Chin Med J (Taipei) 1998;61:S85.

New Insight on the Pathogenesis and Treatment of Diabetic Gastroparesis.

Chung Owyang

University of Michigan Medical Center, Ann Arbor, Michigan 49109

Abstract

Diabetic gastroparesis occurs in about 30% of patients with type I diabetes. Documentation of gastroparesis does not necessarily correlate with the presence of symptoms. Some asymptomatic diabetics exhibit markedly delayed gastric emptying while others with severe nausea have normal gastric scintigraphy. Delays in emptying of solid foods are generally believed to result from impaired phasic antral motor activity and this may result in early postprandial fullness, nausea and vomiting. Both phase III of the interdigestive migrating motor complex and phasic activities of the postprandial antral motility are impaired in diabetic gastroparesis. These abnormalities may respond to prokinetic agents such as metoclopramide and cisapride. In patients who fail to respond to prokinetic agents, gastric electrical pacing may be considered. Epigastric pain is another complaint common among patients with diabetic gastroparesis. Recent studies suggest that pain is not related to gastroparesis in most cases. In an investigation of type I diabetics with dyspepsia and autonomic dysfunction, gastric distention, evoked greater nausea, bloating and epigastric pain than in healthy controls suggestive of defects in visceral afferent function. As this abnormality is likely to be secondary to sensory neuropathy, it showed little or no response to prokinetic agents. Potential therapy for pain in diabetic gastroparesis include the use of peripheral kappa agonist, gabapentin and gastric electrical pacing. A common observation in diabetic gastroparesis is that stable motor defects often exhibit wide day to day variation in severity of symptoms of nausea and vomiting,. Frequently this is caused by abnormal gastric electrical activities (tachygastria) due to ectopic pacemakers originate from the antrum resulting in nausea and loss of gastric contractions. Clinical studies indicate that 50-90% of diabetics with gastroparesis developed tachygastria (pacemaker activities disturbances) at one time or another and this may be due to uncontrolled hyperglycemia. The increased dysrhythmic activity associated with hyperglycemia could be prevented by the prostaglandin synthesis inhibitor, indomethacin. This suggests that prostaglandin over production in gastric smooth muscle may be responsible for gastric dysrhythmias in diabetic conditions. In addition, domperidone, a dopamine 2 receptors also appears to be effective in the treatment of tachygastria in diabetic gastroparesis. Therefore the pathogenesis of symptoms of diabetic gastroparesis is multifactorial. In general nausea and vomiting may be due to gastroparesis and these can be exacerbated by development of tachygastrias. On the other hand, pain is usually not related to gastroparesis but appears to be secondary to sensory neuropathy. Treatment of these symptoms should be tailored according to their causes.

[Chin Med J (Taipei) 1998;61:S85.]