Roberts Michael S, Magnusson Beatrice M, Burczynski Frank J, Weiss Michael
Department of Medicine, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland, Australia.
Clin Pharmacokinet. 2002;41(10):751-90. doi: 10.2165/00003088-200241100-00005.
Enterohepatic recycling occurs by biliary excretion and intestinal reabsorption of a solute, sometimes with hepatic conjugation and intestinal deconjugation. Cycling is often associated with multiple peaks and a longer apparent half-life in a plasma concentration-time profile. Factors affecting biliary excretion include drug characteristics (chemical structure, polarity and molecular size), transport across sinusoidal plasma membrane and canniculae membranes, biotransformation and possible reabsorption from intrahepatic bile ductules. Intestinal reabsorption to complete the enterohepatic cycle may depend on hydrolysis of a drug conjugate by gut bacteria. Bioavailability is also affected by the extent of intestinal absorption, gut-wall P-glycoprotein efflux and gut-wall metabolism. Recently, there has been a considerable increase in our understanding of the role of transporters, of gene expression of intestinal and hepatic enzymes, and of hepatic zonation. Drugs, disease and genetics may result in induced or inhibited activity of transporters and metabolising enzymes. Reduced expression of one transporter, for example hepatic canalicular multidrug resistance-associated protein (MRP) 2, is often associated with enhanced expression of others, for example the usually quiescent basolateral efflux MRP3, to limit hepatic toxicity. In addition, physiologically relevant pharmacokinetic models, which describe enterohepatic recirculation in terms of its determinants (such as sporadic gall bladder emptying), have been developed. In general, enterohepatic recirculation may prolong the pharmacological effect of certain drugs and drug metabolites. Of particular importance is the potential amplifying effect of enterohepatic variability in defining differences in the bioavailability, apparent volume of distribution and clearance of a given compound. Genetic abnormalities, disease states, orally administered adsorbents and certain coadministered drugs all affect enterohepatic recycling.
肠肝循环是通过溶质的胆汁排泄和肠道重吸收来实现的,有时还伴随着肝脏结合和肠道去结合过程。在血浆浓度-时间曲线上,循环通常与多个峰以及较长的表观半衰期相关。影响胆汁排泄的因素包括药物特性(化学结构、极性和分子大小)、跨肝血窦质膜和胆小管膜的转运、生物转化以及肝内胆小管的可能重吸收。肠道重吸收以完成肠肝循环可能取决于肠道细菌对药物结合物的水解。生物利用度还受肠道吸收程度、肠壁P-糖蛋白外排和肠壁代谢的影响。最近,我们对转运体的作用、肠道和肝脏酶的基因表达以及肝脏分区的理解有了相当大的进展。药物、疾病和遗传因素可能导致转运体和代谢酶的活性被诱导或抑制。例如,一种转运体(如肝小管多药耐药相关蛋白(MRP)2)表达降低,通常会伴随着其他转运体(如通常静止的基底外侧外排MRP3)表达增强,以限制肝脏毒性。此外,已经建立了生理相关的药代动力学模型,该模型根据其决定因素(如偶发性胆囊排空)来描述肠肝循环。一般来说,肠肝循环可能会延长某些药物及其代谢产物的药理作用。肠肝循环变异性对确定给定化合物的生物利用度、表观分布容积和清除率差异的潜在放大作用尤为重要。基因异常、疾病状态、口服吸附剂和某些同时服用的药物都会影响肠肝循环。