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Supportive Oncology Chemotherapy-induced Nausea and Vomiting—Where We Stand Now Rita Wickham, PhD, RN, AOCN Adjunct Faculty, Rush College of Nursing, Chicago, Illinois Abstract Chemotherapy-induced nausea and vomiting (CINV) has been a major supportive care concern since the development of cisplatin, which was probably the major factor that drove antiemetic research. If strategies, particularly using combination antiemetic therapy, had not been developed and studied, cancer chemotherapy research would also likely to have been stymied. The past 30 years or more have seen our understanding of the physiology of vomiting grow from the understanding of the medullary brain structures we call the chemoreceptor trigger zone and the vomiting center, as well as the neurotransmitters located about that site. The current view of chemotherapy-induced vomiting is that two main pathways are involved—a peripheral pathway from the gut to the vomiting center that is mediated by increased release of serotonin by enterochromaffin cells in the gastrointestinal tract mucosa that binds to vagal terminals terminating in the nucleus tractus solitarius, and a central pathway in the brain that involves substance P binding at neurokinin 1 receptors near the vomiting center. Development of antiemetics that target these specific receptors, plus the use of dexamethasone, has resulted in prevention of acute vomiting in 70–80 % of patients receiving highly emetogenic chemotherapy. The scientific evidence resulting from this antiemetic research, along with clinical application knowledge, forms the basis of current chemotherapy antiemetic guidelines. Although these are useful to clinical practice, they do no replace clinical assessment and follow up of individual patients. Furthermore, about half of patients receiving moderately or highly emetogenic chemotherapy experience distressing delayed nausea, which can alter a patient’s life activities, cause debilitating physical consequences, and interfere with their ability and willingness to undergo chemotherapy. Keywords Nausea, vomiting, CINV, chemoreceptor trigger zone, vomiting center, serotonin, 5HT3 receptors, substance, NK1 receptors, emetogenicity, antiemetic guidelines Disclosure: The author has no conflicts of interest to declare. Received: May 13, 2013 Accepted: July 20, 2013 Citation: Oncology Hematology Review (US), 2013;9(2):154–60 Correspondence: Rita Wickham, PhD, RN, AOCN, 8039 Garth Point Ln, Rapid River, Michigan, US. E: rita_wickham@yahoo.com It has been almost 50 years since the first study of an antiemetic (prochlorperazine versus placebo) for chemotherapy-induced nausea and vomiting (CINV) was published. 1 However, we have not reached the point where CINV is never a problem for any patient receiving antineoplastic therapies. On the other hand, momentous discoveries during the intervening years have increased our understanding of the physiology of chemotherapy- related emesis, and have led to the corresponding development of receptor- targeted antiemetics, and resulted in evidence-based antiemetic guidelines from several professional oncology organizations in Europe and the US. Nausea and vomiting (N&V) are relatively common for patients with cancer and may occur from progressive disease, radiation therapy—especially when fields include the upper abdomen—and from MEC/HEC. CINV is this article’s focus, but clinicians should remember other possible causes that may worsen CINV or radiation therapy-induced N&V (RINV), or increase the risk for N&V secondary to advanced disease. 2,3 near the nucleus tractus solitarius (NTS) of the vagus nerve in brainstem medulla, which may also influence nausea, taste, salivation, swallowing and gagging, and gut motility. The chemoreceptor trigger zone (CTZ), a circumventricular organ in the area postrema (AP), is near the VC. Together the CTZ, NTS, and VC make up the final common pathway for vomiting. 6 The Physiology of Vomiting Afferent neural inputs to the central nervous system (CNS) and the VC include the gastrointestinal (GI) tract—particularly via the vagus nerve and stretch receptors, the vestibular apparatus of the inner ear that plays a role in motion sickness, and several sites in the brain including the limbic region that assigns emotion to distressing events, the cortex, and other receptor Emesis is an important, highly conserved reflex in vertebrates that protects against accidental ingestion of harmful substances. Borison’s and Wang’s sentinel works 4,5 were critical to understanding how it occurs. They identified the so-called vomiting center (VC), which is not an organ but a group of neurons 154 Given the importance of emesis, it is not surprising that there are multiple peripheral and central sites that can transmit neural signals to the CTZ, NTS, and VC, and with direct or indirect contributions of several neurotransmitters and receptors. 7 In addition, emetic chemical stimuli in the bloodstream or the cerebral spinal fluid can reach the CTZ, which has a relatively permeable blood–brain barrier. 8 Numerous neurotransmitters (e.g. acetylcholine, dopamine, serotonin [5HT], histamine [H1], gamma-aminobutyric acid [GABA], and substance P [SP]) have been identified near and in the NTS and AP and may play some role in N&V. © TOU C H M E D ICA L ME D IA 2013