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Br J Clin Pharmacol. 1987 Mar;23(3):358-61. doi: 10.1111/j.1365-2125.1987.tb03059.x.
2
Studies in porphyria. V. Drug oxidation rates in hereditary hepatic porphyria.卟啉症研究。V. 遗传性肝卟啉症中的药物氧化速率。
Clin Pharmacol Ther. 1976 Jan;19(1):47-54. doi: 10.1002/cpt197619147.
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Effect of haem arginate therapy on porphyrin metabolism and mixed function oxygenase activity in acute hepatic porphyria.精氨酸血红素疗法对急性肝卟啉病患者卟啉代谢及混合功能氧化酶活性的影响
Lancet. 1987 Nov 21;2(8569):1178-9. doi: 10.1016/s0140-6736(87)91320-1.
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The reversal of experimental porphyria and the prevention of induction of hepatic mixed-function oxidase by acetate.实验性卟啉症的逆转以及乙酸盐对肝混合功能氧化酶诱导的预防。
Arch Biochem Biophys. 1974 Sep;164(1):351-6. doi: 10.1016/0003-9861(74)90041-1.
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Urinary excretion of porphyrins, porphobilinogen and δ-aminolaevulinic acid following an attack of acute intermittent porphyria.急性间歇性卟啉症发作后卟啉、卟啉原和 δ-氨基酮戊酸的尿排泄。
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[Urinary excretion of porphyrins and their precursors. Longterm observations in acute intermittent porphyrias (author's transl)].[卟啉及其前体的尿排泄。急性间歇性卟啉病的长期观察(作者译)]
MMW Munch Med Wochenschr. 1979 Mar 30;121(13):457-8.
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"Glucose effect" and rate limiting function of uroporphyrinogen synthase on porphyrin metabolism in hepatocyte culture: relationship with human acute hepatic porphyrias.“葡萄糖效应”及尿卟啉原合酶在肝细胞培养中对卟啉代谢的限速作用:与人类急性肝卟啉症的关系
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Acute hepatic porphyria syndrome with porphobilinogen synthase defect.
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10
Erythropoietin treatment in the neuropsychiatric porphyrias.神经精神性卟啉病的促红细胞生成素治疗
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引用本文的文献

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Haem arginate improves hepatic oxidative metabolism in variegate porphyria.精氨酸血红素可改善混合型卟啉病患者的肝脏氧化代谢。
Br J Clin Pharmacol. 1988 Dec;26(6):753-7. doi: 10.1111/j.1365-2125.1988.tb05315.x.
2
Influences of diet and nutrition on clinical pharmacokinetics.饮食和营养对临床药代动力学的影响。
Clin Pharmacokinet. 1988 Jun;14(6):325-46. doi: 10.2165/00003088-198814060-00002.
3
Clinical pharmacokinetics in patients with liver disease.肝病患者的临床药代动力学
Clin Pharmacokinet. 1991 Jul;21(1):42-69. doi: 10.2165/00003088-199121010-00004.

本文引用的文献

1
Comparison of the in vivo and in vitro rates of formation of the three main oxidative metabolites of antipyrine in man.人体内安替比林三种主要氧化代谢物的体内和体外生成速率比较。
Br J Clin Pharmacol. 1981 Dec;12(6):771-7. doi: 10.1111/j.1365-2125.1981.tb01305.x.
2
Screening for latent acute intermittent porphyria: the value of measuring both leucocyte delta-aminolaevulinic acid synthase and erythrocyte uroporphyrinogen-1-synthase activities.潜伏性急性间歇性卟啉病的筛查:同时检测白细胞δ-氨基乙酰丙酸合酶和红细胞尿卟啉原-1-合酶活性的价值。
J Med Genet. 1982 Aug;19(4):271-6. doi: 10.1136/jmg.19.4.271.
3
Abnormalities in liver function and morphology and impaired aminopyrine metabolism in hereditary hepatic porphyrias.遗传性肝卟啉症患者的肝功能和形态异常以及氨基比林代谢受损。
Gastroenterology. 1983 Nov;85(5):1131-7.
4
Effects of cimetidine on carbamazepine auto- and hetero-induction in man.西咪替丁对人体中卡马西平自身诱导和异体诱导的影响。
Br J Clin Pharmacol. 1984 Sep;18(3):411-9. doi: 10.1111/j.1365-2125.1984.tb02483.x.
5
The kinetics of organic anion excretion by the liver in acute intermittent porphyria.急性间歇性卟啉症中肝脏对有机阴离子的排泄动力学。
Clin Sci. 1970 Jun;38(6):677-86. doi: 10.1042/cs0380677.
6
Salicylamide metabolism in acute intermittent porphyria.急性间歇性卟啉病中的水杨酰胺代谢
Clin Pharmacol Ther. 1974 Apr;15(4):431-5. doi: 10.1002/cpt1974154431.
7
Studies in porphyria. V. Drug oxidation rates in hereditary hepatic porphyria.卟啉症研究。V. 遗传性肝卟啉症中的药物氧化速率。
Clin Pharmacol Ther. 1976 Jan;19(1):47-54. doi: 10.1002/cpt197619147.
8
Is porphobilinogen deaminase activity a secondary control mechanism in haem biosynthesis in humans? [proceedings].胆色素原脱氨酶活性是人类血红素生物合成中的一种次级调控机制吗?[会议论文集]
Biochem Soc Trans. 1977;5(5):1466-8. doi: 10.1042/bst0051466.
9
Hereditary coproporphyria. Demonstration of the abnormalities in haem biosynthesis in peripheral blood.遗传性粪卟啉病。外周血中血红素生物合成异常的证明。
Q J Med. 1977 Apr;46(182):229-41.
10
Enzyme abnormalities in the porphyrias.卟啉症中的酶异常。
Lancet. 1977 Oct 1;2(8040):699-701. doi: 10.1016/s0140-6736(77)90507-4.

急性肝性卟啉病复发期与缓解期的安替比林代谢

Antipyrine metabolism in acute hepatic porphyria in relapse and remission.

作者信息

Birnie G G, McColl K E, Thompson G G, Moore M R, Goldberg A, Brodie M J

出版信息

Br J Clin Pharmacol. 1987 Mar;23(3):358-61. doi: 10.1111/j.1365-2125.1987.tb03059.x.

DOI:10.1111/j.1365-2125.1987.tb03059.x
PMID:3567053
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1386238/
Abstract

Antipyrine kinetics following a single oral dose were obtained in porphyric patients in attack and in remission and in controls. The clearance of antipyrine was significantly lower during an acute porphyric attack (median: 0.34 ml min-1 kg-1; range: 0.1-0.71, P less than 0.05) than in patients in remission (median: 0.53 ml min-1 kg-1; range: 0.28-0.87) or controls (median: 0.52 ml min-1 kg-1; range: 0.32-0.93). There was a significant negative correlation between weight-adjusted antipyrine clearance and the urinary excretion of the porphyrin precursors, delta-aminolaevulinic acid (r = 0.86, P less than 0.001) and porphobilinogen (r = 0.82, P less than 0.002). These data suggest that the more severe the porphyric attack, the greater the impairment of hepatic monooxygenase activity.

摘要

在急性发作期和缓解期的卟啉症患者以及对照组中,获取了单次口服安替比林后的动力学数据。在急性卟啉症发作期间,安替比林的清除率(中位数:0.34 ml min⁻¹ kg⁻¹;范围:0.1 - 0.71,P < 0.05)显著低于缓解期患者(中位数:0.53 ml min⁻¹ kg⁻¹;范围:0.28 - 0.87)或对照组(中位数:0.52 ml min⁻¹ kg⁻¹;范围:0.32 - 0.93)。体重校正后的安替比林清除率与卟啉前体δ-氨基乙酰丙酸的尿排泄量(r = 0.86,P < 0.001)和胆色素原(r = 0.82,P < 0.002)之间存在显著负相关。这些数据表明,卟啉症发作越严重,肝单加氧酶活性的损害就越大。