Hypoglycemia after gastric bypass: an old problem resurfaces.

et al. Severe hypoglycaemia post-gastric bypass requiring partial pancreatectomy: evidence for inappropriate insulin secretion and pancreatic islet hyperplasia. Effects of ingestion of hyper-osmotic glucose solution on the splanchnic circulation in normal subjects and in partially gastrectomized patients reacting with circulatory collapse. glucose to lerance, insulin response, and insulin sensitivity after massive weight reduction subsequent to gastric bypass. Patients with neuroglycopenia after gastric bypass surgery have exaggerated incretin and insulin secretory responses to a mixed meal. Abbasi F, et al. Plasma glucose and insulin regulation is abnormal following gastric bypass surgery with or without neuroglycopenia. hypoglycemia after Roux-en-Y gastric bypass: unraveling the role of gut hormonal and pancreatic endocrine dysfunction. A clinical diagnostic index in the diagnosis of the dumping syndrome. Changes in plasma volume and blood sugar after a test meal. Rate of fall in blood glucose and recurrent hypoglycemia affect glucose dynamics and noradrener-gic activation in the ventromedial hypothalamus. Hypoglycemia after gastric bypass: an old problem resurfaces Roux-en-Y gastric bypass (RYGB) has established itself as the standard for the surgical treatment of morbid obesity and its complications. The overwhelming success of RYGB in adult and pediatric patients has been accompanied by much interest in the mechanism(s) by which this and other bariatric procedures reverse the abnormal glucose metabolism seen in about half of the patients. The early resolution of type 2 diabetes mellitus after RYGB has been shown to be independent of the loss of body fat, and likely involves alterations of one or more systems, which include incretin secretion [1], bile acid absorption [2], or gut microflora [3] to name just a few. As gratifying as the resolution of type 2 diabetes mellitus after RYGB is, it remains to be seen whether this effect is permanent or merely temporary despite sustained weight loss, or whether the system(s) responsible for the reversal of abnormal glucose metabolism ever reverts to a normal or baseline condition. Evidence that it may not is deduced from the observation that an unknown number of both diabetic and nondiabetic patients who have undergone RYGB subsequently develop hypoglycemia and neuroglycopenia months to years after their surgery [4]. Some of these patients, the number of which is also unknown, develop such profound neuroglycopenia that they sustain life-threatening injuries or are disabled by their postbypass condition. The syndrome of postbypass hyperinsulinemic hypoglyce-mia is now well recognized, but the details of its prevalence and even of its definition remain …