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galactosemias/edema
Veza se sprema u međuspremnik
15 rezultati
Computed tomographic demonstration of cerebral edema in a child with galactosemia.
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An eight-day-old male infant with galactosemia presented with signs of increased intracranial pressure and no evidence of intracranial infection or hemorrhage. Computed tomographic scans demonstrated the presence of diffuse cerebral edema. With treatment, the edema gradually resolved, although it
Cerebral edema and galactosemia.
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[Anasarca of fatal course in a newborn infant. Possible role of a congenital galactosemia].
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Brain MRI in a patient with classical galactosemia: acute event of unilateral hemispheric cerebral edema.
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Teaching NeuroImages: Galactitol peak and fatal cerebral edema in classic galactosemia: Too much sugar in the brain.
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Proton magnetic resonance spectroscopy of brain metabolites in galactosemia.
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Brain edema may occur in infants with galactosemia and has been associated with accumulation of galactitol. Proton magnetic resonance spectra were obtained from 12 patients (four newly diagnosed neonates and eight patients on galactose-restricted diets, age range 1.7-47 years) and control subjects
Suckling rat brain regional distribution of Na+,K+-atpase activity in the in vitro galactosaemia: the effect of L-cysteine and glutathione.
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Inhibition of Na+,K+-ATPase activity causes edema and cell death in central nervous system. We determined the in vitro effects of galactose-l-phosphate (Gal-1-P), galactitol (Galtol) and galactose (Gal) (mix A = classical galactosaemia) or Galtol and Gal (mix B = galactokinase deficiency
In vivo evidence of brain galactitol accumulation in an infant with galactosemia and encephalopathy.
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In a newborn infant with galactose-1-phosphate uridyltransferase deficiency and encephalopathy, brain magnetic resonance imaging revealed cytotoxic edema in white matter. Using in vivo proton magnetic resonance spectroscopy, we detected approximately 8 mmol galactitol per kilogram of brain tissue,
Evidence of cataplerosis in a patient with neonatal classical galactosemia presenting as citrin deficiency.
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Classical galactosemia is an autosomal recessive disorder caused by a deficiency of the enzyme galactose-1-phosphate uridyltransferase. Undoubtedly, some of the short term complications are linked to the toxic effects of the accumulated abnormal metabolites (galactose-1-phosphate and galactitol).
Cerebellar herniation after lumbar puncture in galactosemic newborn.
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Cerebral edema resulting in elevated intracranial pressure is a well-known complication of galactosemia. Lumbar puncture was performed for the diagnosis of clinically suspected bacterial meningitis. Herniation of cerebral tissue through the foramen magnum is not a common problem in neonatal
Expanding the Spectrum of PMM2-CDG Phenotype.
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Congenital Disorders of Glycosylation (CDG) are a group of recently described inborn errors of metabolism affecting glycosylation. CDG are disorders that have been reported with a great variability in the clinical presentation, especially for the most common PMM2-CDG. The classical form is
Subfertility and growth restriction in a new galactose-1 phosphate uridylyltransferase (GALT) - deficient mouse model.
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The first GalT gene knockout (KO) mouse model for Classic Galactosemia (OMIM 230400) accumulated some galactose and its metabolites upon galactose challenge, but was seemingly fertile and symptom free. Here we constructed a new GalT gene-trapped mouse model by injecting GalT gene-trapped mouse
Lens changes in a galactosemic fetus.
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The first child of a Spanish-American couple died presumbably from galactosemia. Early in the mother's fourth pregnancy, the parents' red blood cell levels of galactose 1-phosphate uridyl transferase were measured and both parents were found to be heterozygous (carriers) for transferase deficiency.
[Prenatal symptoms and diagnosis of inherited metabolic diseases].
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Inherited metabolic diseases are mostly due to enzyme deficiency in one of numerous metabolic pathways, leading to absence of a compound downstream from and the accumulation of a compound upstream from the deficient metabolite(s). Diseases of intoxication by proteins (aminoacidopathies, organic
Inborn errors of metabolism in infancy: a guide to diagnosis.
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Recent advances in the diagnosis and treatment of inborn errors of metabolism have improved substantially the prognosis for many of these conditions. This makes it essential that the practicing pediatrician be familiar with the clinical presentation of these disorders. A practical clinical approach
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