Pisani F, Perucca E, Primerano G, D'Agostino A A, Petrelli R M, Fazio A, Oteri G, Di Perri R
Eur J Clin Pharmacol. 1984;27(4):465-9. doi: 10.1007/BF00549596.
The pharmacokinetics of primidone (PRM) after oral administration of a single 500 mg dose was studied in 7 patients with acute viral hepatitis and 7 healthy control subjects. The elimination half-life and the apparent clearance of unchanged PRM in the patients were 18.0 +/- 3.1 h and 42 +/- 14 ml X h-1 X kg-1, respectively (mean +/- SD) and did not differ significantly from the values in the controls (half-life 17.0 +/- 2.4 h; clearance 35 +/- 8 ml X h-1 X kg-1). The metabolite phenylethylmalonamide (PEMA) was detected in the serum of all normal subjects within 2-24 h. By contrast, serum levels of this metabolite were undetectable (less than 2 mumol/1) in all but one of the patients. Serum levels of phenobarbital (PB) remained below the limit of detection (less than 2 mumol/1) in all subjects. The findings indicate that accumulation of PRM with its attendant toxicity is unlikely to occur in epileptic patients who develop acute viral hepatitis, despite evidence that the metabolism of the drug is affected by this condition. The possibility of impaired conversion to PB and its implications are discussed.
对7例急性病毒性肝炎患者和7名健康对照者进行了研究,以观察单次口服500mg剂量的扑米酮(PRM)后的药代动力学。患者体内未变化的PRM的消除半衰期和表观清除率分别为18.0±3.1小时和42±14ml·h⁻¹·kg⁻¹(均值±标准差),与对照组的值(半衰期17.0±2.4小时;清除率35±8ml·h⁻¹·kg⁻¹)无显著差异。在所有正常受试者的血清中,2至24小时内均可检测到代谢产物苯乙丙二酰胺(PEMA)。相比之下,除1例患者外,所有患者血清中该代谢产物的水平均检测不到(低于2μmol/L)。所有受试者血清中苯巴比妥(PB)的水平均低于检测限(低于2μmol/L)。研究结果表明,尽管有证据表明药物代谢受这种疾病影响,但急性病毒性肝炎患者发生癫痫时,PRM及其伴随毒性不太可能发生蓄积。文中讨论了转化为PB受损的可能性及其影响。