Novel surgical treatment and gastric pathology in diabetic gastroparesis
Article first published online: 24 DEC 2001
Volume 16, Issue 6, pages 488–495, June 1999
How to Cite
Ejskjaer, N. T., Bradley, J. L., Buxton-Thomas, M. S., Edmonds, M. E., Howard, E. R., Purewal, T., Thomas, P. K. and Watkins, P. J. (1999), Novel surgical treatment and gastric pathology in diabetic gastroparesis. Diabetic Medicine, 16: 488–495. doi: 10.1046/j.1464-5491.1999.00086.x
- Issue published online: 24 DEC 2001
- Article first published online: 24 DEC 2001
- Received 9 October 1998; revised 11 January 1999; accepted 17 January 1999
- diabetic gastroparesis;
- gastric surgical reconstruction;
Aims Observations are made on four Type 1 diabetic patients with the rare syndrome of intractable vomiting from confirmed gastroparesis, to determine whether radical surgery would alleviate their symptoms and subsequently to examine in detail the gastric histopathology.
Methods The surgical approach consisted of an ≈ 70% resection of the stomach, including the antrum and pylorus, with closure of the duodenum and restoration of gastrointestinal continuity with a 60-cm Roux-en-Y jejunal loop. Four longstanding Type 1 diabetic patients were examined and treated as described. They were all women in the age range 27–41 years with grossly abnormal autonomic function tests in whom other causes for gastric paresis had been excluded.
Results Vomiting episodes leading to multiple hospital admissions (6–8) in the year preceeding surgery were eliminated in three of the four patients, while in the fourth initial success was followed by the need for dialysis for renal failure. Gastric histopathology showed evidence of smooth muscle degeneration and fibrosis, with eosinophilic inclusion bodies (M-bodies) which appear to be unique to this condition. The findings suggest the presence of a gastromyopathy.
Conclusions Satisfactory relief of intractable vomiting from diabetic gastroparesis was achieved by a novel radical surgical procedure. Histopathological findings suggest that gastromyopathy may contribute to the production of this syndrome.