Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2009) 19 P159

SFEBES2009 Poster Presentations Diabetes, Metabolism and Cardiovascular (49 abstracts)

Metformin attenuates hypoglycaemia secondary to dumping syndrome

S Gonzalez 1 , N Mizban 2 , R King 2 & C Rajeswaran 1


1Pinderfield Hospital Mid Yorkshire NHS Trust, Wakefield, UK; 2Dewsbury District Hospital, Mid Yorkshire NHS Trust, Dewsbury, UK.


Dumping syndrome is a common complication following gastric bypass surgery. Rapid gastric emptying in dumping syndrome triggers an inappropriate hyperinsulinaemic response which leads to hypoglycaemia. This can be very disabling and challenging to manage in clinical practice. Here we present a lady with dumping syndrome whose post meal hypoglycaemia improved with metformin.

A 42-year-old female presented with eight months history of increasing mood swings, short term memory loss and craving for sugary food. She underwent a Roux-en-Y gastric bypass surgery for morbid obesity 7 years previously which was followed by sustained weight loss. Only past medical illness was vitamin B12 deficiency and she was adequately replaced. Alcohol comsuption was minimal. BMI was 29 kg/m2. Physical examination was unremarkable in particular there was no postural drop in blood pressure. Post prandial capillary blood glucose (CBG) were usually between 1.6 and 2.4 mmol/l. Glucose tolerance test revealed a fasting glucose of 4.6 mmol/l and a 2 h sample of 2.2 mmol/l. All investigations for recurrent hypoglycaemia were normal except for an elevated C-Peptide-2166, Insulin-155 during a hypoglycaemic episode. CT abdomen was reported normal. Therefore, late dumping syndrome was diagnosed. Dietary modification, low glycaemic index food, restriction of fluid intake following a meal and avoidance of physical activity immediately after oral intake was recommended. Octreotide was introduced when she was unable to tolerate acarbose. However, her symptoms remained refractory to these interventions. A trial of metformin was initiated which dramatically improved her symptoms and stabilised her CBG levels post meal.

Metformin acts primarily by decreasing hepatic glucose output largely by inhibiting gluconeogenesis and thereby reducing glycaemic excursions and hyperinsulinaemia. Other effects include inhibition of intestinal active transport systems, delayed gastric emptying and decreased intestinal motility and gastric acid secretion, however exact mechanism by which metformin improves hypoglycaemia following gastric bypass surgery remains unclear.

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