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Gastric bypass determines an increase in incretin secretion and glucose excursions throughout the day and may sometimes entail the development of severe post-bariatric hypoglycemia (PBH). However, there is no consensus on the gold standard method for its diagnosis. In this study, we evaluated the usefulness of a mixed meal tolerance test (MMTT) and continuous glucose monitoring (CGM) for the diagnosis of PBH, defined as glucose levels <54 mg/dL (3.0 mmol/L). We found that hypoglycemia occurred in 60% of patients after the MMTT and in 75% during CGM, and it was predominantly asymptomatic. The MMTT confirmed the diagnosis of PBH in 88.9%of patients in whom surgery had been performed more than three years ago, in comparison to 36.4% in cases with a shorter postsurgical duration. CGM diagnosed nocturnal asymptomatic hypoglycemia in 70% of patients, and daytime postprandial hypoglycemia in 25% of cases. The mean duration of asymptomatic hypoglycemia was more than 30 min a day. Patients with ≥2% of their CGM readings with hypoglycemia exhibited a higher degree of glucose variability than those with <1% of the time in hypoglycemia. Our results show that the MMTT may be a useful dynamic test to confirm the occurrence of hypoglycemia in a large number of patients with persistent and recurrent PBH during long-term follow-up after gastric bypass. CGM, on its part, helps identify hypoglycemia in the real-world setting, especially nocturnal asymptomatic hypoglycemia, bringing to light that PBH is not always postprandial. [ABSTRACT FROM AUTHOR]

Postprandial reactive hypoglycemia, or late dumping syndrome, is a common but underrecognized complication from bypass surgery. We report an unusual case of postprandial reactive hypoglycemia in a patient with a severe esophageal stricture from corrosive agent ingestion who underwent ileocolic interposition and an antecolic Billroth‐II gastrojejunostomy. A 22‐year‐old male patient with a one‐year history of corrosive ingestion was referred to the hospital for a surgical correction of severe esophageal stricture. After the patient underwent ileocolic interposition and an antecolic Billroth‐II gastrojejunostomy, he experienced multiple episodes of gastroesophageal refluxsymptoms during nasogastric feeding and had onset of hypoglycemic symptoms. His plasma glucose level was 59 mg/dL. After we had intraoperatively re‐inserted a jejunostomy tube bypassing the ileocolic interposition, and reintroduced enteral nutrition, his hypoglycemic symptoms resolved. We performed a mixed meal tolerance test by nasogastric tube, but the results did not show postprandial hypoglycemia. Although the specific mechanism is unclear, this case suggests gastroesophageal reflux to the ileal interposition may have caused a state of exaggerated hyperinsulinemic response and rebound hypoglycemia. To the best of our knowledge, we are the first to report case of postprandial hypoglycemia after ileocolic interposition, which may have been caused by exaggerated hyperinsulinemic response due to gastroesophageal reflux to the ileal interposition. This syndrome should be considered in the patient who has had ileocolic interposition surgery and has developed postprandial hypoglycemia. [ABSTRACT FROM AUTHOR]