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.
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- Anderson K. E., Alvares A. P., Sassa S., Kappas A. Studies in porphyria. V. Drug oxidation rates in hereditary hepatic porphyria. Clin Pharmacol Ther. 1976 Jan;19(1):47–54. doi: 10.1002/cpt197619147. [DOI] [PubMed] [Google Scholar]
- Boobis A. R., Brodie M. J., Kahn G. C., Toverud E. L., Blair I. A., Murray S., Davies D. S. Comparison of the in vivo and in vitro rates of formation of the three main oxidative metabolites of antipyrine in man. Br J Clin Pharmacol. 1981 Dec;12(6):771–777. doi: 10.1111/j.1365-2125.1981.tb01305.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Brodie M. J., Moore M. R., Goldberg A. Enzyme abnormalities in the porphyrias. Lancet. 1977 Oct 1;2(8040):699–701. doi: 10.1016/s0140-6736(77)90507-4. [DOI] [PubMed] [Google Scholar]
- Brodie M. J., Moore M. R., Thompson G. G., Campbell B. C., Goldberg A. Is porphobilinogen deaminase activity a secondary control mechanism in haem biosynthesis in humans? [proceedings]. Biochem Soc Trans. 1977;5(5):1466–1468. doi: 10.1042/bst0051466. [DOI] [PubMed] [Google Scholar]
- Brodie M. J., Thompson G. G., Moore M. R., Beattie A. D., Goldberg A. Hereditary coproporphyria. Demonstration of the abnormalities in haem biosynthesis in peripheral blood. Q J Med. 1977 Apr;46(182):229–241. [PubMed] [Google Scholar]
- Macphee G. J., Thompson G. G., Scobie G., Agnew E., Park B. K., Murray T., McColl K. E., Brodie M. J. Effects of cimetidine on carbamazepine auto- and hetero-induction in man. Br J Clin Pharmacol. 1984 Sep;18(3):411–419. doi: 10.1111/j.1365-2125.1984.tb02483.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- McColl K. E., Moore M. R., Thompson G. G., Goldberg A. Screening for latent acute intermittent porphyria: the value of measuring both leucocyte delta-aminolaevulinic acid synthase and erythrocyte uroporphyrinogen-1-synthase activities. J Med Genet. 1982 Aug;19(4):271–276. doi: 10.1136/jmg.19.4.271. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Ostrowski J., Kostrzewska E., Michalak T., Zawirska B., Medrzejewski W., Gregor A. Abnormalities in liver function and morphology and impaired aminopyrine metabolism in hereditary hepatic porphyrias. Gastroenterology. 1983 Nov;85(5):1131–1137. [PubMed] [Google Scholar]
- Song C. S., Bonkowsky H. L., Tschudy D. P. Salicylamide metabolism in acute intermittent porphyria. Clin Pharmacol Ther. 1974 Apr;15(4):431–435. doi: 10.1002/cpt1974154431. [DOI] [PubMed] [Google Scholar]
- Stein J. A., Bloomer J. R., Berk P. D., Corcoran P. L., Tschudy D. P. The kinetics of organic anion excretion by the liver in acute intermittent porphyria. Clin Sci. 1970 Jun;38(6):677–686. doi: 10.1042/cs0380677. [DOI] [PubMed] [Google Scholar]