Diabetes is one of the most common causes of gastroparesis. 40% of patients with long term diabetes mellitus type I and 20% with diabetes mellitus type II have delayed gastric emptying. In 1995, 21% patient of gastroparesis patients had DM; in 2004, 26.7%.
Diabetes patients are more likely to have nausea and vomiting as the cardinal GP symptoms, rather than epigastric pain seen more frequently in idiopathic GP. `Diabetic GP is known to cause more severe gastric retention than idiopathic GP.
Diabetic patients with gastroparesis are at risk for developing difficulty in managing sugar levels. Poor control of blood sugar can contribute to delayed gastric emptying. Hyperglycemia is associated with decreased movement of the stomach, an effect more pronounced above 250 mg/dL. Additionally, some medications used for diabetes, like exenatide for type II diabetes, can delay gastric emptying. Persistent hyperglycemia is often cited as contributing to vagus nerve damage, which can also result in GP.
In one series, 58% of DM patients had increased tone in the pyloric sphincter, through which food passes from the stomach into the small intestine. Pyloric tone is often elevated in GP patients. Botox injections into the pyloric sphincter has been associated with increased gastric emptying and relief of symptoms in diabetic GP patients.
Gastric electric stimulation is more likely to be successful in diabetic patients versus those whose GP is not associated with diabetes, showing 50% reduction in symptoms over those with idiopathic GP. Patients also experience better glycemic control when GP is more controlled, as reflected by reduction in hemoglobin A1C.
Gastroparesis in diabetes patients is well studied. Curiously, improving glycemic control is not associated with symptom improvement (or change at all) in patients with type II diabetes. In type I diabetics, symptom change has only correlated well with depression.
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