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pyridoxine/hemorragia
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[Treatment of functional uterine hemorrhages with pyridoxine].
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Roth spots in pyridoxine dependent epilepsy.
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Pyridoxine dependent epilepsy (PDE) is a rare metabolic defect in the degradation of lysine. The authors report a patient with metabolic and DNA confirmed PDE, on the fifth day of life ophthalmoscopy showed bilateral multiple white centred retinal haemorrhages, so called Roth spots. Roth spots are
[Immunomodulating effect of pyridoxine, folate, and cobalamin in various forms of anemia].
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Hemorrhage and toxic lesions of hemopoietic tissues inhibit the development of various types of immune response and induce immunosuppressive properties in light erythrocytes, while not influencing the immunological activity of heavy erythrocytes. The immunomodulant action of pyridoxine, folate and
[Actual vitamin and main foodstuffs consumption by recovered patients suffered from hemorrhagic fever with renal syndrome].
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Actual consumption of vitamins A, E, beta-carotene, ascorbic acid, thiamin, pyridoxine and main foodstuffs by recovered patients suffered from hemorrhagic fever with renal syndrome has been given. Frequency analysis of foodstuffs consumption was used to study actual nourishment of recovered
Infantile convulsion suspected of pyridoxine responsive seizures.
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A 6-month-old boy, having suffered repeated convulsive siezures since birth, died of severe epilepsy, the disease remaining unknown. However, when a brother, born after the death of the present case, displayed the same clinical symptoms and was diagnosed clinically as having pyridoxine dependent
Superiority of bromocriptine over pyridoxine in the treatment of patients with acromegaly or galactorrhea.
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Sixteen patients, eight with acromegaly and eight with galactorrhea, were treated with pyridoxine (600 mg/day) for a three-month period. The clinical and biochemical changes induced by the drug were compared with those induced by bromocriptine (2.5 to 50 mg/day) administered for the same length of
Fetal onset ventriculomegaly and subependymal cysts in a pyridoxine dependent epilepsy patient.
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Pyridoxine dependent epilepsy (PDE) is caused by mutations in the ALDH7A1 gene encoding α-aminoadipic semialdehyde dehydrogenase. The classic clinical presentation is neonatal seizures responsive only to pyridoxine therapy. White matter abnormalities, corpus callosum agenesis or hypoplasia,
Effect of oral pyridoxine hydrochloride supplementation on in vitro platelet sensitivity to different agonists.
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Effect of vitamin B6 (pyridoxine-HCl, CAS 58-56-0) on platelet aggregation, plasma lipids and serum zinc level was investigated. The trial comprised 24 healthy male volunteers, aged between 19-24 years. The subjects were randomized in two groups of 12 and treated for 4 weeks by a single daily oral
B6 and Bleeding: A Case Report of a Novel Vitamin Toxicity.
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Pyridox(am)ine-5-phosphate oxidase deficiency is an inborn error of vitamin B6 metabolism that is characterized by neonatal seizures, requiring lifelong therapy with pyridoxal-5-phosphate. We present the first case of a patient with pyridox(am)ine-5-phosphate oxidase deficiency and mild hemophilia
A case of pyridoxine-dependent epilepsy with novel ALDH7A1 mutations.
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Pyridoxine-dependent epilepsy (PDE) is a rare autosomal-recessive disorder typically presenting with neonatal seizures and is sometimes difficult to diagnose, because the clinical features mimic those of birth asphyxia. A Japanese newborn boy presented with pulmonary haemorrhage and convulsions on
Profound neonatal hypoglycemia and lactic acidosis caused by pyridoxine-dependent epilepsy.
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Pyridoxine-dependent epilepsy (PDE) was first described in 1954. The ALDH7A1 gene mutations resulting in α-aminoadipic semialdehyde dehydrogenase deficiency as a cause of PDE was identified only in 2005. Neonatal epileptic encephalopathy is the presenting feature in >50% of patients with classic
Pyridoxine-Dependent Epilepsy: An Expanding Clinical Spectrum.
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Pyridoxine-dependent epilepsy is a rare autosomal recessive epileptic encephalopathy caused by antiquitin (ALDH7A1) deficiency. In spite of adequate seizure control, 75% of patients suffer intellectual developmental disability. Antiquitin deficiency affects lysine catabolism resulting in
Pyridoxine-dependent seizures: demographic, clinical, MRI and psychometric features, and effect of dose on intelligence quotient.
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A regional population-based survey identified six patients with pyridoxine dependency. Four presented on the first day of life and the other two at 1 and 8 months of age. Apart from multiple seizure types, other presenting features included jitteriness; encephalopathy, at first thought to be
VITAMIN B6 (PYRIDOXINE HYDROCHLORIDE) TOXICOSIS IN FALCONS.
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This manuscript reports three independent accidental cases of vitamin (Vit) B6 toxicosis in gyrfalcons (Falco rusticolus) and peregrine falcons (Falco peregrinus) and a toxicology study that was conducted to characterize the clinical responses of gyrfalcons and gyrfalcon × peregrine falcons to a
Myelodysplastic syndrome and acquired factor VIII inhibitor with severe subcutaneous haemorrhage.
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A case of acquired haemophilia A presenting with extensive spontaneous bruising and anaemia is reported. The anaemia was due to myelodysplastic syndrome (FAB: refractory anaemia with ringed sideroblasts). A factor-VII:C-specific inhibitor was also found. Prednisone and pyridoxine were given, and the
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