Hiperinsulinemic hypoglycaemia is a rare complication in late postoperative bariatric surgery (0.2-0.36% after LRYGB). It may be triggered by an increase in incretin levels but its physopathology is still unknown. In some cases pancreatectomy is the only therapeutic option. In these cases the anatomopathological report showed a condition of hyperplasia and hyperfunction called Nesidioblastosis.
Another peptide that might be involved is GIP, which promotes islet augmentation and reduces apoptosis.
Classically hypoglycaemia after bariatric surgery presents with the Whipple’s tirad: confusion, low plasma glucose concentration and resolution of symptoms after glucose intake.
Time from surgery may be variable (1-3 years). The post-prandial timing of the symptoms varies from 1-3 hours.
Rapid gastric emptying of partially digested food after gastric surgeries triggers an alteration in intestinal hormones secretion developing dumping syndrome. These changes could also contribute to the development of postoperative hypoglycemia after gastric bypass.
Post-prandial hypoglycemia (≤ 2.2 mmol/L) demands a clinical evaluation with continuous glucose monitoring during 3 days while the patient is eating normally. Nesidioblastosis is suspected when C-petide is elevated (> 5ng/mL), insulin is > 6 μU/mL and Proinsulin is low (< 5 pmol/L).
Differential diagnosis with insulinoma is mandatory and imaging with CT scan or MRI is needed.
Pancreatic hyperfunction can be located with selective intraarterial calcium stimulus and suprahepatic venous collection angiographically.
Treatment includes carbohydrates restriction, acarbose, nifedipine, diazoxide and octreotide. Conservative treatment can have good results but severe cases of nesidioblastosis with elevated postprandial insulin may need surgery. The preferred technique is the conversion of RYGBP to sleeve gastrectomy.