Diabetic<unk>  was first discovered by Kassander in 1958 in diabetic patients with delayed gastric emptying and gastric stasis but without mechanical obstruction, and was named<unk>  diabeticorum. The definition has been changing by adding new symptoms such as severe abdominal pain. Based on the rate of gastric emptying, abnormalities of gastric emptying in<unk>  may be classified as: transient slow gastric emptying, transient rapid gastric emptying, persistent slow or delayed gastric emptying<unk> , and persistent rapid gastric emptying. Persistent hyperglycemia results in molecular and metabolic changes in neurons, interstitial cells of Cajal, and smooth muscle cells. Theses changes are caused by oxidative stress and products (cytokines) of the polarized M1 (proinflammatory) and M2 (prohealing, or repair) macrophages.<unk>  is not a separate category and is considered a part of functional dyspepsia. The most common symptoms "cardinal symptoms" of<unk>  include early satiety, postprandial fullness, nausea, vomiting, and bloating. Gastric scintigraphy or stable-isotope 13C breath test can detect different gastric emptying abnormalities. The most effective symptomatic treatment of diabetic<unk>  is the same as the treatment of functional dyspepsia.
Gastroparesis in diabetes
Diabetes mellitus type 1 pathophysiology
Chronic functional abdominal pain
Gastric dumping syndrome
Mallory-Weiss syndrome epidemiology and demographics
Gastric dumping syndrome epidemiology and demographics
Mallory–Weiss syndrome
Functional gastrointestinal disorder