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The endocrine pancreata of five overweight newborns (birthweight ranging from 3,800 g to 4,500 g) have been studied. Basal blood glucose and insulin levels were normal in these newborns. A marked and widespread B-cell nesidioblastosis was observed in relation to ten controls (birthweight ranging
The anatomical and physiological changes after Roux-en-Y gastric bypass for morbid obesity can lead to severe hyperinsulinemic hypoglycemia with neuroglycopenia in a small percentage of patients. The exact physiologic mechanism is not completely understood. Surgical reversal to the original anatomy
BACKGROUND
Hyperinsulinemic hypoglycemia after Roux-en-Y gastric bypass (RYGB) has been increasingly reported. It is induced by β-cell hyperplasia often referred to as nesidioblastosis. Positron emission tomography (PET) with [11C]-5-hydroxytryptophan ((11)C-HTP) and
Persistent hyperinsulinemic hypoglycemia in adults is usually caused by solitary benign insulinomas. Nesidioblastosis, a term that has been used to designate a functional disorder of the beta cells, is a rare cause of persistent hyperinsulinemic hypoglycemia in adults, but seems to have increased in
Persistent hyperinsulinemic hypoglycaemia is caused most commonly by an insulinoma in adults or by nesidioblastosis in neonates. In adults, localised islet cell hyperplasia is a rare disorder characterised by localised proliferation of islet cells. The authors present the case of a previously
BACKGROUND
Severe hypoglycemia after Roux-en-Y gastric bypass surgery (RYGB) is an increasingly recognized condition, characterized by neuroglycopenia and inappropriately elevated insulin concentrations that occur primarily in the postprandial state. Both pathophysiology and treatment of this
The New Zealand obese mouse (NZO/Hl) is characterised by hereditary obesity and type-2 diabetes, including insulin resistance, hyperinsulinaemia, and glucose intolerance. In other diabetic models, it has been revealed that the proper functioning of the glucose transporter isoform 2 (GLUT2) is
We describe six patients (five women and one man; median age, 47 years; range, 39 to 54) with postprandial symptoms of neuroglycopenia owing to endogenous hyperinsulinemic hypoglycemia after Roux-en-Y gastric bypass surgery. Except for equivocal evidence in one patient, there was no radiologic
BACKGROUND
Postprandial hyperinsulinemic hypoglycemia (PHH) is an increasingly recognized complication of gastric bypass surgery in obese adults, distinct from the "dumping syndrome".
METHODS
Upon birth, primary repair of esophageal atresia was performed, and at the age of 14 months definite
In summary, the present review provides evidence in support of the proposition that pancreatic islet cell hyperplasia precedes the development of insulin insensitivity in the obese mouse and, it is likely, that similar events occur in obese humans. Moreover, the hyperplastic pancreatic islet appears
Roux-en-Y gastric bypass (RYGBP) is the most commonly performed type of bariatric surgery, which is used in the treatment of obesity and type 2 diabetes. Recent case reports and case series have described a rare complication of RYGBP, status post-gastric-bypass hyperinsulinemic hypoglycemia, which
Roux-en-Y gastric bypass (RYGB) is an efficient treatment for morbid obesity and reduces obesity-related co-morbidities. With the growing number of patients undergoing gastric bypass, complications now demand further attention. Postprandial hyperinsulinemic hypoglycemia (PHH) after Roux-en-Y gastric
Here, we present the case of a 31-year-old woman patient who underwent distal pancreatectomy with the history of gastric bypass surgery for obesity. The final histopathological diagnosis of the lesion was nesidioblastosis. Nesidioblastosis is the most common cause of organic persistent