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Gastroparesis: a turning point in understanding and treatment
  1. Madhusudan Grover1,
  2. Gianrico Farrugia1,
  3. Vincenzo Stanghellini2
  1. 1 Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA
  2. 2 Department of Digestive Diseases and Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy
  1. Correspondence to Dr Madhusudan Grover, Division of Gastroenterology and Hepatology, Enteric NeuroScience Program, Mayo Clinic, Rochester, MN 55905, USA; grover.madhusudan{at}


Gastroparesis is defined by delayed gastric emptying (GE) and symptoms of nausea, vomiting, bloating, postprandial fullness, early satiety and abdominal pain. Most common aetiologies include diabetes, postsurgical and postinfectious, but in many cases it is idiopathic. Clinical presentation and natural history vary by the aetiology. There is significant morbidity and healthcare utilisation associated with gastroparesis. Mechanistic studies from diabetic animal models of delayed GE as well as human full-thickness biopsies have significantly advanced our understanding of this disorder. An innate immune dysregulation and injury to the interstitial cells of Cajal and other components of the enteric nervous system through paracrine and oxidative stress mediators is likely central to the pathogenesis of gastroparesis. Scintigraphy and 13C breath testing provide the most validated assessment of GE. The stagnant gastroparesis therapeutic landscape is likely to soon see significant changes. Relatively newer treatment strategies include antiemetics (aprepitant), prokinetics (prucalopride, relamorelin) and fundic relaxants (acotiamide, buspirone). Endoscopic pyloromyotomy appears promising over the short term, especially for symptoms of nausea and vomiting. Further controlled trials and identification of the appropriate subgroup with pyloric dysfunction and assessment of long-term outcomes are essential. This review highlights the clinical presentation, diagnosis, mechanisms and treatment advancements for gastroparesis.


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  • Contributors All authors contributed equally to this manuscript.

  • Funding MG and GF are supported by NIH DK068055 and DK74008. MG is also supported by NIH K23 DK 103911 and R03 DK 120745. GF is also supported by NIH DK057061.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.