Patients with enteropathies caused by diabetes mellitus present with a spectrum of clinical manifestations with diverse pathophysiologies. A simple test to document the mechanism contributing to these symptoms is helpful in the selection of therapy. Patients need a single physician to coordinate and prioritize treatment of the protean manifestations and complications of diabetes mellitus. In particular, medications used to treat depression and hypertension have marked effects on gut motor function, and alternatives without such effects may correct the disturbance and relieve symptoms. Despite specific approaches to the treatment of diabetic enteropathy and the availability of prokinetic agents to treat motility disorders, management has been only partially successful. Reversal of the derangements that cause the abnormal gut functions would clearly be preferable, but no medical therapy is of proven benefit in restoring the underlying disorders of nerve function. Therefore, current therapy is based on restoration of euglycemia and symptomatic control. The prospect of complete euglycemic control with pancreas transplantation offers the chance of better control in the future. With improved immunosuppressive regimens and surgical technique, graft survival rates are now similar to those of other organ transplants. Whether pancreatic transplantation reverses the enteropathy caused by diabetes is uncertain. Pancreatic transplantations have been performed for indications other than the management of diabetic enteropathy. Most patients undergoing pancreas transplantation have had chronic renal failure and also have undergone kidney transplantation. Because uremia and other metabolic derangements are corrected at the same time, it is uncertain whether pretransplant gastric stasis was solely caused by diabetic enteropathy. The data from pretransplantation and post-transplantation symptom assessments in diabetic enteropathy are limited. In a study of 32 patients, Zehr and co- workers reported that 96% of 24 patients with gastrointestinal symptoms improved after a pancreatic transplant. On the other hand, objective evaluation of gastrointestinal motor function revealed conflicting results. Gaber and co-workers studied gastric emptying of solids and gastrointestinal symptoms in 10 patients before and 12 months alter combined renal and pancreatic transplantation. Symptoms improved significantly, and gastric emptying kinetics improved in the six patients who had gastric stasis pretransplant. On the other hand, in a study of 32 patients with diabetes mellitus and end-stage renal failure, Murat and co-workers found that at 6 and 12 months alter transplantation, emptying of solids remained abnormal but liquid emptying improved significantly. These findings suggest that glycemic control or correction of uremia may normalize the emptying of liquids, whereas impaired emptying of solids and antral hypomotility (which depends on vagal input) persist, because the autovagotomy is not reversed by the transplantation. In the absence of markers that accurately predict which patients with diabetes are at risk for a secondary complication, such as enteropathy, the selection of patients for transplantation in an attempt to achieve maximal benefit remains difficult. Moreover, because some data suggest that patients with abnormal autonomic (cardiorespiratory) reflexes and an unsuccessful pancreatic transplantation have a greater mortality rate than similar patients who do not undergo transplantation, the role of transplantation in the management of diabetic enteropathy requires further study.
|Number of pages
|Endocrinology and Metabolism Clinics of North America
|Published - 1996
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism