Recent advances in the management of nausea and vomiting caused by antineoplastic agents.

The pathophysiology of nausea and vomiting caused by antineoplastic therapy is described, and the literature on selected recent pharmacologic approaches to antiemetic therapy is reviewed. Nausea and vomiting associated with antineoplastic therapy remain serious deterrents to continued, potentially curative therapy for many patients. Although much research has been conducted in the area of antiemetic therapy over the past decade, the mechanisms by which antineoplastic agents cause nausea and vomiting are still not well defined. The most effective antiemetic agents to date are those that antagonize dopamine receptors. Metoclopramide is a dopamine antagonist that has been widely studied for the prevention of antineoplastic-agent-induced nausea and vomiting. Recent studies with this agent focus on routes of administration other than the traditional high-dose intermittent bolus intravenous injections. Continuous intravenous infusions of the drug and high-dose oral administration have been studied in an attempt to decrease the adverse effects associated with the traditional regimen and to allow administration on an outpatient basis. Prochlorperazine, a phenothiazine derivative, has been a mainstay of antiemetic therapy for many years. Although it is generally reserved for use with regimens that cause mild to moderate emesis, recent data suggest that higher-than-traditional doses given intravenously impart greater antiemetic protection. Perhaps the most promising antiemetic research has been conducted with a new group of agents, the serotonin antagonists. Preliminary trials suggest that these agents are comparable in efficacy to high doses of metoclopramide but devoid of many of the adverse effects commonly associated with metoclopramide. Further research in the area of neuropharmacology is necessary to direct the development of the most effective antiemetic agents.