Review article: An analysis of the pharmacological rationale for selecting drugs to inhibit vomiting or increase gastric emptying during treatment of gastroparesis

Summary Background Drugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly ‘off‐label’. Within each category, they act at different targets and modulate different physiological mechanisms. Aims Address the questions: In gastroparesis, why shou...

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Published inAlimentary pharmacology & therapeutics Vol. 57; no. 9; pp. 962 - 978
Main Authors Sanger, Gareth J., Andrews, Paul L. R.
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.05.2023
Subjects
Acetylcholine receptors (muscarinic)
Agonists
Amitriptyline
Antagonists
aprepitant
domperidone
Drugs
Erythromycin
Gastric Emptying
gastroparesis
Gastroparesis - drug therapy
Humans
Metoclopramide
Motilin - pharmacology
Motilin - therapeutic use
Movement disorders
Nausea
Nausea - etiology
Pacemakers
prucalopride
Sensory neurons
Serotonin
Tardive dyskinesia
Vagus nerve
Vomiting
Vomiting - drug therapy
Vomiting - etiology
prucalopride
aprepitant
domperidone
gastric emptying
gastroparesis
nausea
vomiting
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Abstract Summary Background Drugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly ‘off‐label’. Within each category, they act at different targets and modulate different physiological mechanisms. Aims Address the questions: In gastroparesis, why should blocking one pathway causing vomiting, be more appropriate than another? Why might increasing gastric emptying via one mechanism be more appropriate than another? Methods Drugs used clinically were identified via consensus opinions and reviews, excluding the poorly characterised. Their pharmacology was defined, mapped to mechanisms influencing vomiting and gastric emptying, and rationale developed for therapeutic use. Results Vomiting: Rationale for 5‐HT3, D2, H1 or muscarinic antagonists, and mirtazapine, amitriptyline, nortriptyline, are poor. Arguments for inhibiting central consequences of vagal afferent transmission by NK1 antagonism are complicated by doubts over effects on nausea. Gastric emptying: Confusion emerges because of side‐effects of drugs increasing gastric emptying: Metoclopramide (5‐HT4 agonist, D2 and 5‐HT3 antagonist; also blocks some emetic stimuli and causes tardive dyskinesia) and Erythromycin (high‐efficacy motilin agonist, requiring low doses to minimise side‐effects). Limited trials with selective 5‐HT4 agonists indicate variable efficacy. Conclusions Several drug classes inhibiting vomiting have no scientific rationale. NK1 antagonism has rationale but complicated by limited efficacy against nausea. Studies must resolve variable efficacy of selective 5‐HT4 agonists and apparent superiority over motilin agonists. Overall, lack of robust activity indicates a need for novel approaches targeting nausea (e.g., modulating gastric pacemaker or vagal activity, use of receptor agonists or new targets such as GDF15) and objective assessments of nausea. Summary of the pharmacological rationale for selecting drugs to inhibit vomiting or increase gastric emptying during the treatment of gastroparesis.
AbstractList BACKGROUNDDrugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly 'off-label'. Within each category, they act at different targets and modulate different physiological mechanisms. AIMSAddress the questions: In gastroparesis, why should blocking one pathway causing vomiting, be more appropriate than another? Why might increasing gastric emptying via one mechanism be more appropriate than another? METHODSDrugs used clinically were identified via consensus opinions and reviews, excluding the poorly characterised. Their pharmacology was defined, mapped to mechanisms influencing vomiting and gastric emptying, and rationale developed for therapeutic use. RESULTSVomiting: Rationale for 5-HT3 , D2 , H1 or muscarinic antagonists, and mirtazapine, amitriptyline, nortriptyline, are poor. Arguments for inhibiting central consequences of vagal afferent transmission by NK1 antagonism are complicated by doubts over effects on nausea. Gastric emptying: Confusion emerges because of side-effects of drugs increasing gastric emptying: Metoclopramide (5-HT4 agonist, D2 and 5-HT3 antagonist; also blocks some emetic stimuli and causes tardive dyskinesia) and Erythromycin (high-efficacy motilin agonist, requiring low doses to minimise side-effects). Limited trials with selective 5-HT4 agonists indicate variable efficacy. CONCLUSIONSSeveral drug classes inhibiting vomiting have no scientific rationale. NK1 antagonism has rationale but complicated by limited efficacy against nausea. Studies must resolve variable efficacy of selective 5-HT4 agonists and apparent superiority over motilin agonists. Overall, lack of robust activity indicates a need for novel approaches targeting nausea (e.g., modulating gastric pacemaker or vagal activity, use of receptor agonists or new targets such as GDF15) and objective assessments of nausea.
Summary Background Drugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly ‘off‐label’. Within each category, they act at different targets and modulate different physiological mechanisms. Aims Address the questions: In gastroparesis, why should blocking one pathway causing vomiting, be more appropriate than another? Why might increasing gastric emptying via one mechanism be more appropriate than another? Methods Drugs used clinically were identified via consensus opinions and reviews, excluding the poorly characterised. Their pharmacology was defined, mapped to mechanisms influencing vomiting and gastric emptying, and rationale developed for therapeutic use. Results Vomiting: Rationale for 5‐HT 3 , D 2 , H 1 or muscarinic antagonists, and mirtazapine, amitriptyline, nortriptyline, are poor. Arguments for inhibiting central consequences of vagal afferent transmission by NK 1 antagonism are complicated by doubts over effects on nausea. Gastric emptying: Confusion emerges because of side‐effects of drugs increasing gastric emptying: Metoclopramide (5‐HT 4 agonist, D 2 and 5‐HT 3 antagonist; also blocks some emetic stimuli and causes tardive dyskinesia) and Erythromycin (high‐efficacy motilin agonist, requiring low doses to minimise side‐effects). Limited trials with selective 5‐HT 4 agonists indicate variable efficacy. Conclusions Several drug classes inhibiting vomiting have no scientific rationale. NK 1 antagonism has rationale but complicated by limited efficacy against nausea. Studies must resolve variable efficacy of selective 5‐HT 4 agonists and apparent superiority over motilin agonists. Overall, lack of robust activity indicates a need for novel approaches targeting nausea (e.g., modulating gastric pacemaker or vagal activity, use of receptor agonists or new targets such as GDF15) and objective assessments of nausea.
Summary Background Drugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly ‘off‐label’. Within each category, they act at different targets and modulate different physiological mechanisms. Aims Address the questions: In gastroparesis, why should blocking one pathway causing vomiting, be more appropriate than another? Why might increasing gastric emptying via one mechanism be more appropriate than another? Methods Drugs used clinically were identified via consensus opinions and reviews, excluding the poorly characterised. Their pharmacology was defined, mapped to mechanisms influencing vomiting and gastric emptying, and rationale developed for therapeutic use. Results Vomiting: Rationale for 5‐HT3, D2, H1 or muscarinic antagonists, and mirtazapine, amitriptyline, nortriptyline, are poor. Arguments for inhibiting central consequences of vagal afferent transmission by NK1 antagonism are complicated by doubts over effects on nausea. Gastric emptying: Confusion emerges because of side‐effects of drugs increasing gastric emptying: Metoclopramide (5‐HT4 agonist, D2 and 5‐HT3 antagonist; also blocks some emetic stimuli and causes tardive dyskinesia) and Erythromycin (high‐efficacy motilin agonist, requiring low doses to minimise side‐effects). Limited trials with selective 5‐HT4 agonists indicate variable efficacy. Conclusions Several drug classes inhibiting vomiting have no scientific rationale. NK1 antagonism has rationale but complicated by limited efficacy against nausea. Studies must resolve variable efficacy of selective 5‐HT4 agonists and apparent superiority over motilin agonists. Overall, lack of robust activity indicates a need for novel approaches targeting nausea (e.g., modulating gastric pacemaker or vagal activity, use of receptor agonists or new targets such as GDF15) and objective assessments of nausea. Summary of the pharmacological rationale for selecting drugs to inhibit vomiting or increase gastric emptying during the treatment of gastroparesis.
Drugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly 'off-label'. Within each category, they act at different targets and modulate different physiological mechanisms. Address the questions: In gastroparesis, why should blocking one pathway causing vomiting, be more appropriate than another? Why might increasing gastric emptying via one mechanism be more appropriate than another? Drugs used clinically were identified via consensus opinions and reviews, excluding the poorly characterised. Their pharmacology was defined, mapped to mechanisms influencing vomiting and gastric emptying, and rationale developed for therapeutic use. Vomiting: Rationale for 5-HT , D , H or muscarinic antagonists, and mirtazapine, amitriptyline, nortriptyline, are poor. Arguments for inhibiting central consequences of vagal afferent transmission by NK antagonism are complicated by doubts over effects on nausea. Gastric emptying: Confusion emerges because of side-effects of drugs increasing gastric emptying: Metoclopramide (5-HT agonist, D and 5-HT antagonist; also blocks some emetic stimuli and causes tardive dyskinesia) and Erythromycin (high-efficacy motilin agonist, requiring low doses to minimise side-effects). Limited trials with selective 5-HT agonists indicate variable efficacy. Several drug classes inhibiting vomiting have no scientific rationale. NK antagonism has rationale but complicated by limited efficacy against nausea. Studies must resolve variable efficacy of selective 5-HT agonists and apparent superiority over motilin agonists. Overall, lack of robust activity indicates a need for novel approaches targeting nausea (e.g., modulating gastric pacemaker or vagal activity, use of receptor agonists or new targets such as GDF15) and objective assessments of nausea.
Author Andrews, Paul L. R.
Sanger, Gareth J.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/36919196$$D View this record in MEDLINE/PubMed
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Keywords prucalopride
aprepitant
domperidone
gastric emptying
gastroparesis
nausea
vomiting
Language English
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2014; 20
2010; 22
2018; 9
1993; 34
2018; 3
1990; 46
1994; 268
2018; 4
2007; 292
2013; 56
1993; 33
2019; 23
2008; 27
2022; 34
2019; 27
2002; 302
2008; 20
2006; 325
2014; 94
1991; 104
2010; 6
2019; 156
2016; 151
2016; 150
2017; 62
1990; 30
2011; 2
1992; 261
2019; 31
2013; 108
2009; 60
2002; 2
1995
2020; 33
2020; 32
2011; 4
1999; 106
2022; 117
1998; 65
2016; 13
1996; 97
1995; 5
2004; 53
2021; 53
2021; 55
2022; 180
2021; 379
2010; 299
2005; 524
1999; 33
2003; 28
2008; 378
2013; 170
2016; 28
2012; 46
2022; 588
1998; 77
2016; 22
2017; 8
1990; 99
2013; 25
2012; 167
2022; 67
2003; 13
2009; 155
2013; 168
2008; 6
2018; 84
2022; 65
2023; 3
2014; 61
1998; 43
2003; 98
2012; 208
2017; 239
2021; 38
2014; 722
2021; 33
1999; 19
2019; 68
1980; 78
1994; 34
2013; 310
2014; 59
2019; 114
1996; 24
2021; 9
2009; 21
2011
2023; 245
2013; 386
2006; 18
2011; 33
1995; 115
2011; 32
2017; 29
2004
1995; 114
2003
2007; 52
1999; 60
2007; 56
2018; 154
1988; 3
2015; 27
2014; 109
2012; 1
2021; 11
2023
2022
2001; 4
2017; 11
2002; 22
2017; 12
2022; 56
2006; 141
1996; 271
1996; 40
2015
2009; 5
2020; 65
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Snippet Summary Background Drugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly ‘off‐label’. Within each...
Drugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly 'off-label'. Within each category, they act at...
BackgroundDrugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly ‘off‐label’. Within each category,...
BACKGROUNDDrugs which can inhibit nausea/vomiting and/or increase gastric emptying are used to treat gastroparesis, mostly 'off-label'. Within each category,...
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SubjectTerms Acetylcholine receptors (muscarinic)
Agonists
Amitriptyline
Antagonists
aprepitant
domperidone
Drugs
Erythromycin
Gastric Emptying
gastroparesis
Gastroparesis - drug therapy
Humans
Metoclopramide
Motilin - pharmacology
Motilin - therapeutic use
Movement disorders
Nausea
Nausea - etiology
Pacemakers
prucalopride
Sensory neurons
Serotonin
Tardive dyskinesia
Vagus nerve
Vomiting
Vomiting - drug therapy
Vomiting - etiology
Title Review article: An analysis of the pharmacological rationale for selecting drugs to inhibit vomiting or increase gastric emptying during treatment of gastroparesis
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fapt.17466
https://www.ncbi.nlm.nih.gov/pubmed/36919196
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https://search.proquest.com/docview/2787212122
Volume 57
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