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Recurrent Intracranial Bleed in 3 Siblings: Short of a Shot of Vitamin K!
Mahajan, V, Tahlan, A, Azad, C, Ahluwalia, J, Watzka, M, Oldenburg, J
Journal of pediatric hematology/oncology. 2021;(4):e580-e582
Abstract
We present a family who suffered recurrent sibling losses due to vitamin K deficiency bleed. The index child was asymptomatic at presentation, had normal clinical examination, and was investigated for coagulation disorders in view of previous 3 sibling losses as a result of intracranial hemorrhage. His investigations showed deranged coagulogram and clotting factors' assay. The baby was given vitamin K1 1 mg intramuscularly following which his coagulogram and clotting factors' assay returned to normal. The genetic analysis did not identify any inherited cause of bleeding tendency. The significant family history, exclusive breastfeeding, no diarrhea, failure to thrive or drug use, no prophylaxis with vitamin K at birth, recovery of clotting factors on vitamin K administration, and a corroborative molecular analysis confirmed diagnosis of vitamin K deficiency in the index child. This case gives a strong reminder not to miss birth dose of vitamin K in any neonate.
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Evidence-Based Minireview: Are DOACs an alternative to vitamin K antagonists for treatment of venous thromboembolism in patients with MPN?
Schieppati, F, Falanga, A
Hematology. American Society of Hematology. Education Program. 2021;(1):448-452
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3.
Vitamin K deficiency bleeding in an apparently healthy newborn infant: the compelling need for evidence-based recommendation.
Ceratto, S, Savino, F
Italian journal of pediatrics. 2019;(1):30
Abstract
BACKGROUND Vitamin K is a key point for guarantee normal blood clotting and its level in newborns is commonly low, so a supplementation after delivery is mandatory. Vitamin K prophylaxis in newborns is still an open field of debate: many types of protocol have been proposed in different years and Countries, and sometimes with great variability inside the same Nation (for instance, in Italy a national consensus is not available, so different protocols are employed). Recommendations include different protocols for healthy newborns born at term, but the unpreventable presence of bleeding favouring factors (i.e. blood vessels malformations) or limiting intestinal absorption of liposoluble vitamins (i.e. cholestasis), which could be unrecognized or subclinical in the perinatal period, rises some concerning about the most precautionary route of administration and the timing of further doses after the first one given at birth. The purpose of this report is to underline the most recent evidences available in literature and to arise a debate about this topic, in order to stimulate the production of evidence-based guidelines concerning the prophylaxis with vitamin K1 in newborn infants, considering that many bleeding risk factors are not recognizable at birth. CASE PRESENTATION We are hereby presenting an emblematic case concerning the risk of intracranial bleeding in an apparently healthy newborn: the described infant did not show any pathological elements in pregnancy history or perinatal life which suggest a possible increased risk of bleeding and the needing of a particular approach in the administration of vitamin K1, but at the end of the first week of life presented an intracranial bleeding with neurological symptoms that required treatment for vitamin K deficiency. CONCLUSIONS Univocal recommendations about vitamin K prophylaxis are not available and the contrast between oral and intramuscular routes persists unsolved. The difficulty to certainly identify an infant eligible for oral administration of vitamin K1 at birth suggests that the intramuscular route should be preferred. How to prosecute the supplementation in the first months of life is still an open topic of debate.
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4.
Acute non-cirrhotic portal vein thrombosis : review.
Salembier, A, Verhamme, M, Verhamme, P, Van Moerkercke, W
Acta gastro-enterologica Belgica. 2018;(2):318-322
Abstract
A 35-year-old man with a medical history of myocardial infarction, presenting with fever, general malaise and vague abdominal discomfort, was diagnosed with a portomesenteric venous thrombosis and acute cytomegalovirus (CMV) infection. Thrombophilia screening resulted in detection of heterozygosity for factor II G20210A gene mutation. Low molecular weight heparin in therapeutic dose was started, followed by disappearance of thrombus on imaging CT two months after diagnosis. The multifactorial origin of portal thrombosis and the importance of awareness of the link between CMV infection and an increased risk of thrombosis is emphasized with this case and review of the literature. Identifying CMV infection as a trigger for thrombosis can help to avoid extended anticoagulation. Acute non-cirrhotic PVT is a rare but probably underestimated condition as symptoms may be discrete or non-specific. The origin of portal thrombosis is frequently multifactorial. Recent literature has emphasized the increasing prevalence of CMV-induced PVT in immunocompetent patients. The multifactorial origin of portal thrombosis and the importance of awareness of the link between CMV infection and an increased risk of thrombosis is emphasized with this review of the literature and included case. Identifying CMV infection as a trigger for thrombosis can help to avoid extended anticoagulation.
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5.
Unexpected Problems of Antithrombotic Therapy with An Unusual Side Effect of Vitamin K Antagonists after Mitral Valve Replacement.
Marchandot, B, Messas, N, Jesel, L, Trinh, A, Kibler, M, Reydel, A, Ohlmann, P, Morel, O
The Journal of heart valve disease. 2017;(3):309-313
Abstract
Except for bleeding complications, vitamin K antagonists (VKAs) are known to have few undesirable side effects. Herein is presented the case of a 45-year-old woman in whom liver damage was induced by fluindione and warfarin after mitral valve replacement. Hepatotoxicity is a rare complication of VKAs, both in the French National and Drug Safety registry and the medical literature. A diagnosis of VKA-induced drug damage was confirmed by the absence of other etiologies, the chronological sequence, recurrence after re-exposure to VKA, and rapid improvements after discontinuation of the drug. Despite possible cross-reactions between VKAs, the re-introduction of acenocoumarol was successfully achieved, with no recurrence of biological disturbances.
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6.
[Not Available].
Santos Lopes, B, Steffel, J
Therapeutische Umschau. Revue therapeutique. 2016;(10):551-559
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7.
[Not Available].
Rickli, H, Maeder, MT
Therapeutische Umschau. Revue therapeutique. 2016;(10):589-594
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8.
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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9.
Life-threatening bleeding under vitamin K antagonists in spite of an INR in the therapeutic range.
Gavillet, M, Abbal, C, Schmidt, S, Nötzli, J, Lambert, JF, Angelillo-Scherrer, A
Journal of thrombosis and thrombolysis. 2011;(2):232-7
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10.
[General practitioner's considerations if INR doesn't change].
Dick, A, Spannagl, M
MMW Fortschritte der Medizin. 2009;(26-29):32-3