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患有急性乳糜泻、乳糜泻缓解期的儿童以及十二指肠黏膜正常儿童的维生素B6营养状况。

Vitamin B6 nutriture of children with acute celiac disease, celiac disease in remission, and of children with normal duodenal mucosa.

作者信息

Reinken L, Zieglauer H, Berger H

出版信息

Am J Clin Nutr. 1976 Jul;29(7):750-3. doi: 10.1093/ajcn/29.7.750.

Abstract

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.

摘要

成年乳糜泻患者在摄入这种氨基酸后,色氨酸代谢产物的排泄量异常,这表明这些患者存在维生素B6缺乏。事实上,给予维生素B6后,色氨酸代谢产物的排泄恢复正常。通过测定14例急性乳糜泻患儿以及6例处于临床和生化缓解期的乳糜泻患儿血清和十二指肠黏膜中的磷酸吡哆醛及吡哆醇激酶活性,来评估维生素B6营养状况。以10例十二指肠黏膜正常的儿童作为对照。与缓解期儿童和对照组相比,乳糜泻患儿血清和十二指肠黏膜中的磷酸吡哆醛显著降低。然而,与对照组相比,乳糜泻患儿血清和十二指肠黏膜中的吡哆醇激酶活性显著升高,但与缓解期儿童相比则无显著差异。这些患儿的吡哆醇激酶活性升高程度与急性乳糜泻患儿相同。这些数据有力地证明了急性乳糜泻患儿存在维生素B6缺乏。处于缓解期的乳糜泻患儿的吡哆醇激酶活性仍然升高,这似乎是无麸质饮食前维生素B6缺乏所导致的一种代偿机制。

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