Diabetic gastroparesis.

ABSTRACT

Our understanding of gastric motility disorder--diabetic gastroparesis has advanced in the last ten to fifteen years, but the published data regarding pathogenesis are confusing and show conflicting results. The pathogenesis is sometimes linked with hyperglycemia, autonomic neuropathy, gastrointestinal hormone or myogenic mechanism. Antral hypomotility is often associated with hyperglycemia which is often accompanied by reduction in duodenal waves. Varying level of motilin, a gastrokinetic hormone has been reported. However none of the mechanism could explain the exact pathogenesis. The relationship of this mortality disorder with clinical symptoms is not always established, however nausea and vomiting lasting for days or weeks are the prominent symptoms. Other symptoms are post-prandial fullness, early satiety, bloating, belching, and vague abdominal discomfort. In a few cases, it may be the cause of poor nutrition, uncontrolled diabetes and recurrent ketoacidosis. Last one or two decades have seen some advancement in the investigational procedures like scintigraphy, radio-opaque markers, breath test, electrogastrography and MRI. Which can lead to a proper diagnosis. Such objective assessment is all the more important as nearly half of the patients do not have any symptom. Symptomatic improvement of gastroparetic patients should be the aim and in asymptomatic patients, treatment is often not recommended. Some dietary advice and prokinetic agents like metoclopramide, cisapride etc. are often prescribed but much needs to be further known as management is not always uniformly rewarding.