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BMJ. 1988 Jul 9;297(6641):105-7. doi: 10.1136/bmj.297.6641.105.
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本文引用的文献

1
A family and population study of the genetic polymorphism of debrisoquine oxidation in a white British population.对英国白人人群中异喹胍氧化遗传多态性的家系及群体研究。
J Med Genet. 1980 Apr;17(2):102-5. doi: 10.1136/jmg.17.2.102.
2
Defective oxidation of drugs: pharmacokinetic and therapeutic implications.药物氧化缺陷:药代动力学及治疗学意义
Clin Pharmacokinet. 1982 Jan-Feb;7(1):1-22. doi: 10.2165/00003088-198207010-00001.
3
The contribution of genetically determined oxidation status to inter-individual variation in phenacetin disposition.遗传决定的氧化状态对非那西丁处置个体间差异的影响。
Br J Clin Pharmacol. 1983 Aug;16(2):157-66. doi: 10.1111/j.1365-2125.1983.tb04980.x.
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Food hypersensitivity.食物过敏
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5
Genetic aspects of the polymodally distributed sulphoxidation of S-carboxymethyl-L-cysteine in man.人体中S-羧甲基-L-半胱氨酸多峰分布硫氧化的遗传因素
Br J Clin Pharmacol. 1984 Oct;18(4):507-21. doi: 10.1111/j.1365-2125.1984.tb02498.x.
6
Substrate specificity of the form of cytochrome P-450 catalyzing the 4-hydroxylation of debrisoquine in man.人肝脏中催化异喹胍4-羟化反应的细胞色素P-450形式的底物特异性
Mol Pharmacol. 1983 Mar;23(2):474-81.
7
Systemic allergic reactions to ingested antigens.对摄入抗原的全身性过敏反应。
J Allergy. 1969 Aug;44(2):96-107. doi: 10.1016/0021-8707(69)90005-7.
8
Cytosolic sulphoxidation of S-carboxymethyl-L-cysteine in mammals.哺乳动物中S-羧甲基-L-半胱氨酸的胞质硫氧化作用。
Biochem Pharmacol. 1986 Sep 15;35(18):2999-302. doi: 10.1016/0006-2952(86)90377-1.
9
IgE complexes in food allergy.食物过敏中的IgE复合物。
Ann Allergy. 1987 Aug;59(2):110-7.

食物敏感患者的硫氧化能力较差。

Poor sulphoxidation ability in patients with food sensitivity.

作者信息

Scadding G K, Ayesh R, Brostoff J, Mitchell S C, Waring R H, Smith R L

机构信息

Department of Immunology, Middlesex Hospital Medical School, London.

出版信息

BMJ. 1988 Jul 9;297(6641):105-7. doi: 10.1136/bmj.297.6641.105.

DOI:10.1136/bmj.297.6641.105
PMID:3408928
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1833819/
Abstract

Patients with well defined reactions to foods were examined for their ability to carry out both sulphur and carbon oxidation reactions by using carbocisteine and debrisoquine as probe compounds. The proportion of poor sulphoxidisers (58 of 74) was significantly greater than that of a previously determined normal control population (67 of 200; p less than 0.005). The proportion of poor carbon oxidisers was not significantly different from the controls. Metabolic defects may play a part in the pathogenesis of adverse reactions to foods.

摘要

对食物有明确反应的患者,通过使用羧甲司坦和异喹胍作为探针化合物,检测他们进行硫和碳氧化反应的能力。硫氧化能力差的患者比例(74例中有58例)显著高于先前确定的正常对照人群(200例中有67例;p<0.005)。碳氧化能力差的患者比例与对照组无显著差异。代谢缺陷可能在食物不良反应的发病机制中起作用。