Table 2. Comparison of Aprepitant and Standard Regimens continued...
Much of the research on this class of agent was conducted in the late 1970s and 1980s and compared Cannabis to older antiemetic agents that targeted the dopamine receptor, such as prochlorperazine (Compazine) and metoclopramide (Reglan).[89,93,94,95,96,97,98,99,100] This group of studies demonstrated that Cannabis was as effective for moderately emetogenic chemotherapy as dopaminergic antiemetics or was more effective than placebo. Side effects of Cannabis products included euphoria, dizziness, dysphoria, hallucinations, and hypotension. Despite earlier reports of efficacy, in at least one study, patients did not significantly prefer Cannabis agents because of the side effects.
Research in nausea and vomiting since the 1990s has elucidated newer and more physiologic targets, namely 5-HT3 and NK-1 receptors. Subsequently, 5-HT3 and NK-1 receptor antagonists have become standard prophylactic therapy for CINV. Studies investigating the role of Cannabis with these newer agents are few; therefore, limited conclusions can be drawn. In published trials, however, Cannabis has not demonstrated more efficacy than 5-HT3 receptor antagonists, and synergistic or additive effects have not been fully investigated.[90,101,102]
In summary, the place of Cannabis in today's arsenal of antiemetics for the prevention and treatment of CINV is not known. Discussions with patients about its use should include responses to available agents, known side effects of Cannabis, and an assessment of the risks versus benefits of this therapy.
For a broader discussion of the issues surrounding Cannabis use, refer to the PDQ summary on Cannabis and Cannabinoids.
Benzodiazepines such as lorazepam, midazolam, and alprazolam have become recognized as valuable adjuncts in the prevention and treatment of anxiety and the symptoms of anticipatory nausea and vomiting (ANV) associated with chemotherapy, especially with the highly emetogenic regimens given to children.[104,105,106] Benzodiazepines have not demonstrated intrinsic antiemetic activity as single agents. Therefore, their place in antiemetic prophylaxis and treatment is adjunctive to other antiemetic agents. Benzodiazepines presumably act on higher CNS structures, the brainstem, and spinal cord, and they produce anxiolytic, sedative, and anterograde amnesic effects. In addition, they markedly decrease the severity of EPRs, especially akathisia, associated with dopaminergic receptor antagonist antiemetics.