Betamethasone does not prevent nausea and vomiting induced by ipecacuanha

Axelsson, Patric; Thörn, Sven‐Egron; Wattwil, Magnus

doi:10.1111/j.1399-6576.2004.00527.x

Cited by 5 publications

(5 citation statements)

References 20 publications

(42 reference statements)

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“…Later studies using high-dose dexamethasone in patients receiving cisplatin alone or in combination with other cytotoxic drugs reported impressive responses with excellent or good control of nausea and vomiting in 50% of patients who had failed on standard anti-emetics and 71% in patients who had not received anti-emetics previously (Aapro and Alberts, 1981 ). Notably, synthetic corticosteroids do not inhibit the acute, rapid-onset forms of vomiting induced by apomorphine or ipecacuanha (Axelsson et al, 2003 ; Sam et al, 2003 ), suggesting involvement of an “inflammatory” component in the mechanisms of chemotherapy-induced emesis (Sanger and Andrews, 2006 ).…”

Section: Early Serendipidous Discoveries Of Anti-emetic Drugsmentioning

confidence: 99%

A History of Drug Discovery for Treatment of Nausea and Vomiting and the Implications for Future Research

Sanger

Andrews

2018

Front. Pharmacol.

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The origins of the major classes of current anti-emetics are examined. Serendipity is a recurrent theme in discovery of their anti-emetic properties and repurposing from one indication to another is a continuing trend. Notably, the discoveries have occurred against a background of company mergers and changing anti-emetic requirements. Major drug classes include: (i) Muscarinic receptor antagonists–originated from historical accounts of plant extracts containing atropine and hyoscine with development stimulated by the need to prevent sea-sickness among soldiers during beach landings; (ii) Histamine receptor antagonists–searching for replacements for the anti-malaria drug quinine, in short supply because of wartime shipping blockade, facilitated the discovery of histamine (H1) antagonists (e.g., dimenhydrinate), followed by serendipitous discovery of anti-emetic activity against motion sickness in a patient undergoing treatment for urticaria; (iii) Phenothiazines and dopamine receptor antagonists–investigations of their pharmacology as “sedatives” (e.g., chlorpromazine) implicated dopamine receptors in emesis, leading to development of selective dopamine (D2) receptor antagonists (e.g., domperidone with poor ability to penetrate the blood-brain barrier) as anti-emetics in chemotherapy and surgery; (iv) Metoclopramide and selective 5-hydroxytryptamine3 (5-HT3) receptor antagonists–metoclopramide was initially assumed to act only via D2 receptor antagonism but subsequently its gastric motility stimulant effect (proposed to contribute to the anti-emetic action) was shown to be due to 5-hydroxytryptamine4 receptor agonism. Pre-clinical studies showed that anti-emetic efficacy against the newly-introduced, highly emetic, chemotherapeutic agent cisplatin was due to antagonism at 5-HT3 receptors. The latter led to identification of selective 5-HT3 receptor antagonists (e.g., granisetron), a major breakthrough in treatment of chemotherapy-induced emesis; (v) Neurokinin1 receptor antagonists–antagonists of the actions of substance P were developed as analgesics but pre-clinical studies identified broad-spectrum anti-emetic effects; clinical studies showed particular efficacy in the delayed phase of chemotherapy-induced emesis. Finally, the repurposing of different drugs for treatment of nausea and vomiting is examined, particularly during palliative care, and also the challenges in identifying novel anti-emetic drugs, particularly for treatment of nausea as compared to vomiting. We consider the lessons from the past for the future and ask why there has not been a major breakthrough in the last 20 years.

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Section: Early Serendipidous Discoveries Of Anti-emetic Drugsmentioning

confidence: 99%

A History of Drug Discovery for Treatment of Nausea and Vomiting and the Implications for Future Research

Sanger

Andrews

2018

Front. Pharmacol.

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“…The antiemetic mechanism of action still remains unclear, but previous studies have excluded dopamine-and/or 5HT-3 antagonistic effects [17,18].…”

Section: Discussionmentioning

confidence: 99%

Betamethasone in prevention of postoperative nausea and vomiting following breast surgery

Olanders

Lundgren

Johansson

2014

Journal of Clinical Anesthesia

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“…In the present study we could not demonstrate any dopamine antagonistic effects of betamethasone, and in a previous study we also showed that betamethasone does not abolish serotonin-induced nausea and vomiting. 15 The role of metoclopramide as a prophylaxis for PONV has been previously questioned, and in a review paper by Henzi et al it was concluded that "metoclopramide, although used as an antiemetic for almost 40 years in the prevention of PONV, has no clinically relevant antiemetic effect and a continuous use of metoclopramide in the dose ranges tested in these studies is inadequate". 16 In the present study, pretreatment with metoclopramide, 10 mg iv, prevented nausea and vomiting induced by the D 2 -receptor agonist apomorphine.…”

Section: Discussionmentioning

confidence: 99%

Betamethasone does not prevent nausea and vomiting induced by the dopamine-agonist apomorphine

Axelsson

Thörn

Lövqvist

et al. 2006

Can J Anesth/J Can Anesth

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Purpose:The mechanism of the antiemetic actions of corticosteroids is not known. The purpose of this study was to evaluate if betamethasone can prevent nausea, vomiting or increase of vasopressin induced by apomorphine. Metoclopramide, a dopamine antagonist, was used as a control substance. Methods:Ten healthy volunteers were studied on three occasions. In a randomized order they were allocated to receive pretreatment with betamethasone 8 mg iv, metoclopramide 10 mg iv, and normal saline 2 mL as placebo on the three different occasions, 15 min before the administration of apomorphine 30 µg·kg -1 sc. After administration of apomorphine, episodes of vomiting were recorded, and the intensity of nausea was estimated by the subject on a visual analogue scale (VAS 0-10 cm). Blood samples for analysis of plasma concentrations of vasopressin were analyzed. Results:One volunteer decided to withdraw, as he experienced akathisia after receiving metoclopramide. During the first two hours after apomorphine, eight of nine volunteers vomited both after betamethasone and placebo. One volunteer did not vomit after betamethasone and placebo but he experienced nausea. None of the volunteers vomited after metoclopramide (P < 0.01 vs betamethasone and placebo). The maximum VAS for nausea was significantly higher after betamethasone and placebo compared to metoclopramide (P < 0.01). The vasopressin levels increased after betamethasone and placebo, but there was no increase in any volunteer after pretreatment with metoclopramide. Conclusion:This study demonstrates that betamethasone does not prevent nausea, vomiting and increase of vasopressin induced by apomorphine, whereas metoclopramide prevents apomorphine-induced emesis. Our work suggests that betamethasone does not have dopamine-antagonistic effects. Objectif

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Betamethasone does not prevent nausea and vomiting induced by ipecacuanha

Abstract: This study in volunteers has shown that betamethasone does not prevent nausea and vomiting induced by oral intake of ipecacuanha syrup. As ipecacuanha releases 5-hydroxytryptamin, it can be concluded that betamethasone does not have 5-HT3 antagonistic effects.

Cited by 5 publications

References 20 publications

A History of Drug Discovery for Treatment of Nausea and Vomiting and the Implications for Future Research

A History of Drug Discovery for Treatment of Nausea and Vomiting and the Implications for Future Research

Betamethasone in prevention of postoperative nausea and vomiting following breast surgery

Betamethasone does not prevent nausea and vomiting induced by the dopamine-agonist apomorphine

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