Vitamin B6 nutriture of children with acute celiac disease, celiac disease in remission, and of children with normal duodenal mucosa.
Patients with adult celiac disease excrete abnormal amounts of tryptophan metabolites after loading with this amino acid, suggesting vitamin B6 deficienty in these patients, In fact, the excretion of tryptophan metabolites returns to normal after administration of vitamin B6. The vitamin B6 nutriture was measured by means of determination of pyridoxal phosphate and activity of pyridoxalkinase in serum and in duodenal mucosa of 14 children with acute celiac disease and of six children with celiac disease in clinical and biochemical remission. Ten children with normal duodenal mucosa were studied as controls. Children with celiac disease had significantly decreased pyridoxal phosphate in serum and in duodenal mucosa when compared both with children in remission and controls. Activity of pyridoxalkinase, however, was significantly increased in serum and in duodenal mucosa when compared with controls but not when compared with children in remission. These children had the same increase in pyridoxalkinase activity as children with acute celiac disease. These data provide a strong evidence for the occurrence of vitamin B6 deficienty in children with acute celiac disease. The children with celiac disease in remission still had an increased activity of pyridoxalkinase which seems to be a compensating mechanism in consequence of vitamin B6 deficiency prior to the gluten-free diet.
D002446:Celiac Disease / Q000150:complications / Q000378:metabolism*; D002648:Child; D004386:Duodenum / Q000378:metabolism*; D006801:Humans; D007223:Infant; D007413:Intestinal Mucosa / Q000378:metabolism; D010770:Phosphotransferases / Q000378:metabolism*; D011732:Pyridoxal Phosphate / Q000378:metabolism*; D012075:Remission, Spontaneous; D026681:Vitamin B 6 Deficiency / Q000150:complications
D011732:Pyridoxal Phosphate; D010770:Phosphotransferases