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• W2016120999 abstract "Vitamin B 6 deficiency in uremia and its implications for the depression of immune responses. By serial determinations of the glutamic oxaloacetic transaminase (GOT) activity of erythrocytes, we found a marked biochemical vitamin B 6 deficiency in 48 out of 69 patients with advanced chronic azotemia (serum creatinine >4 mg/100 ml), 37 on chronic intermittent dialysis and 32 being treated conservatively. As an index for vitamin B 6 status, we used the stimulation effect of pyridoxal-5′ phosphate on the erythrocyte EGOT activity (activation coefficient, α egot ), with values ≧1.7 indicating a biochemical vitamin B 6 deficiency. Increased activation coefficients were restored to normal by the oral administration of 300 mg of vitamin B 6 (pyridoxine HCl) daily for two weeks. From measurements of the GOT activity of nondeficient erythrocytes after incubation with plasma of uremic patients, we can exclude any inhibitory effect of plasma constituents in uremia on the enzyme activity. Hemodialysis improved elevated EGOT ratios significantly. On the basis of these findings we suggest that inhibition of pyridoxal kinase activity rather than insufficient vitamin B 6 supply is the most likely explanation for the depletion of vitamin B 6 coenzyme in uremia. Diminution of reactivity in mixed lymphocyte cultures of uremics could be reversed by treating the patients with vitamin B 6 orally. We conclude that suppression of cellmediated immunity in uremia is probably in part due to vitamin B 6 depletion. Deficit en vitamine B 6 dans l'uremie et ses implications quant a la diminution des responses immunes. Au moyen de determinations repetees de la transaminase glutamate-oxaloacetique (GOT) des erythrocytes nous avons mis en evidence un deficit important en vitamine B 6 chez 48 malades parmi 69 atteints d'insuffisance renale chronique (creatininemie > 4 mg/100 ml), 37 d'entre eux sont soumis a l'hemodialyse periodique et 32 sont traites par des moyens conservateurs. Comme parametre de la situation de la vitamine B 6 nous utilisons l'effet stimulateur du pyridoxal-5′ phosphate sur l'activite de la transaminase glutamate-oxaloacetique des erythrocytes (coefficient d'activation α egot ), des valeurs ≧1,7 indiquent un deficit biochimique en vitamine B 6 . Des coefficients d'activation augmentes sont normalises par l'administration orale de 300 mg de vitamine B 6 quotidiennement pendant deux semaines. A partir de mesures de l'activite de la GOT d'erythrocytes sans deficit incubes avec du plasma de malades uremiques nous pouvons exclure un quelconque effet inhibiteur des constituants plasmatiques au cours de l'uremie sur l'activite enzymatique. Sur la base de ces constations nous suggerons que l'inhibition de l'activite de la pyridoxal-kinase, plutot qu'un apport insuffisant de vitamine B 6 , est l'explication la plus probable de la depletion en coenzyme de la vitamine B 6 au cours de l'uremie. La diminution de reactivite de cultures mixtes de lymphocytes d'uremiques pourrait etre abolie par le traitement prealable des malades par la vitamine B 6 . Nous concluons que la suppression de l'immunite cellulaire au cours de l'uremie est probablement en partie liee a une depletion en vitamine B 6 ." @default.
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• W2016120999 title "Vitamin B6 deficiency in uremia and its implications for the depression of immune responses" @default.
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• W2016120999 doi "https://doi.org/10.1038/ki.1974.28" @default.
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