Current pharmacotherapy for chemotherapy-induced nausea and vomiting in cancer patients

Abstract

Introduction: Nausea and vomiting are two of the most frequent and troubling side effects patients experience during chemotherapy, interfering with compliance with cancer therapies and quality of life. While newly available treatments have improved our ability to manage nausea and vomiting, anticipatory and delayed nausea and vomiting are still major problems for patients receiving chemotherapy. Many cancer patients consider delaying future chemotherapy cycles and some contemplate stopping chemotherapy altogether because of their fear of experiencing further nausea and vomiting.

Areas covered: The purpose of this article is to provide an overview of the pathopsychophysiology of chemotherapy-induced nausea and vomiting (CINV), the recommended guidelines for treatment, and current agents in late-stage clinical trials, and future research needs to address the continued challenges of treatment-related nausea and vomiting.

Expert opinion: Despite advances in pharmaceutical and behavioral therapies, and the provision of standard clinical guidelines for effectively managing CINV, patients continue to experience it. Moreover, control of nausea, acute and delayed, and anticipatory nausea and vomiting remains an important, unmet need among cancer patients. It is critical to focus attention on better understanding the mechanisms underlying nausea, anticipatory symptoms and delayed symptoms.

Figure 1. Emetic Pathways

Cytotoxic chemotherapies can damage the gastrointestinal (GI) tract and cause the Enterochromaffin cells (EC), distributed throughout the GI lining, to release neural signals via neurotransmitter release. These neurotransmitters activate the vagal afferents, by binding to the receptors, which then conduct the stimuli to the dorsal vagal complex consisting of emetic/vomiting center (VC), the area postrema (CTZ) and the nucleus tractus solitarius (NTS). These sensory inputs are then integrated resulting in the activation of the emetic response.

Figure 2. Summary of Current Clinical Guidelines