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接受抗惊厥药物治疗患者的代谢性酸中毒。

Metabolic acidosis in patients receiving anticonvulsants.

作者信息

Nagai B, Matsuda I, Kondo T, Taniguchi N, Arashima S, Mitsuyama T, Oka Y, Honma M

出版信息

Eur J Pediatr. 1979 Nov;132(3):161-8. doi: 10.1007/BF00442432.

DOI:10.1007/BF00442432
PMID:41717
Abstract

Blood pH, bicarbonate, PCO2, serum calcium, alkaline phosphatase and red cell carbonic anhydrase were measured in 37 selected patients receiving anticonvulsants. Patients with metabolic acidosis showed a high incidence of hypocalcemia with increased alkaline phosphatase and a significant reduction of carbonic anhydrase-B activity. High iPTH levels were found in 13 patients, but this was not correlated with acid-base balance status. Anticonvulsant drugs seemed to inactive carbonic anhydrase-B activity. Metabolic acidosis might be one of the factors causing a disturbance of calcium metabolism in these patients.

摘要

对37例服用抗惊厥药的特定患者进行了血液pH值、碳酸氢盐、二氧化碳分压、血清钙、碱性磷酸酶和红细胞碳酸酐酶的检测。代谢性酸中毒患者低钙血症发生率较高,碱性磷酸酶升高,碳酸酐酶-B活性显著降低。13例患者甲状旁腺激素水平升高,但这与酸碱平衡状态无关。抗惊厥药物似乎使碳酸酐酶-B活性失活。代谢性酸中毒可能是导致这些患者钙代谢紊乱的因素之一。

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Metabolic acidosis in patients receiving anticonvulsants.接受抗惊厥药物治疗患者的代谢性酸中毒。
Eur J Pediatr. 1979 Nov;132(3):161-8. doi: 10.1007/BF00442432.
2
[Studies on the mechanism of metabolic acidosis observed in the children treated with anticonvulsants].[关于接受抗惊厥药物治疗的儿童中观察到的代谢性酸中毒机制的研究]
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引用本文的文献

1
Pseudohypoparathyroidism type II and anticonvulsant rickets.II型假性甲状旁腺功能减退症与抗惊厥药所致佝偻病
Eur J Pediatr. 1979;132(4):303-8. doi: 10.1007/BF00496854.

本文引用的文献

1
Purification and properties of human erythrocyte carbonic anhydrases.人红细胞碳酸酐酶的纯化及性质
J Biol Chem. 1966 Nov 10;241(21):5137-49.
2
Activation and phosphorylation of carbonic anhydrase by adenosine 3',5'-monophosphate-dependent protein kinases.3',5'-环磷酸腺苷依赖性蛋白激酶对碳酸酐酶的激活与磷酸化作用。
Biochim Biophys Acta. 1974 May 20;350(1):215-24. doi: 10.1016/0005-2744(74)90219-8.
3
Vitamin D-dependency rickets in institutionalized, mentally retarded children on long term anticonvulsant therapy. II. The response to 25-hydroxycholecalciferol and to vitamin D2.
长期接受抗惊厥治疗的机构收容智障儿童中的维生素D依赖性佝偻病。II. 对25-羟胆钙化醇和维生素D2的反应
Pediatr Res. 1973 Nov;7(11):914-22. doi: 10.1203/00006450-197311000-00008.
4
Enzymatically inactive red cell carbonic anhydrase B in a family with renal tubular acidosis.一个患有肾小管酸中毒的家族中的无酶活性红细胞碳酸酐酶B
J Clin Invest. 1974 Jan;53(1):59-63. doi: 10.1172/JCI107559.
5
Osteomalacia associated with anticonvulsant drug therapy in mentally retarded children.智障儿童抗惊厥药物治疗相关的骨软化症
Pediatrics. 1975 Jul;56(1):45-50.
6
Letter: Anticonvulsants, acetazolamide and osteomalacia.信函:抗惊厥药、乙酰唑胺与骨软化症
N Engl J Med. 1975 Sep 25;293(13):668. doi: 10.1056/nejm197509252931320.
7
Plasma 1,25-dihydroxyvitamin D levels in patients receiving anticonvulsant drugs.接受抗惊厥药物治疗患者的血浆1,25-二羟维生素D水平
J Clin Endocrinol Metab. 1977 Apr;44(4):617-21. doi: 10.1210/jcem-44-4-617.
8
Radioimmunoassay of bovine parathyroid hormone.牛甲状旁腺激素的放射免疫测定法。
Natl Inst Anim Health Q (Tokyo). 1975 Fall;15(3):151-8.
9
Estimations of active and inactive carbonic anhydrase isozyme B in human red cells.人体红细胞中活性与非活性碳酸酐酶同工酶B的测定
Clin Chim Acta. 1975 May 1;60(3):347-53. doi: 10.1016/0009-8981(75)90077-7.
10
Effect of correction of metabolic acidosis on bone mineralisation rates in patients with renal osteomalacia.代谢性酸中毒的纠正对肾性骨软化症患者骨矿化率的影响。
Nephron. 1975;15(2):98-110. doi: 10.1159/000180501.