Pyloric Sphincter Abnormalities in Patients With Gastroparesis Symptoms

Overview

About this study

The purpose of this study is to determine if there are pyloric sphincter abnormalities in patients with gastroparesis symptoms and determine how prevalent these abnormalities are using tests to assess the pyloric sphincter - endoluminal functional luminal imaging probe (Endoflip™), water load satiety testing (WLST), and high-resolution cutaneous electrogastrography (HR-EGG) using Gastric Alimetry™ System.

Participation eligibility

Participant eligibility includes age, gender, type and stage of disease, and previous treatments or health concerns. Guidelines differ from study to study, and identify who can or cannot participate. There is no guarantee that every individual who qualifies and wants to participate in a trial will be enrolled. Contact the study team to discuss study eligibility and potential participation.

Inclusion Criteria FOR SYMPTOMATIC PARTICIPANTS:

1. Provision of signed and dated informed consent form.
2. Stated willingness to comply with all study procedures and availability for the duration of the study.
3. Male or female, aged 18-85
4. Symptoms of gastroparesis, either diabetic or idiopathic etiology
5. Symptoms of gastroparesis with minimum Gastroparesis Cardinal Symptom Index (GCSI) score of 2.0 (18/45 x 5)
6. Individual will have had a prior 4-hour gastric emptying scintigraphy test performed for clinical evaluation within the last 6 months. This gastric emptying test would be done for clinical evaluation and is not part of the research study. From these participants with gastroparesis symptoms, we will include those with delayed gastric emptying as well as those with normal gastric emptying.
7. Participant must not initiate any new treatments until completion of the study procedures.
8. Willingness to:

1. Stop histamine 2 antagonists, prokinetics (e.g., metoclopramide, erythromycin, domperidone, prucalopride), narcotics, anticholinergics, constipation medications (over the counter laxatives, isotonic polyethylene glycol (PEG) electrolyte preparations (e.g. MiraLax), prescription laxatives (e.g. lubiprostone), proton pump inhibitors, cannabinoids, and cannabidiol (CBD) for 3 days prior to each visit;
2. Abstain from food and water after midnight (at least for 8 hours) before the start of each visit until after the visit.

INCLUSION CRITERIA FOR CONTROL PARTICIPANTS:

1. Provision of signed and dated informed consent form
2. Male or female, aged 18 or older
3. Undergoing an upper endoscopy for their clinical evaluation of diarrhea, GI bleed, or iron-deficiency anemia, or evaluation for bariatric surgery.
4. Do not have upper GI symptoms greater than 1 as assessed by the Gastroparesis Cardinal Symptom Index (GCSI) of PAGI-SYM questionnaire.

EXCLUSION CRITERIA:

1. Prior gut lumen surgery on the esophagus or the stomach, including Nissen fundoplication.
2. Prior surgery on the pylorus (G-POEM, surgical pyloroplasty, surgical pyloromyotomy)
3. Known history of achalasia or esophageal stricture
4. Known history of physiological or mechanical GI obstruction
5. Abnormalities seen on a prior upper endoscopy placing patient at increased risk:

* Ulcer of the esophagus, stomach, or duodenum
* Esophageal varices

6. Individuals at risk for prolonging the endoscopy procedure: severe chronic pulmonary disease, severe food retention in the stomach on endoscopy.
7. Presence of significant gastric or duodenal pathology that could be expected to cause dysmotility (e.g. significant inflammation, infiltrate disorders etc)
8. Individuals with a history of other chronic disease potentially causative of gastrointestinal symptom
9. Acute or chronic renal insufficiency
10. Current eating disorders
11. Females who are pregnant. A urine pregnancy test is routinely obtained on all females immediately prior to endoscopic procedures.
12. Individuals with contraindications for endoscopy, including bleeding abnormalities
13. Allergy to eggs preventing sedation with propofol and/or gastric emptying test
14. Significant dysphagia
15. Prior inflammatory bowel disease, Crohn's
16. History of any esophageal/gastric/pyloric injection of botulinum toxin
17. Patients on daily opioid use or \>3 day/week use
18. Use of glucagon-like peptide 1 (GLP1) receptor agonists or Sodium-Glucose Transport Protein 2 (SGLT2); Gastric inhibitory polypeptide (GIP)- glucagon-like peptide (GLP) combo

Note: Other protocol defined Inclusion/Exclusion Criteria may apply.

Eligibility last updated 12/05/2024. Questions regarding updates should be directed to the study team contact.

 

Participating Mayo Clinic locations

Study statuses change often. Please contact the study team for the most up-to-date information regarding possible participation.

Mayo Clinic Location Status Contact

Scottsdale/Phoenix, Ariz.

Mayo Clinic principal investigator

Pankaj Pasricha, M.B.B.S., M.D.

Contact us for the latest status

Contact information:

Clinical Studies Unit

(904) 953-2255

More information

Publications

  • Manometric recording from the pyloric channel is challenging and is usually performed with a sleeve device. Recently, a solid-state manometry system was developed, which incorporates 36 circumferential pressure sensors spaced at 1-cm intervals. Our aim was to use this system to determine whether it provided useful manometric measurements of the pyloric region. We recruited 10 healthy subjects (7 males:3 females). The catheter (ManoScan(360)) was introduced transnasally and, in the final position, 15-20 sensors were in the stomach and the remainder distributed across the pylorus and duodenum. Patients were recorded fasting and then given a meal and recorded postprandially. Using pressure data and isocontour plots, the pylorus was identified in all subjects. Mean pyloric width was 2.1 +/- 0.1 cm (95% CI: 1.40-2.40). Basal pyloric pressure during phase I was 9.4 +/- 1.1 mmHg, while basal antral pressure was significantly lower (P = 0.003; 95% CI: 2.4-8.4). Pyloric pressure was always elevated relative to antral pressure in phase I. For phases II and III, pyloric pressure was 7.7 +/- 2.3 mmHg and 9.4 +/- 1.1 mmHg, respectively. Pyloric pressure increased similarly after both the liquid and solid meal. In addition, isolated pressure events and waves, which involve the pylorus, were readily identified. Read More on PubMed
  • This literature review and the recommendations herein were prepared for the American Gastroenterological Association Clinical Practice Committee. The paper was approved by the Committee on May 16, 2004, and by the AGA Governing Board on September 23, 2004. Read More on PubMed
  • Diabetes mellitus has been associated with a variety of gastrointestinal motor disturbances. Pyloric activity, however, has not been specifically investigated. We have quantified the pyloric manometric profile in 24 diabetics with recurrent nausea or vomiting, or both, without evidence of mechanical obstruction. Twelve healthy volunteers served as controls. A multilumen pneumohydraulic perfusion assembly with five side openings, each 1 cm apart, was positioned fluoroscopically across the antroduodenal junction and used to monitor pressure activity for 5 h (3 h fasting and 2 h fed). Three patterns of pyloric activity were defined and quantified: (a) baseline elevation of greater than or equal to 3 mmHg for greater than or equal to 1 min (tonic pattern); (b) antral-type phasic pressure activity mixed with duodenal phasic activity (phasic pattern); and (c) phasic pattern superimposed on tonic activity (combined tonic-phasic pattern). The duration of the total pyloric activity before and after the meal was greater in diabetics than in controls (p less than 0.005). Furthermore, episodes of unusually prolonged (greater than or equal to 3 min) and intense (greater than or equal to 10 mmHg) tonic contraction, "pylorospasm," were observed in 14 of 24 diabetics but in only 1 control (p = 0.025). In diabetics, episodes of pylorospasm had a peak amplitude of tonic activity of 13 +/- 1 mmHg and a duration of 7 +/- 0.7 min (mean +/- SE). We conclude that pyloric dysmotility forms part of the widespread disruption of gut motility that affects some patients with diabetes. Read More on PubMed
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CLS-20585144

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