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1.
Medicina (B.Aires) ; 62(2): 149-153, 2002.
Artigo em Espanhol | LILACS, BINACIS | ID: biblio-1165113

RESUMO

Homocysteine is a risk factor for cardiovascular disease. Mutations in a key enzyme in homocysteine metabolism, methylenetetrahydrofolate reductase, may contribute to hyperhomocysteinemia and alter folate and cobalamin levels. After starting hemodialysis, 10 mg oral folate daily and 500 micrograms intravenous methylcobalamin once weekly were prescribed to 27 hemodialysis patients (time on hemodialysis > or = 12 months) and two groups were defined: Group A normal; Group B heterozygous. Initial, third and twelfth month measurements of homocysteine, serum folate and vitamin B12 levels were collected and analyzed. Heterozygous state of methylenetetrahydrofolate reductase prevalence was 48


. Hyperhomocysteinemia was present in both groups. Cobalamin final levels were significantly lower in Group B compared to Group A. Homocysteine, serum folate and cobalamin levels at third and twelfth month were significantly different from baseline levels but non-different between them in both groups. In Group B, vitamin B12 at third month was significantly higher than initial, but final measurements were not different from baseline determinations. In conclusion, the heterozygous prevalence of the enzyme in hemodialysis patients is similar to that reported in the general population; hyperhomocysteinemia is frequent in hemodialysis patients and final levels in heterozygous patients are significantly higher than in normal patients. Cobalamin levels are lower in the heterozygous group. After one year of treatment, homocysteine tends to increase, suggesting a secondary resistance phenomenon to vitamin supplementation in heterozygous patients.


Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Vitamina B 12/análogos & derivados , Vitamina B 12/sangue , Ácido Fólico/sangue , Oxirredutases atuantes sobre Doadores de Grupo CH-NH/genética , Homocisteína/sangue , Falência Renal Crônica/enzimologia , Vitamina B 12/uso terapêutico , Distribuição de Qui-Quadrado , Diálise Renal , Mutação Puntual/genética , Estatísticas não Paramétricas , Hiper-Homocisteinemia/prevenção & controle , Metilenotetra-Hidrofolato Redutase (NADPH2) , Ácido Fólico/uso terapêutico , Heterozigoto , Homocisteína/genética , Falência Renal Crônica/sangue , Falência Renal Crônica/terapia
2.
Rev. nefrol. diál. traspl ; (49): 9-12, dic. 1999.
Artigo em Espanhol | LILACS | ID: lil-253563

RESUMO

La eritrocitosis post-transplante es una entidad caracterizada por un hematocrito superior al 51 por ciento, tiene una prevalencia del 10 al 15 por ciento en los pacientes transplantados renales, y puede manifestarse en cualquier momento post-transplante. La eritrocitosis post-transplante se asocia a hipertensión arterial, por aumento de la volemia, y es un factor predisponente a la trombosis vascular, por aumento de la viscosidad sanguínea. Tanto la angiotensina II como el Insulin Growth Factor I y otros compuestos han sido postulados como posibles mediadores del aumento de la eritropoyesis. La eritropoyetina se encuentra en valores aumentados en esta entidad, aunque existen casos en los cuales la misma se encuentra en valores normales o disminuídos. Independientemente de estos niveles, los inhibidores de la enzima convertidora de angiotensina, o recientemente los inhibidores del receptor de angiotensina II, son las drogas de elección para tratar en forma efectiva y segura la eritrocitosis post-trasnplante.


Assuntos
Humanos , Policitemia/etiologia , Policitemia/terapia , Transplante de Rim/efeitos adversos , Angiotensina II/antagonistas & inibidores , Inibidores da Enzima Conversora de Angiotensina , Eritropoetina
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