Chemotherapy-induced nausea and vomiting: incidence and characteristics of persistent symptoms and future directions NCCTG N08C3 (Alliance)

Abstract

Background Despite newer agents, chemotherapy-induced nausea and vomiting (CINV) continues to remain a distressing side effect to a proportion of patients undergoing systemic anti-cancer therapy. Methods We recently performed an unplanned secondary analysis on a previously reported negative phase III trial (N08C3) looking at the efficacy of gabapentin/placebo in combination with dexamethasone and a 5HT3 receptor antagonist in the prevention of CINV for 413 patients undergoing regimens with highly emetogenic chemotherapy (HEC). In the current study, we attempted to better understand the higher than expected rate of overall patient satisfaction, despite a low complete response rate in both arms. Additionally, we looked at patient variables and their relationship to rates of CINV. Results Approximately one third of patients experienced more than mild nausea and reported scores on the Functional Living Index–Emesis that indicated interference with activities. Thirty-five percent reported nausea greater than 2.5 on a scale of 0 to 10 (0 being none), 19 % reported at least one emetic episode, and 49 % reported taking rescue medication. Nausea and vomiting on day 1, cisplatin therapy, and history of motion sickness significantly predicted delayed CINV. Age, combination chemotherapy (HEC with moderately emetogenic), and getting treatment for breast cancer predicted CINVon day 1. Discussion These data confirm previous reports that subgroups of patients may be more prone to acute and delayed CINV. Future CINV study design may benefit from a more individualized approach to CINV management, targeting those patients who are truly at risk for CINV despite continued drug development efforts.

Impact of Chemotherapy on Diet and Nutritional Status of Women with Breast Cancer: A Prospective Study

“…Studies evaluating changes in eating patterns after the diagnosis of breast cancer showed different results, but most found favorable changes with a reduced consumption of high-fat and high-sugar foods, and an increase in vegetables and fruits [ 6 , 7 ]. Certain food groups, are often rejected or preferred during chemotherapy [ 8 – 10 ], because of side effects of treatment, such as nausea and vomiting [ 11 ]. These changes in diet can interfere with an adequate diet and influence the nutritional status of the patient, and there may be consequences for the prognosis of the disease.…”

Granulin A Synergizes with Cisplatin to Inhibit the Growth of Human Hepatocellular Carcinoma

“…It is used for the treatment of ovarian cancer, prostate cancer, testicular cancer, lung cancer, nasopharyngeal cancer, esophageal cancer, malignant lymphoma, and thyroid cancer, as well as HCC [ 6 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 ]. However, the severe emetic side effect and drug resistance limits its efficacy in the treatment of HCC [ 17 , 18 , 19 , 20 ]. In recent years, combination therapy of cisplatin with other anticancer agents have been developed as novel therapeutic strategies for many human cancers [ 16 , 21 , 22 ].…”

Role of Calcium in Vomiting

“…Acute (≤24 h) and delayed (>24 h) phases of chemotherapy-induced nausea and vomiting cause distressing side-effects which affect the well-being and quality of life of cancer patients receiving chemotherapy, especially cisplatin [1]. Major neurotransmitter mechanisms underlying chemotherapy-induced nausea and vomiting have been subject of considerable research over the past 45 years.…”

“…The dorsal motor nucleus of the vagus receives axonal projections from nucleus tractus solitarius [7] and sends emetic signals via motor efferent pathways to the gastrointestinal tract and modulates vomiting behaviors [2,5,8,9] (Figure 1). In addition, chemotherapeutic drugs may evoke release of emetic neurotransmitters/mediators from the gastrointestinal tract into the blood to be directly delivered to the area postrema via a Mechanisms underlying cisplatin-induced vomiting can be simplified as: (1) cisplatin can increase cytoplasmic Ca 2+ level to evoke Ca 2+ -dependent release of emetic neurotransmitters/mediators at the brainstem emetic loci, the dorsal vagal complex, and subsequently activates diverse receptors and their corresponding signaling pathways. These emetic signals are output to the gastrointestinal tract via efferents to trigger vomiting [2,[4][5][6][7][8][9]; (2) cisplatin-induced peripheral release of neurotransmitters/mediators from the gastrointestinal tract into the blood can directly stimulate the dorsal vagal complex, activate receptors signaling pathways and trigger vomiting [2,10]; and (3) the peripherally-released emetic neurotransmitters/mediators stimulate their corresponding receptors present on vagal afferents in the gastrointestinal tract which indirectly activate brainstem emetic nuclei and trigger vomiting [6].…”