Allopurinol is the drug most widely used to lower the blood concentrations of urate and, therefore, to decrease the number of repeated attacks of gout. Allopurinol is rapidly and extensively metabolised to oxypurinol (oxipurinol), and the hypouricaemic efficacy of allopurinol is due very largely to this metabolite. The pharmacokinetic parameters of allopurinol after oral dosage include oral bioavailability of 79 +/- 20% (mean +/- SD), an elimination half-life (t((1/2))) of 1.2 +/- 0.3 hours, apparent oral clearance (CL/F) of 15.8 +/- 5.2 mL/min/kg and an apparent volume of distribution after oral administration (V(d)/F) of 1.31 +/- 0.41 L/kg. Assuming that 90 mg of oxypurinol is formed from every 100mg of allopurinol, the pharmacokinetic parameters of oxypurinol in subjects with normal renal function are a t((1/2)) of 23.3 +/- 6.0 hours, CL/F of 0.31 +/- 0.07 mL/min/kg, V(d)/F of 0.59 +/- 0.16 L/kg, and renal clearance (CL(R)) relative to creatinine clearance of 0.19 +/- 0.06. Oxypurinol is cleared almost entirely by urinary excretion and, for many years, it has been recommended that the dosage of allopurinol should be reduced in renal impairment. A reduced initial target dosage in renal impairment is still reasonable, but recent data on the toxicity of allopurinol indicate that the dosage may be increased above the present guidelines if the reduction in plasma urate concentrations is inadequate. Measurement of plasma concentrations of oxypurinol in selected patients, particularly those with renal impairment, may help to decrease the risk of toxicity and improve the hypouricaemic response. Monitoring of plasma concentrations of oxypurinol should also help to identify patients with poor adherence. Uricosuric drugs, such as probenecid, have potentially opposing effects on the hypouricaemic efficacy of allopurinol. Their uricosuric effect lowers the plasma concentrations of urate; however, they increase the CL(R) of oxypurinol, thus potentially decreasing the influence of allopurinol. The net effect is an increased degree of hypouricaemia, but the interaction is probably limited to patients with normal renal function or only moderate impairment.

译文

:别嘌呤醇是最广泛用于降低血尿酸盐浓度的药物,因此可减少痛风的反复发作次数。别嘌呤醇被迅速广泛地代谢为氧嘌呤醇(oxipurinol),别嘌呤醇的降尿血药功效在很大程度上归因于这种代谢产物。口服后别嘌醇的药代动力学参数包括79 /-20%(平均/-SD)的口服生物利用度,1.2 /-0.3小时的消除半衰期(t((1/2))),明显的口腔清除率( CL / F)为15.8 /-5.2 mL / min / kg,口服后的表观分布体积(V(d)/ F)为1.31 / 0.41 L / kg。假设每100mg别嘌呤醇可形成90mg羟嘌呤醇,那么在肾功能正常的受试者中,氧嘌呤醇的药代动力学参数为((1/2))为23.3 /-6.0小时,CL / F为0.31 /-0.07 mL / min / kg,V(d)/ F为0.59 /-0.16 L / kg,相对于肌酐清除率的肾清除率(CL(R))为0.19 /-0.06。氧嘌呤醇几乎全部通过尿排泄清除,多年来,建议在肾功能不全时应减少别嘌呤醇的剂量。降低肾功能不全的初始目标剂量仍然是合理的,但是有关别嘌呤醇毒性的最新数据表明,如果血浆尿酸盐浓度的降低不足,则可以将剂量增加到当前指导值以上。在选定的患者中,特别是患有肾功能不全的患者中,测定氧嘌呤醇的血浆浓度可能有助于降低中毒的风险并改善低尿毒症反应。监测氧嘌呤醇的血浆浓度也应有助于确定依从性差的患者。尿酸药物,如丙磺舒,对别嘌呤醇的降尿血药功效具有潜在的相反作用。它们的尿尿排尿作用降低了血浆尿酸盐的浓度。但是,它们会增加氧嘌呤醇的CL(R),因此有可能降低别嘌呤醇的影响。净效应是低尿酸血症程度的增加,但这种相互作用可能仅限于肾功能正常或仅有中度损害的患者。

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