Domination of gastric Complications Among Diabetic Patients

Abdul Kader Mohiuddin

doi:10.26717/bjstr.2019.19.003331

Abstract

This article covers the epidemiology, pathophysiology/complications and management of diabetic gastroparesis (DGP), and more broadly diabetic gastroenteropathy, which encompasses all the gastrointestinal manifestations of diabetes mellitus (DM). Hyperglycemia, autonomic neuropathy, and enteric neuromuscular inflammation and injury are implicated in the pathogenesis of delayed gastric emptying (GE). Initial options include dietary modifications, supplemental oral nutrition, and antiemetic and prokinetic medications. Patients with more severe symptoms may require a venting gastrostomy or jejunostomy and/or gastric electrical stimulation (GES). To date, few population-based studies have estimated the true prevalence and incidence of gastroparesis. Nonetheless, its prevalence appears to be rising, as does its incidence among minority populations, documented via hospitalizations, which can impose significant economic burdens on patients.

Highlights

T to improve gastric health by using the ubiquitously prescribed proton pump inhibitors, H2 receptor antagonists, and sucralfate or aluminum hydroxide-based antacids
Most patients respond to conservative treatment with frequent small meals and an upright eating position, in combination with motility agents, such as oral erythromycin analogs, metoclopramide, and domperidone [19]
Metoclopramide and domperidone, a D2 dopamine receptor antagonist, are the most widely used but only metoclopramide is FDA approved in the US while domperidone is available in Europe, Canada, Mexico, and New Zealand

Summary

Introduction

T to improve gastric health by using the ubiquitously prescribed proton pump inhibitors, H2 receptor antagonists, and sucralfate or aluminum hydroxide-based antacids. It is critical to clearly distinguish patients with functional dyspepsia (FD) from those with GP and to better understand the relationship among alterations in specific symptoms, GE, and altered peripheral and central sensory responses to gastric stimuli [15]. These drugs are a cause of delayed gastric emptying.

Results

Conclusion