Gastroparesis is a chronic disabling condition of impaired gastric motility. It is defined as delayed gastric emptying of solids from the stomach in the absence of a mechanical obstruction.
It may result from the presence of lifelong diabetes mellitus, (sugar diabetes) vagal nerve injury or can be idiopathic (no known reason). It leads to gastrointestinal symptoms: postprandial (after eating) nausea and vomiting, easy satiety (feeling full quickly), weight loss, and malnutrition. It can progress to the need for frequent hospitalizations for treatment of dehydration and malnutrition.
The current conventional medical treatment consists of nutritional support along with prokinetic (stimulatory) and antiemetic (anti-nausea) medications combined with dietary modifications and nutritional supplements. These therapeutic approaches are often limited by their side effects and questionable therapeutic effects.
Diabetic gastroparesis is clinically important because it may be associated with gastrointestinal symptoms as listed above, alterations in glycemic (blood sugar) control, and changes in oral drug absorption. Until relatively recently, gastroparesis was thought to be an infrequent complication of diabetes, occurring only in patients with long-standing diabetes who had severe microvascular complications. Today it has been demonstrated that gastric emptying of solid and/or nutrient liquid meals is delayed in about 50% of outpatients with long-standing type 1 or type 2 diabetes.
In the diagnostic work-up of a patient with upper gastrointestinal symptoms a diagnosis of gastroparesis can not be assigned to that patient until all the other diagnostic studies have been exhausted. This list includes the CCK Stimulation Test which demonstrates the function or dysfunction of the gallbladder. Gallbladder disease, in its own right, greatly contributes to a delay in stomach emptying.
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