Postprandial hypoglycemia after upper gastrointestinal tract surgery: diagnosis and treatment (part 2)

Abstract

The causes of postprandial hyperinsulinemic hypoglycemia (PHH) in patients who have undergone an upper gastrointestinal tract surgery are still a matter of debate in the scientific community. Low postoperative body mass index, high postprandial beta-cell activity before the surgery, and younger age are all have been associated with higher PHH risk. It is hypothesized that the insulin-like growth factor-1 increases the tissue sensitivity to insulin and indirectly promotes the development of hypoglycemia. An increase in postprandial secretion of enteropancreatic hormones is still considered to be the main reason for PHH manifestation; however, a particular contribution has been ascribed to glycentin, which could be used as a marker of PHH risk in the future.At present, there are no clinical guidelines for the diagnosis of PHH. Undoubtedly, the first step in this direction should be the collection of the disease history. The provocative tests have been proposed for the detection of PHH. Today, the 72-hour fast test is still the gold standard in the diagnosis of hypoglycemia. However, most post-bariatric patients do not have fasting hypoglycemia, and insulinoma is extremely rare in this patient category. The use of a prolonged oral glucose tolerance test as the main method is associated with a risk of a false diagnosis, because about 12% of healthy individuals may have their glycemic levels at below 2.8 mmol/l. The mixed meal test has not been validated yet. The best results in the assessment of glucose variability have been obtained with “real time” continuous glucose monitoring the interstitial fluid for several days.The goal of PHH treatment is to reduce the stimulated insulin secretion. First of all, patients are advised to eat small meals consisting of carbohydrates with a low glycemic index in combination with proteins and lipids, with high fiber content. Should the nutritional modification be ineffective, it is possible to prescribe medical treatment, such as acarbose or somatostatin analogs. Diazoxide and slow calcium channel blockers can be used as the third line of therapy. A recent study has suggested that exogenous agonists of glucagon-like peptide-1 (GLP-1) receptors by stronger bonds with receptors, compared to those with endogenous GLP-1, could enhance glucagon response to hypoglycemia, thereby stabilizing glucose levels. In severe refractory PHH, reconstructive surgery and gastric banding are to be considered. If the expected decrease in insulin hypersecretion by reconstructive surgery is not achieved, partial or complete pancreatectomy remains the only possible approach to prevent hypoglycemia. However, due to the small number and short duration of the studies, effectiveness and safety of these techniques for PHH treatment have not yet been proven.