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Evidence-Based Minireview: Should warfarin or a direct oral anticoagulant be used in patients presenting with thrombosis in the splanchnic or cerebral veins?
Mathew, C, Zumberg, M
Hematology. American Society of Hematology. Education Program. 2021;(1):100-105
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Abstract
Case 1: A 23-year-old female third-year medical student who has no medical history seeks treatment for abdominal distention. She takes an estrogen-containing birth control pill and does not smoke or consume alcohol. Family history is unremarkable. Physical examination is significant for abdominal distention, and an abdominal fluid wave is detected. Complete blood count is normal. Imaging confirms occlusive thrombosis of the main portal vein. On endoscopy, grade 1 to 2 esophageal varices are noted and banded. Unfractionated heparin is begun. Subsequent workup reveals a homozygous factor V Leiden mutation. Long-term anticoagulation is planned, and she asks if warfarin can be avoided given her hectic ward rotations, erratic diet, and need for monitoring. Case 2: A 35-year-old woman who has no medical history seeks treatment for progressively worsening posterior headaches for 1 week. Magnetic resonance imaging of the brain shows dural sinus thrombosis with associated small areas of petechial cerebral hemorrhage. She is started on a continuous unfractionated heparin infusion and admitted to the hospital for further observation. Her grandmother is on warfarin for atrial fibrillation, and the patient would prefer to avoid warfarin because she does not think she can comply with the frequent monitoring that will be required. She inquires about other oral anticoagulant options for her condition.
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High-dose steroid therapy for CNS inflammatory diseases increases INR in patients taking oral vitamin K antagonist.
Gelibter, S, Orrico, M, Croese, T, Bosco, L, Martinelli, V, Sangalli, F, Filippi, M
Journal of neurology. 2019;(12):3160-3161
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The critical interaction between valproate sodium and warfarin: case report and review.
Zhou, C, Sui, Y, Zhao, W, Dong, C, Ren, L, Song, P, Xu, B, Sun, X
BMC pharmacology & toxicology. 2018;(1):60
Abstract
BACKGROUND Valproic acid (VPA) and warfarin are commonly prescribed for patients with epilepsy and concomitant atrial fibrillation (AF). When VPA and warfarin are prescribed together, clinically important interactions may occur. VPA may replace warfarin from the protein binding sites and result in an abnormally increased anticoagulation effect. This is commonly underrecognized. CASE PRESENTATION In our case, we report a 78-year-old woman with a glioma who presented with status epilepticus. The patient was on warfarin to prevent cardiogenic embolism secondary to AF. Intravenous loading dose of VPA was administered, but international normalized ratio (INR) increased significantly to 8.26. Intravenous vitamin K1 was then given and the patient developed no overt bleeding during the hospitalization. CONCLUSION By reviewing the literature and discussing the critical interaction between valproate sodium and warfarin, we conclude that intravenous VPA and the co-administrated warfarin may develop critical but underrecognized complications due to effects on the function of hepatic enzymes and displacement of protein binding sites.
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Warfarin-Associated Nonuremic Calciphylaxis.
Yu, WY, Bhutani, T, Kornik, R, Pincus, LB, Mauro, T, Rosenblum, MD, Fox, LP
JAMA dermatology. 2017;(3):309-314
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Abstract
IMPORTANCE Classic calciphylaxis associated with renal failure is a life-threatening disease. Warfarin-associated calciphylaxis without renal injury has been described, but whether it is a subset of classic calciphylaxis or a different entity remains unknown. We describe 1 case of warfarin-associated calciphylaxis, present data from 2 others from our institution, and review all cases of warfarin-associated calciphylaxis available in the literature. Our review indicates that warfarin-associated calciphylaxis is clinically and pathophysiologically distinct from classic calciphylaxis. OBJECTIVE To review warfarin-associated calciphylaxis and determine its relationship to classic calciphylaxis. DESIGN, SETTING, AND PARTICIPANTS We searched MEDLINE and Ovid without language or date restrictions for case reports of calciphylaxis from the inpatient setting using the terms "calciphylaxis and warfarin," "non-uremic calciphylaxis," and "nonuremic calciphylaxis." We defined nonuremic calciphylaxis as a histopathologic diagnosis of calciphylaxis without severe kidney disease (serum creatinine level >3 mg/dL; glomerular filtration rate <15 mL/min; acute kidney injury requiring dialysis; and renal transplantation). EXPOSURES Each patient had been exposed to warfarin before the onset of calciphylaxis. MAIN OUTCOMES AND MEASURES Patient data were abstracted from published reports. Original patient medical records were requested and reviewed when possible. RESULTS We identified 18 patients with nonuremic calciphylaxis, 15 from the literature, and 3 from our institution. Patients were predominantly female (15 of 18 [83%]) with ages ranging from 19 to 86 years. Duration of warfarin therapy prior to calciphylaxis onset averaged 32 months. Lesions were usually located below the knees (in 12 of 18 [67%]). No cases reported elevated calcium-phosphate products (0 of 17 [0%]). Calcifications were most often noted in the tunica media (n = 8 [44%]) or in the vessel lumen and tunica intima (n = 7 [39%]). The most common treatments included substitution of heparin or low-molecular weight heparin for warfarin (n = 13 [72%]), intravenous sodium thiosulfate (n = 9 [50%]), and hyperbaric oxygen (n = 3 [17%]). The survival rate on hospital discharge was remarkably high, with 15 cases (83%) reporting full recovery and 3 cases ending in death. CONCLUSIONS AND RELEVANCE Warfarin-associated calciphylaxis is distinct from classic calciphylaxis in pathogenesis, course, and, particularly, outcome. This finding should influence clinical management of the disease and informs targeted treatment of the disease.
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Warfarin related nephropathy: a case report and review of the literature.
Ng, CY, Tan, CS, Chin, CT, Lim, SL, Zhu, L, Woo, KT, Tan, PH
BMC nephrology. 2016;:15
Abstract
BACKGROUND Warfarin related nephropathy is one of the potential complications of warfarin therapy. Despite the well described histological entity, the clinical course and approach to warfarin related nephropathy in patients requiring life-long anticoagulation is however not well described in the literature. CASE PRESENTATION We report the clinical course of a 56 years old Chinese lady who presented with over anti-coagulation and acute kidney injury while on warfarin therapy for permanent atrial fibrillation and mechanical valve replacement. Renal biopsy was performed as the acute kidney injury was persistent despite normalization of the International Normalized Ratio and the diagnosis of warfarin related nephropathy was made. Temporary interruption of anti-coagulation, in combination with oral N-acetylcysteine resulted in subsequent stabilization of renal function. CONCLUSION The diagnosis of warfarin induced nephropathy should be considered in patients presenting with unexplained acute kidney injury and over anti-coagulation. Awareness of this clinical entity is important for clinician managing anti-coagulation therapy and renal function should be monitored regularly in patients who are on warfarin therapy.
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[Reinforcement of warfarin action in a patient administered S-1].
Watanabe, H, Itoh, H, Tsuchiya, Y, Miyagi, N, Sugiyama, T, Nakai, Y, Shinozaki, Y, Noguchi, T, Jinbu, Y, Kusama, M
Gan to kagaku ryoho. Cancer & chemotherapy. 2015;(1):131-3
Abstract
A case showing reinforcement of the action of warfarin and potassium in a patient administered S-1 is reported.The patient was a 71-year-old man with left upper gingival cancer.He had ventricular tachycardia (VT), hypertrophic cardiomyopathy, and a cerebellar infarction.He underwent a pacemaker implantation, and was administered warfarin.After the operation, in mid-March 2010, he was administered with S-1 and warfarin. However, the international normalized ratio of prothrombin time (PT-INR) increased to an extremely high level of 5.82, and S-1 and warfarin were stopped. They were re-administered at the end of April, and the PT-INR stabilized to approximately 2.
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Interaction of vitamin K antagonists and trimethoprim-sulfamethoxazole: ignore at your patient's risk.
Hale, SF, Lesar, TS
Drug metabolism and drug interactions. 2014;(1):53-60
Abstract
The aim of the study was to summarize available literature regarding the interaction between vitamin K antagonists (VKAs) and trimethoprim-sulfamethoxazole (co-trimoxazole, TMP-SMX), and to provide recommendations for managing patient risk from this interaction. Data sources were English-language publications in the medical literature and Internet databases. Relevant publications that directly or indirectly addressed the VKA-TMP-SMX interaction were selected and reviewed. The mechanism of the VKA-TMP-SMX interaction, frequency of concurrent use, effect on international normalized ratio (INR), increased risk of bleeding, and strategies for risk reduction are summarized. The concurrent use of VKA and TMP/SMX rapidly and consistently raises INR and is associated with a two- to five-fold increase in bleeding. Concurrent use of VKA and TMP-SMX should be avoided when possible. When VKA and TMP-SMX are co-prescribed, VKA dose reduction is usually required. Patient education as well as early and frequent INR monitoring is recommended to reduce risk from this interaction.
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Management of anticoagulation around pacemaker and defibrillator surgery.
Birnie, DH, Healey, JS, Essebag, V
Circulation. 2014;(20):2062-5
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Effects of amiodarone, thyroid hormones and CYP2C9 and VKORC1 polymorphisms on warfarin metabolism: a review of the literature.
Tomisti, L, Del Re, M, Bartalena, L, Tanda, ML, Pucci, A, Pambianco, F, Danesi, R, Braverman, LE, Martino, E, Bogazzi, F
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2013;(6):1043-9
Abstract
OBJECTIVE To review the literature regarding the interaction among amiodarone therapy, thyroid hormone levels, and warfarin metabolism. METHODS A 73-year-old male with type 2 after describing an unusual case of amiodarone-induced thyrotoxicosis (AIT) who experienced a severe rise in international normalized ratio (INR) values after initiating warfarin therapy due to an unusual combination of excessive thyroid hormones, amiodarone therapy, and a genetic abnormality affecting warfarin metabolism. RESULTS Genetic analysis revealed that the patient was CYP2C9*2 wild-type, CYP2C9*3/*3 homozygous mutant, and VKORC1*3/*3 homozygous mutant. A review of the literature revealed that both mutations can independently affect warfarin metabolism. In addition, amiodarone therapy and the presence of thyrotoxicosis per se can affect warfarin metabolism and reduce the dose needed to maintain INR in the therapeutic range. The association of the 2 genetic polymorphisms in a patient with AIT is extremely rare and strongly impairs warfarin metabolism, exposing the patient to a high risk of overtreatment. CONCLUSIONS In patients with AIT, warfarin therapy should be gradually introduced, starting with a very low dose, because of the significant risk of warfarin overtreatment. Whether the genetic analysis of CYP2C9 and VKORC1 polymorphisms should be routinely performed in AIT patients remains conjectural.
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Emergency reversal of vitamin-K antagonists related over-anticoagulation: case report and brief overview on the role of prothrombin complex concentrate.
Di Fusco, SA, Aspromonte, N, Aquilani, S, Mele, L, Colivicchi, F
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace. 2013;(4):184-8
Abstract
Oral anticoagulation is a widely used treatment and atrial fibrillation (AF) is the most frequent indication. We review the therapeutic options on an important clinical challenge: rapid reversal anticoagulation in the setting of an urgent invasive procedure. We report a case of a 71-year-old man treated with warfarin who was over-anticoagulated when presented to the emergency department for syncope due to severe bradiarrhythmia and needed temporary pacing. Intravenous infusion of vitamin-k was not adequate for rapid reversal over anticoagulation whereas the administration of a Prothrombin Complex Concentrate (PCC) was able to quickly reverse anticoagulant activity and allowed the performance of an urgent invasive procedure without hemorrhagic complication. The aim of this paper is to draw attention to possible therapeutic strategies to reduce the risk of bleeding related to over-anticoagulation with vitamin-K antagonists (VKAs) in case of urgent invasive procedure, emphasizing the role of PCC in keeping with national and international guidelines.