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Cited by 151Gastrointestinal motility and disordersGastroesophageal reflux and treatmentsEnhanced Recovery After Surgery

Gastroparesis

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Camilleri, Michael, Sanders, Kenton M.·2022·Gastroenterology
DOI 10.1053/j.gastro.2021.10.028PMC PMC8678360
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Abstract

Gastroparesis is characterized by symptoms suggestive of, and objective evidence of, delayed gastric emptying in the absence of mechanical obstruction. This review addresses the normal emptying of solids and liquids from the stomach and details the myogenic and neuromuscular control mechanisms, including the specialized function of the pyloric sphincter, that result in normal emptying, based predominantly on animal research. A clear understanding of fundamental mechanisms is necessary to comprehend derangements leading to gastroparesis, and additional research on human gastric muscles is needed. The section on pathophysiology of gastroparesis considers neuromuscular diseases that affect nonsphincteric gastric muscle, disorders of the extrinsic neural control, and pyloric dysfunction that lead to gastroparesis. The potential cellular basis for gastroparesis is attributed to the effects of oxidative stress and inflammation, with increased pro-inflammatory and decreased resident macrophages, as observed in full-thickness biopsies from patients with gastroparesis. Predominant diagnostic tests involving measurements of gastric emptying, the use of a functional luminal imaging probe, and high-resolution antral duodenal manometry in characterizing the abnormal motor functions at the gastroduodenal junction are discussed. Management is based on supporting nutrition; dietary interventions, including the physical reduction in particle size of solid foods; pharmacological agents, including prokinetics and anti-emetics; and interventions such as gastric electrical stimulation and pyloromyotomy. These are discussed briefly, and comment is added on the potential for individualized treatments in the future, based on optimal gastric emptying measurement and objective documentation of the underlying pathophysiology causing the gastroparesis.

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  • In the gastric fundus, impaired inhibitory neurotransmission is accompanied by reduced tonic contraction because of defective muscle contractility, whereas in the antrum both cholinergic neuromuscular transmission and smooth muscle strength are altered.

    “in the gastric fundus, impaired inhibitory neurotransmission is accompanied by reduced tonic contraction because of defective muscle contractility, whereas in the antrum both cholinergic neuromuscular transmission and smooth muscle strength are altered [19, 23, 42, 43].”

    From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [42]

    Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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  • Myogenic changes may occur in parallel with neuronal injury, supporting the concept of a partly independent muscular pathway in the disease process.

    “Importantly, these myogenic changes may occur in parallel with neuronal injury, supporting the concept of a partly independent muscular pathway in the disease process [42].”

    From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [42]

    The Pathophysiology section (Pyloric Dysfunction; page not available) reports changes around smooth muscle cells and abnormalities of neurons or nerve endings in gastroparesis. It also suggests that pyloric dysfunction could reflect ICC damage rather than neuropathy. These passages support a possible non-neuronal contribution, but do not establish that myogenic changes occur in parallel with neuronal injury or identify a partly independent muscular pathway. (LLM, conf=0.78)

    Experimental — accuracy not yet measured

  • Advanced diabetic gastroparesis can be associated with smooth-muscle degeneration, fibrosis, collagen deposition, and ultrastructural abnormalities such as thickened basal lamina, changes that likely contribute to a hypocontractile phenotype and delayed gastric emptying.

    “Moreover, advanced diabetic gastroparesis can be associated with smooth-muscle degeneration, fibrosis, collagen deposition, and ultrastructural abnormalities such as thickened basal lamina, changes that likely contribute to a hypocontractile phenotype and delayed gastric emptying [23, 42–45].”

    From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [42]

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Authors
Camilleri, M., & Sanders, K. M.
Affiliations
  • Mayo Clinic (US)
  • University of Nevada, Reno (US)
Corresponding author
Camilleri, Michael
ORCID
Venue
Gastroenterology
Publisher
Elsevier BV
Published
2022-01
Volume
162
Issue
1
Pages
68-87.e1
ISSN
0016-5085 (ISSN-L)
DOI
10.1053/j.gastro.2021.10.028
PMC
PMC8678360
OpenAlex
W4200231661
Cited by
151
References
183
Citations by year
2026: 32 · 2025: 42 · 2024: 40 · 2023: 28 · 2022: 9
FWCI
3.67
Type
journal article
Language
en
Open access
Licence
Locations
  • Gastroenterology (acceptedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (R01-DK057236, R01-DK091336, R01-DK120759, R01-DK122280, R01-DK125680)
  • Mayo Clinic
Topics
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
  • Health Sciences › Medicine › Gastroenterology › Gastroesophageal reflux and treatments
  • Health Sciences › Medicine › Surgery › Enhanced Recovery After Surgery
Keywords
gastroparesis, delayed gastric emptying, pyloric sphincter, gastric smooth muscle, pathophysiology, oxidative stress, inflammation, prokinetic agents, antiemetics, gastric electrical stimulation, pyloromyotomy, dietary intervention, particle size reduction
MeSH terms
Animals, Gastric Emptying, Humans, Predictive Value of Tests, Pylorus, Treatment Outcome, Enteric Nervous System, Gastroparesis

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