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Cited by 14Gastrointestinal motility and disordersNausea and vomiting managementGastroesophageal reflux and treatments

Pharmacologic treatments for gastroparesis

Open access
Camilleri, Michael, Jencks, Kara J.·2025·Pharmacological Reviews
DOI 10.1016/j.pharmr.2024.100019PMC PMC12599987
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Abstract

Gastroparesis is a neurogastrointestinal disorder of motility in which patients experience symptoms of nausea, vomiting, bloating, early satiety, postprandial fullness, upper abdominal discomfort or pain, and delayed gastric emptying of solids based on scintigraphy or stable isotope breath test when mechanical obstruction has been excluded. Symptoms of gastroparesis may result from diverse pathophysiological mechanisms, including antroduodenal hypomotility, pylorospasm, increased gastric accommodation, and visceral hypersensitivity. The most common etiologies of gastroparesis are idiopathic, diabetic, and postsurgical, and less frequent causes are neurodegenerative disorders (Parkinson's disease), myopathies (scleroderma, amyloidosis), medication-induced (glucagon-like peptide-1 agonists and opioid agents), and paraneoplastic syndrome. This review addresses pharmacologic management of gastroparesis including prokinetic and antiemetic agents, pharmacologic agents targeting the pylorus, and effects of neuromodulators. SIGNIFICANCE STATEMENT: Gastroparesis is a neurogastrointestinal motility disorder characterized by delayed gastric emptying without mechanical obstruction with numerous upper gastrointestinal symptoms, including nausea and vomiting. The management of gastroparesis involves nutritional support, medications, and procedures. The only Food and Drug Administration-approved medication for gastroparesis is metoclopramide. This article reviews the pharmacology and efficacy of all classes of antiemetics or prokinetic effects used in gastroparesis. There is still a considerable unmet need for efficacious medications specifically for the treatment of gastroparesis, especially in refractory cases.

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Crossref · 10.1016/j.pharmr.2024.100019

Cites

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  • Prokinetics, such as metoclopramide and erythromycin, modify emptying times and may require earlier or split bolus dosing to avoid early hypoglycemia.

    “Prokinetics, such as metoclopramide and erythromycin, modifies emptying times and may require earlier or split bolus dosing to avoid early hypoglycemia [2, 3, 14, 119, 120]”

    From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [120]

    The Management of gastroparesis > Pharmacologic agents section describes metoclopramide as a prokinetic and reports that erythromycin accelerates gastric emptying; the Targeting the fundus section also describes erythromycin’s acceleration of emptying. Our copy does not link either drug to earlier or split insulin bolus dosing to avoid early hypoglycemia (searched for bolus timing, insulin, and hypoglycemia). The supplied passages have no page numbers. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Metoclopramide is the only drug approved by the FDA for gastroparesis, and its use is limited to <12 weeks due to extrapyramidal and tardive dyskinesia risk.

    “Metoclopramide, the only drug approved by the FDA for gastroparesis, is limited to < 12 weeks due to extrapyramidal and tardive dyskinesia risk [3, 14, 120, 121]”

    From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [120]

    The Pharmacologic agents section identifies metoclopramide as the only FDA-approved drug for gastroparesis and links its neurological risks, including extrapyramidal symptoms and tardive dyskinesia, to an approval limit. It states a maximum of 12 weeks, not strictly fewer than 12 weeks, and discusses intermittent use beyond that period. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • The efficacy of prokinetics is often limited and long-term use requires careful monitoring for adverse effects.

    “although their efficacy is often limited and long-term use requires careful monitorg for adverse effects [2, 14, 120].”

    From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [120]

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Research works printed but not linked: 1

  1. Portincasa P, Mearin F, Robert M, Plazas MJ, Mas M, and Heras J (2009) Efficacy and tolerability of cinitapride in the treatment of functional dyspepsia and delayed gastric emptying. Gastroenterol Hepatol 32: 669– 676. 19819042

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Authors
Camilleri, M., & Jencks, K. J.
Affiliations
Mayo Clinic (US)
Corresponding author
Camilleri, Michael
ORCID
Venue
Pharmacological Reviews
Publisher
Elsevier BV
Published
2025-03
Volume
77
Issue
2
Pages
100019
ISSN
0031-6997 (ISSN-L)
DOI
10.1016/j.pharmr.2024.100019
PMC
PMC12599987
OpenAlex
W4406090389
Cited by
14
References
226
Citations by year
2026: 9 · 2025: 4 · 2024: 1
FWCI
3.09
Type
journal article
Language
en
Open access
Licence
Locations
  • Pharmacological Reviews (acceptedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
Funders
National Institutes of Health
Topics
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
  • Health Sciences › Medicine › Surgery › Nausea and vomiting management
  • Health Sciences › Medicine › Gastroenterology › Gastroesophageal reflux and treatments
Keywords
gastroparesis, delayed gastric emptying, prokinetic agents, antiemetics, metoclopramide, neuromodulators, diabetic gastroparesis, visceral hypersensitivity, GLP-1 receptor agonists, refractory gastroparesis
MeSH terms
Animals, Antiemetics, Gastric Emptying, Gastrointestinal Agents, Humans, Gastroparesis

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