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Food Interactions, Sirtuins, Genes, Homeostasis, and General Discussion
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Warfarin is an anticoagulant drug used to treat blood clots such as vein thrombosis and pulmonary thrombosis, and to prevent stroke in cardiac patients. The most notorious food-drug interaction regarding warfarin occurs with green, leafy vegetables, due to their rich vitamin K content (24). Vitamin K is used for blood coagulation and to treat or prevent hemorrhage. Warfarin and vitamin K present in vegetable foods have opposite mechanisms of action. Increasing vitamin K-rich food intake will result in reducing the efficacy of warfarin (24). Therefore, people under warfarin therapy are advised to consume leafy vegetables moderately for the good efficacy of warfarin therapy. Soy milk, char grilled foods, and sushi containing seaweed may also decrease the effect of warfarin (24). Cranberry juice, in contrast, can significantly potentiate the anticoagulant effects of warfarin (24). Dried goji berries may potentiate the anticoagulant effect of warfarin and increase the risk of bleeding.
Atrial fibrillation
Published in Henry J. Woodford, Essential Geriatrics, 2022
The anticoagulant response to warfarin is increased with advanced age. This difference is still apparent after correction for confounding variables such as body weight, medication interactions and comorbidity. Part of this difference may be due to dietary changes. Vitamin K, which opposes the effect of warfarin, is found in leafy green vegetables. Therefore, a diet containing less of these may make the effects of warfarin more pronounced.
Enteral nutrition
Published in David Westaby, Martin Lombard, Therapeutic Gastrointestinal Endoscopy A problem-oriented approach, 2019
Significant coagulopathy precludes PEG insertion, but can usually be corrected – PEG should be considered as a semi-elective procedure and can always be delayed for a day or two while coagulation status is improved. Patients on warfarin should omit the drug for 3–5 days until the INR falls below 1.3. If the indication for anticoagulation is strong (for example, a prosthetic heart valve), heparin can be substituted during this period and discontinued 5 hours before the procedure. Recommencing heparin 2 hours after the procedure does not seem to increase the risk of significant bleeding. Warfarin therapy can generally be resumed on the night of the procedure. Patients on drugs that inhibit platelet function should ideally have these stopped, but experience has shown that PEG can be performed safely in patients on low-dose aspirin.
Management of pulmonary arterial hypertension during pregnancy
Published in Expert Review of Respiratory Medicine, 2023
Kaushiga Krishnathasan, Andrew Constantine, Isma Rafiq, Ana Barradas Pires, Hannah Douglas, Laura C Price, Konstantinos Dimopoulos
While anticoagulation was previously recommended in patients with idiopathic PAH, this is no longer the case for this or other forms of PAH, including Eisenmenger syndrome, which carries an especially high risk of bleeding [1,7]. Pregnancy is, however, a hypercoagulable state and venous thromboembolism is a cause of maternal mortality in PAH [20], therefore the benefits of anticoagulation should be balanced against the risk of bleeding [1,61]. Women who are already on anticoagulation should generally remain anticoagulated [1,24]. Warfarin should be avoided in the early stages of pregnancy, owing to its teratogenicity, and unfractionated or low molecular weight heparin is preferred, with monitoring of anti-Xa levels. Direct-acting oral anticoagulants are not recommended during pregnancy [7,25,64].
The association of non-vitamin K antagonist oral anticoagulants vs. warfarin and the risk of fractures for patients with atrial fibrillation: a systematic review and meta-analysis
Published in Acta Cardiologica, 2023
Nana Yang, Ying Zhao, Zhaohui Bai, Haokun Chen, Haoyu Ning, Meijuan Zou, Gang Cheng
In bone physiology, osteocalcin may limit bone formation without impairing bone resorption or mineralization [55], regulate the rate of mineral maturation, and increase bone toughness by forming a complex between bone matrix and collagen [56]. Osteocalcin is gamma-carboxylated by the vitamin K-dependent gamma-glutamyl (VKDP) carboxylase. Warfarin is an endogenous vitamin K epoxide reductase complex antagonist. So warfarin may increase the proportion of uncarboxylated osteocalcin in bone by blocking the vitamin K metabolic pathway. It exerts harmful effects on bone metabolism and impairs bone material hardness leading to an increased risk of fractures [20,57,58]. In addition, patients taking warfarin are recommended to limit dietary intake of vitamin K to achieve an optimal anticoagulation effect [18]. So some patients may choose to avoid foods rich in vitamin K, although they are advised the least daily allowance of vitamin K, which induced osteocalcin and other relevant proteins deficiency and then increased the risk of bone loss and fracture [20,59,60].
A correlation of thrombin generation assay and clot waveform analysis in patients on warfarin
Published in Hematology, 2022
May Anne Cheong, Chuen Wen Tan, Wan Hui Wong, Ming Chai Kong, Edmund See, Shu Hui Yeang, Sei Keng Koh, Yuan Tying Shim, Lai Heng Lee, Heng Joo Ng
Apart from our present study, there is currently minimal data available comparing CWA and other GCAs. However, Matsumoto et al. demonstrated a strong correlation, with Pearson's r approaching 0.9, between CWA and CAT, in response to the addition of single factor FVIII or FIX to the respective factor deficient plasmas in vitro [10]. With a few notable differences in study methods, we showed a more modest correlation in the present study. A few factors can explain these differences. Firstly, warfarin interacts with multiple clotting factors through a more complex pathway to influence the eventual clot formation than just a single factor deficiency. Secondly, our CWA was performed on Sysmex analysers rather than the MDA analysers (Organon Teknika, UK), which have since been phased out. Thirdly, Matsumoto et al. performed an in-house modification of the commercially available aPTT-SLA reagent used in their study whilst we employed the Dade Actin FSL commercial reagent in its original form [10]. Significantly, we conducted this study using unmanipulated patient samples.