Control of nausea and vomiting after chemotherapy: what is the evidence?

Bartlett, Nancy L.; Koczwara, Bogda

doi:10.1046/j.1445-5994.2002.00259.x

Cited by 17 publications

(7 citation statements)

References 43 publications

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“…In the other study, tropisetron was more effective than conventional agents such as metoclopramide and chlorpromazine but drug selection was empirical and deficiencies in the study design, as reported, meant the results were at a high risk of bias [21]. Because the chronic nausea associated with advanced cancer is multifactorial and involves many different receptor systems, the large body of evidence for the treatment of acute nausea and vomiting due to highly emetogenic chemotherapy has not been considered [42]. Because of concerns over toxicity, such as constipation, and the cost of therapy, more well-designed studies of the 5HT3 receptor antagonists for the nausea associated with far-advanced cancer are needed.…”

Section: Discussionmentioning

confidence: 96%

Systematic review of the efficacy of antiemetics in the treatment of nausea in patients with far-advanced cancer

Glare

Pereira

Kristjanson

et al. 2004

Supportive Care in Cancer

132

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Section: Discussionmentioning

confidence: 96%

Systematic review of the efficacy of antiemetics in the treatment of nausea in patients with far-advanced cancer

Glare

Pereira

Kristjanson

et al. 2004

Supportive Care in Cancer

132

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“…In clinical trials with humans, treatment with 5‐HT 3 antagonists often combined with the corticosteroid dexamethasone during the first chemotherapy treatment reduced the incidence of acute vomiting by approximately 70% (e.g. Bartlett and Koczwara, 2002; Aapro et al ., 2003; Ballatori and Roila, 2003; Hickok et al ., 2003; Andrews and Horn, 2006). However, the 5‐HT 3 antagonists are less effective at suppressing acute nausea than they are at suppressing acute vomiting (Morrow and Dobkin, 1988; Bartlett and Koczwara, 2002; Hickok et al ., 2003) and they are ineffective at reducing instances of delayed (24 h later) nausea and vomiting (Morrow and Dobkin, 1988; Grelot et al ., 1995; Rudd et al ., 1996; Rudd and Naylor, 1996; Tsukada et al ., 2001; Hesketh et al ., 2003) and anticipatory (conditioned) nausea and vomiting (Nesse et al ., 1980; Morrow and Dobkin, 1988; Hickok et al ., 2003).…”

Section: Introductionmentioning

confidence: 99%

Regulation of nausea and vomiting by cannabinoids

Parker

Rock

Limebeer

2011

British J Pharmacology

217

170

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Considerable evidence demonstrates that manipulation of the endocannabinoid system regulates nausea and vomiting in humans and other animals. The anti-emetic effect of cannabinoids has been shown across a wide variety of animals that are capable of vomiting in response to a toxic challenge. CB1 agonism suppresses vomiting, which is reversed by CB1 antagonism, and CB1 inverse agonism promotes vomiting. Recently, evidence from animal experiments suggests that cannabinoids may be especially useful in treating the more difficult to control symptoms of nausea and anticipatory nausea in chemotherapy patients, which are less well controlled by the currently available conventional pharmaceutical agents. Although rats and mice are incapable of vomiting, they display a distinctive conditioned gaping response when re-exposed to cues (flavours or contexts) paired with a nauseating treatment. Cannabinoid agonists (D 9 -THC, HU-210) and the fatty acid amide hydrolase (FAAH) inhibitor, URB-597, suppress conditioned gaping reactions (nausea) in rats as they suppress vomiting in emetic species. Inverse agonists, but not neutral antagonists, of the CB1 receptor promote nausea, and at subthreshold doses potentiate nausea produced by other toxins (LiCl). The primary non-psychoactive compound in cannabis, cannabidiol (CBD), also suppresses nausea and vomiting within a limited dose range. The anti-nausea/anti-emetic effects of CBD may be mediated by indirect activation of somatodendritic 5-HT1A receptors in the dorsal raphe nucleus; activation of these autoreceptors reduces the release of 5-HT in terminal forebrain regions. Preclinical research indicates that cannabinioids, including CBD, may be effective clinically for treating both nausea and vomiting produced by chemotherapy or other therapeutic treatments. LINKED ARTICLESThis article is part of a themed issue on Cannabinoids in Biology and Medicine. To view the other articles in this issue visit http://dx.doi. org/10.1111/bph.2011.163.issue-7 Abbreviations 2-AG, 2-arachidonolylglycerol; 5-HT, 5-hydroxytryptamine; 5-HT3, 5-hydroxytryptamine receptor 3; 5-HT1A, 5-hydroxytryptamine receptor 1A; 5-HTP, 5-hydroxytryptophan; 5,7-DHT, 5,7-dihydroxytryptamine; 8-OH-DPAT, 8-hydroxy-N,N-dipropyl-2-aminotetralin; D 9-THC, D 9 -tetrahydrocannabinol; AN, anticipatory nausea; AP, area postrema; CB1,cannabinoid receptor 1; CB2, cannabinoid receptor 2; CBD, cannabidiol; DMNX, doral motor nucleus of the vagus; DRN, dorsal raphe nucleus; DVC, dorsal vagal complex; FAAH, fatty acid amide hydrolase; Gi, inhibitory G protein subunit; LiCl, lithium chloride; MAGL, monoacylglycerol-lipase; M6G, morphine-6-glucuronide; MRN, medial raphe nucleus; NADA, n-arachidonoyl-dopamine; NTS, nucleus of the solitary tract; S. murinus, Suncus murinus; TRPV1, transient receptor potential vanilloid 1 IntroductionA major advance in the control of acute emesis in chemotherapy treatment was the finding that blockade of one subtype of the 5-hydroxytryptamine (5-HT) receptor, the 5-HT3 receptor, could suppress the ...

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“…Other risk factors may include chronic alcohol use, female gender, and a history of poor control of nausea and vomiting (Bartlett and Koczwara 2002 ). Other risk factors may include chronic alcohol use, female gender, and a history of poor control of nausea and vomiting (Bartlett and Koczwara 2002 ).…”

Section: Nausea and Vomitingmentioning

confidence: 99%