Prognosis is favorable for most diabetic patients with delayed gastric emptying.

Diabetic gastroparesis with nausea and vomiting that is unresponsive to medical therapy is one of the more challenging complications of diabetes. Repeat visits to the emergency department, numerous hospital admissions, and enteral feeding (1) add to the debility already associated with this condition. Although patients with such severe symptoms are few (2), a poor prognosis is often associated with the diagnosis. Reports of increased mortality among diabetic patients with autonomic neuropathy (3), and the association of diabetic gastroparesis with autonomic neuropathy (4), contribute to this expectation of a poor prognosis for diabetic patients with delayed gastric emptying. Furthermore, the term “gastroparesis” suggests permanent paralysis of the stomach. There are several reasons to reexamine the idea that patients with diabetic gastroparesis have a poor prognosis. First, gastric emptying is impaired by hyperglycemia. The rate of gastric emptying in patients with type 1 diabetes decreases during periods of hyperglycemia (5). The triggering of a gastric electrical rhythm disturbance may be a key mechanism in this hyperglycemia-induced but reversible effect (6). Second, hyperglycemia also leads to reversible impairment in autonomic nerve function. In normal volunteers who underwent glucose clamping to raise their blood glucose levels to the hyperglycemic range, cardiovascular nerve function was impaired (7). Third, normalization of blood glucose levels with pancreas transplantation restores autonomic nerve function in some patients (8,9). Fourth, delayed gastric emptying has not been observed to increase mortality in patients with type 1 or type 2 diabetes (10). When considered together, these reports suggest that patients with diabetic gastroparesis include both those with irreversible and those with reversible (hyperglycemia-induced) impairment of gastric emptying. Jones et al. (11) in this issue of The American Journal of Medicine addresses some of these questions. They studied 20 patients with type 1 or type 2 diabetes, comparing rates of solid and liquid emptying, blood glucose concentration, gastric and esophageal symptoms, and autonomic nerve function at baseline and at follow-up about 12 years later. They found that during this time, there was minimal change in gastric emptying for solids and liquids, glycemic control was mildly improved, there was no change in gastric or esophageal symptoms, and autonomic nerve function worsened. This is an important study from a group that has made notable contributions to our understanding of the effects of diabetes on gastrointestinal motility. Extending their previous work that showed that diabetic gastroparesis was not associated with increased mortality (10), their results further support the promise of a good prognosis for diabetic patients with delayed gastric emptying. Does a good prognosis apply to all diabetic patients with delayed gastric emptying? Likely not. In patients who had undergone pancreas transplantation successfully (9), gastric function, as measured by gastric emptying and electrogastrography, did not improve in about half of patients. However, it is encouraging that even in a group of patients with very severe diabetes and refractory complications, not every patient with delayed gastric emptying had a poor prognosis. An intriguing finding of their study is that autonomic nerve function worsened even as the rate of gastric emptying remained unchanged. This lack of a correlation between the recorded change in autonomic nerve function and the change in gastric emptying raises additional doubts about the suggestion that diabetic gastroparesis, in most patients, is paresis of the stomach due to autonomic neuropathy. Because hyperglycemia may have been responsible for a reversible delay in gastric emptying, future studies in this area should consider adding glucose clamping to their design. With patients maintained at normal blood glucose concentrations, it would be possible to sort patients into either the reversible or irreversible impairment group. Adjusting for the confounding effects of hyperglycemia would allow testing of the hypothesis that a good prognosis may apply to the reversible impairment group but not the irreversible group. As we continue to learn more about this relationship, perhaps the term “diabetic gastroparesis” will eventually be reserved for the rare patient with irreversible paresis of the stomach. Am J Med. 2002;113:525–526. From the GI Motility Program and Section of Nutrition, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, and Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California. Requests for reprints should be addressed to Henry C. Lin, MD, 8635 W. Third Street #770W, Los Angeles, California 90048, or henry.lin@cshs.org.