Cases reported "Vitamin K Deficiency"

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1/29. Novel mutation in the gamma-glutamyl carboxylase gene resulting in congenital combined deficiency of all vitamin K-dependent blood coagulation factors.

    A mutation in the gamma-glutamyl carboxylase gene leading to a combined congenital deficiency of all vitamin K-dependent coagulation factors was identified in a Lebanese boy. He is the first offspring of consanguineous parents and was homozygous for a unique point mutation in exon 11, resulting in the conversion of a tryptophan codon (TGG) to a serine codon (TCG) at amino acid residue 501. Oral vitamin K(1) administration resulted in resolution of the clinical symptoms. Screening of several family members on this mutation with an RFLP technique revealed 10 asymptomatic members who were heterozygous for the mutation, confirming the autosomal recessive pattern of inheritance of this disease. In 50 nonrelated normal subjects, the mutation was not found. This is the second time a missense mutation in the gamma-glutamyl carboxylase gene is described that has serious impact on normal hemostasis.
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2/29. calciphylaxis associated with cholangiocarcinoma treated with low-molecular-weight heparin and vitamin K.

    calciphylaxis is a rare disorder of small-vessel calcification and cutaneous infarction associated with chronic renal failure. Rare cases of calciphylaxis not associated with chronic renal failure have been reported with breast cancer, hyperparathyroidism, and alcoholic cirrhosis. To our knowledge, we report the first case of calciphylaxis without chronic renal failure associated with cholangiocarcinoma and the first attempt to treat calciphylaxis with vitamin K. A 56-year-old woman presented with necrotic leg ulceration. She was treated initially with low-molecular-weight heparin, with no effect. A coagulation work-up showed vitamin k deficiency. During vitamin K therapy, the patient had fulminant progression of the calciphylaxis. She died, and an autopsy showed metastatic cholangiocarcinoma. thrombosis and protein c deficiency have been implicated in the pathophysiology of calciphylaxis. Functional protein c deficiency may be one of several factors contributing to the development of calciphylaxis. Vitamin K therapy was ineffective in our patient and may have been detrimental.
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3/29. Abnormal coagulation in the postoperative period contributing to excessive bleeding.

    This article deals primarily with acquired disorders that disrupt normal hemostasis and cause excessive bleeding in the postoperative period because of the coagulopathy itself or because of drugs needed to treat the hemostatic disorder.
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4/29. Deliberate self-poisoning with rodenticide: a diagnostic dilemma.

    A 71-year-old man presented with a recurrent bleeding diathesis requiring frequent blood transfusions, vitamin K and fresh frozen plasma. Extensive investigations revealed vitamin k deficiency. After repeated interviews the patient admitted to deliberately ingesting rat poison. Superwarfarins are an uncommon cause of deranged clotting and specialised tests are available to identify them. They can cause prolonged coagulation abnormalities and may require treatment with oral vitamin K for several months after just a single dose.
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5/29. Inherited vitamin k deficiency: case report and review of literature.

    Vitamin K is the cofactor for the hepatic carboxylation of glutamic acid residues in a number of proteins including the procoagulants factors II, VII, IX, and X. The role of vitamin K in normal bone function is not fully understood. Inherited deficiency of vitamin K dependent coagulation factors is a rare bleeding disorder reported only in a few patients. Here we present an 18-month old child who presented with osteopeni due to inherited vitamin k deficiency. While the patient had high bone specific alkaline phosphatase and parathyroid hormone levels and low osteocalcin and bone mineral density values, with the regular supplementation of vitamin K all the mentioned parameters returned to normal values.
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6/29. brain haemorrhage in five infants with coagulopathy.

    Most intracranial haemorrhages in infants after the neonatal period are secondary to non-accidental injury. Occasionally brain haemorrhages in non-mobile infants are due to an inherited coagulopathy. This may often be diagnosed with a coagulation screen on admission. Little is known about the neurological outcome of infants in the latter group. Five infants are described who presented with acute spontaneous brain haemorrhage secondary to an inherited coagulopathy (n = 3) and vitamin k deficiency in alpha(1) antitrypsin deficiency (n = 1) and Alagille's syndrome (n = 1). Despite the critical clinical presentation and the severe imaging findings, these five infants made a good neurological recovery. Infants presenting with spontaneous ICH due to a significant (inherited) coagulopathy are usually easy to differentiate from non-accidental shaking injury; their bleeding pattern within the brain seems different from non-accidental shaking injury and neurodevelopment outcome appears better.
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7/29. Bleeding disorder as the first symptom of biliary atresia.

    biliary atresia (BA) is occasionally diagnosed in infants whose first symptom is a bleeding disorder, such as intracranial bleeding, nasal bleeding or gastrointestinal bleeding. The authors describe 3 cases in which a bleeding disorder was the first symptom of BA. The presenting symptom was intracranial bleeding in a male on day 55 after birth, nasal bleeding in a female at 65 days, and gastrointestinal bleeding in a female at 25 days. Coagulation studies revealed a vitamin k deficiency in all patients. After the administration of vitamin K, the results of coagulation tests normalized and the bleeding tendency of the infants ceased. Subsequently, BA was suspected to be the cause of these bleeding disorders based on imaging findings. BA should therefore be considered in all infants with sudden onset of a tendency to bleed.
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ranking = 0.2
keywords = coagulation
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8/29. Congenital vitamin K-dependent coagulation factor deficiency: a case report.

    Congenital vitamin K-dependent coagulation factor deficiency is a very rare bleeding disorder, which usually presents with episodes of intracerebral bleed in the first few weeks of life, sometimes leading to a fatal outcome. We report a case of combined factor deficiency of vitamin K-dependent factors in which the patient presented with both intracerebral bleeding, and possibly also thrombosis, and responded to a vitamin K supplement along with fresh frozen plasma.
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9/29. warfarin skin necrosis: recurrence in the absence of anticoagulant therapy.

    skin necrosis is a well-known yet rare complication of oral anticoagulant therapy. We report the unusual recurrence of lesions typical of warfarin skin necrosis in the absence of anticoagulant therapy. A 59-year-old woman developed skin necrosis while receiving prophylactic warfarin following the detection of a large left ventricular thrombus. The warfarin was discontinued and the lesions improved. One month later new areas of skin necrosis developed although the patient had received no further warfarin. Progressive congestive heart failure, poor nutrition, and prolonged oral antibiotic therapy preceded the recurrence. vitamin k deficiency was present on admission. The potential role of vitamin K-dependent coagulation factors in the pathogenesis of anticoagulant-associated skin necrosis is discussed.
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ranking = 0.2
keywords = coagulation
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10/29. Generalized pseudoxanthoma elasticum with deficiency of vitamin K-dependent clotting factors.

    A patient with generalized cutis laxa-like pseudoxanthoma elasticum was found to have a congenital deficiency of vitamin K-dependent coagulation factors II, VII, IX, and X. This association may not be fortutious and may define a particular subset of pseudoxanthoma elasticum with an autosomal recessive inheritance and the clinical features of generalized cutis laxa.
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