| Autor: |
Dahl-Puustinen ML; Department of Clinical Pharmacology, Karolinska Institutet, Huddinge Hospital, Sweden., Aberg-Wistedt A, Bertilsson L |
| Jazyk: |
angličtina |
| Zdroj: |
Pharmacology & toxicology [Pharmacol Toxicol] 1989 Jul; Vol. 65 (1), pp. 37-9. |
| DOI: |
10.1111/j.1600-0773.1989.tb01123.x |
| Abstrakt: |
The urinary excretion of amitriptyline (AT) as N-glucuronide was studied in healthy volunteers after single oral doses of AT and in patients on continuous treatment with AT. In the volunteers, 8 +/- 3% of a 25 mg dose of AT was recovered in urine as glucuronide during 108 hr. No difference between slow and rapid debrisoquine hydroxylators with respect to the excretion of AT glucuronide was seen. 0.08 to 1.68% of the given AT dose was recovered in urine in unchanged form. The excretion of unchanged AT correlated with the debrisoquine metabolic ratio (rs = 0.61; p less than 0.01). In 5 patients on continuous treatment with AT (125-150 mg/day), 8 +/- 5% of the daily dose was recovered in 24-hr urine as AT glucuronide. The present study shows that direct glucuronidation is a minor metabolic pathway of AT in man in vivo both after single low doses and during continuous treatment with therapeutic doses. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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