activity of osteoclasts This limits the loss of bone substance by performing an anti-rheororbitive action [2,3]. Warfarin (Coumadin, Bristol-Myers Squibb) is a coumarinic anticoagulant intended for the prevention of cardioembolic stroke and for the treatment and prevention of venous thromboembolism. It works by inhibiting the synthesis of vitamin K dependent coagulation factors; its anticoagulant effect is measured by monitoring the Prothrombin Time International Normalized Ratio (INR), which should be maintained in predetermined and defined therapeutic ranges intervals. To the Reports 2018, 1, 20; doi:10.3390/reports1030020 www.mdpi.com/journal/reports
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