Post-GB Hyperinsulinism with Nesidioblastosis

Abstract & Commentary

By Richard Peterson, MD, MPH, Clinical Instructor of Surgery, Department of Surgery, USC. Dr. Peterson reports no financial relationships relevant to this field of study.

Synopsis: The risk of recurrent symptomatic hyperinsulinism after limited pancreatectomy is significant, and relative euglycemia may be achieved with subtotal or total pancreatectomy.

Source: Clancy TE, et al. Post-gastric bypass hyperinsulinism with nesidioblastosis: Subtotal or total pancreatectomy may be needed to prevent recurrent hypoglycemia. Gastrointest Surg. 2006;10:1116-1119.

Symptomatic hyperinsulinemic hypoglycemia and pancreatic nesidioblastosis have recently been described in a small series of patients after gastric bypass surgery for morbid obesity. In the limited published reports of patients with this condition, hyperinsulinism and nesidioblastosis have been managed by distal or subtotal pancreatectomy.

Clancy and colleagues present a very interesting paper, which includes 2 cases from their institution, showing their approach to management. Nesidioblastosis is a rare disorder in and of itself, being far less common than insulinoma (which itself is rare) as a cause for hyperinsulinemic hypoglycemia. However, now there are 11 patients reported in the literature (2 from this series). To this point, there has not been an established causal link between nesidioblastosis and gastric bypass, although the incidence appears more common than in the general population. This brings forward a concern, as the popularity of gastric bypass surgery for morbid obesity continues to rise.

The proposed mechanism is that rapid delivery of food to the distal ileum after bypass surgery may result in elevated systemic levels of glucagons-like peptide 1 [GLP-1], or another intestinal hormone, leading to hyperplasia of the pancreatic islet cells. Clancy et al, in their review, discovered that other reports have recently found hyperinsulinemic hypoglycemia after gastric banding, and have suggested that weight loss reduces insulin resistance in the setting of islet hypertrophy and hyperfunction, which is often seen in obesity. A third suggestion of the mechanism is that hyperinsulinism may be masked in some obese patients. The theory that the anabolic nature of insulin, coupled with the relief of hypoglycemic symptoms from eating, might lead to obesity in a population of patients with primary hyperinsulinism who are subsequently rendered hypoglycemic because the protective mechanism of a high-carbohydrate diet is removed. It is only with the increase in obesity surgery that these patients are now being "noticed."


Clancy et al also discuss the fact that the role of surgery in the treatment of nesidioblastosis in the post-gastric bypass patient is not well defined. Clancy et al were required to perform pancreatectomies for 80-95% of their patients in order to resolve their symptoms. Clancy et al also recognize that one management strategy may not be appropriate for all cases, but it is the recognition of this problem within a growing pool of postoperative patients that needs to be realized.