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Biología, patobiología y bioclínica de la homocisteína eh la especie humana

Biology, pathobiology and subclinical homocysteine in the human species



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García, G. A. (2010). Biología, patobiología y bioclínica de la homocisteína eh la especie humana. Revista Repertorio De Medicina Y Cirugía, 19(2), 115-134. https://doi.org/10.31260/RepertMedCir.v19.n2.2010.586

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Esta obra está bajo una licencia internacional Creative Commons Atribución-NoComercial-CompartirIgual 4.0.

Grégory Alfonso García

    La homocistinuria fue descrita en 19a2 en niños con dificultades de aprendizaje y en 19a9 McCully informó la evidencia en autopsias de trombosis arterial eztensa y aterosclerosis en niños con elevadas concentraciones de homocisteína plasmática y homocistinuria. La homocisteína, un aminoácido de azufre, es un metabolito intermedio de la metionina, y sobre la base de estos hallazgos bioquímicos, ellos propusieron que la homocisteína plasmática elevada puede causar lesión neural y enfermedad vascular aterosclerótica. Hoy se considera un factor de riesgo independiente para esta última. La hiperhomocistinemia leve es bastante prevalente en la población general. Puede deberse a defectos genéticos en las enzimas que participan en el metabolismo de la homocisteína, carencias nutricionales de vitaminas y cofactores, ciertos medicamentos, ingesta rica en metionina o enfermedad renal. La alta concentración puede reducirse con folato, y es así que la suplementación vitamínica ha sido propuesta en individuos con hiperhomocistinemia con el fin de reducir su riesgo de enfermedad cardiovascular. En este artículo hacemos una revisión de la biología, la patobiología y la bioclínica del metabolismo de la homocisteína.


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