Hypoglycemia After Gastric Bypass Surgery
Hyperinsulinemic Hypoglycemia after Roux-en-Y gastric bypass may be due to the following mechanisms:
- late dumping syndrome
- beta cell hyperfunction (insulinoma)
- lack of regression of beta cell mass after weight loss
- underlying familial hypoglycemia syndrome
- GLP-1 mediated beta cell proliferation
Hypoglycemia after weight loss surgery is often referred to as nesidioblastosis. Â This may be a misnomer as it refers to normal beta cell growth during neonatal development and was synomymously used to describe familial hyperinsulinemic hypoglycemia in infants. Â After falling out of favor as a term, it re-emerged to describe the entity of post-gastric bypass hypoglycemia with assumed or confirmed beta cell proliferation.
Incidence
Up to 0.2% of patients after gastric bypass surgery may present with neuroglycopenic symptoms requiring hospitalization, compared to 0.04% of the general population. The risk is not increased after adjustable gastric banding or vertical banded gastroplasty (Marsk et al. Diabetologia. 2010).
GLP-1
Along with gastric inhibitory peptide (GIP), the incretins mediate glucose homeostasis by stimulating insulin secretion and inhibiting glucagon release. Â The incretin glucagon-like peptide 1 (GLP-1) has been associated with beta cell hyperproliferation and islet cell neogenesis.
Diagnosis
Patients presenting with hypoglyemia may have tremors, nervousness, weakness, nausea, altered mental status, cold sweats, or other symptoms. Â When there is suspicion for hypoglycemia, serum fasting and post-prandial insulin, C-peptide, and glucose levels should be obtained. Â Assays for sulfonylureas should also be obtained to rule out iatrogenic hypoglycemia, along with an elevated C-peptide level, especially in patients with previous or current diabetes mellitus. Â Capillary blood glucose monitoring can be obtained to associate low blood glucose (< 40 mg/dL) with symptoms. Â Imaging of the pancreas with computed tomography, MRI, or endoscopic transgastric ultrasound may be used to rule out pancreatic insulinomas. Â Pancreatic histopathology can confirm changes consistent with islet cell neoplasia and beta cell hyperproliferation, with staining for insulin, glucagon, and somatostatin. Â Where suspician is high, transhepatic measurements of insulin in the hepatic vein after injection of calcium intra-arterially in the superior mesenteric artery, gastroduodenal artery, and splenic artery can help localize the areas of the pancreas with increased insulin secretory activity.
Treatment
Small, frequent (4-6 per day), low carbohydrate, and high protein meals may help to avoid symptoms. Â Patients should carry snacks with them.
Pharmacologic treatment may include
- diaxozide
- nifedipine
- octreotide
- glucocorticoids
- glucagon
In refractory patients, reversal of gastric bypass or subtotal or near total pancreatectomy can be considered.