Octreotide treatment for sulfonylurea-induced hypoglycaemia

To the Editor: Prolonged hypoglycaemia in patients taking a sulfonylurea may be refractory to intravenous glucose treatment with fatal consequences, as described by Veitch and Clifton-Bligh.1 Although these authors briefly mention the use of octreotide, we believe that an additional point in the “Lessons from practice” should have been: Octreotide may be an effective therapy in refractory sulfonylurea-induced hypoglycaemia.

We describe the first two patients in whom we used this therapy.

A 76-year-old man with type 2 diabetes was admitted after an acute myocardial infarction and cardiac arrest. He was successfully resuscitated and underwent emergency bypass surgery. His diabetes was controlled with gliclazide 80 mg twice a day. After surgery, he developed cardiac failure, renal impairment (serum creatinine level, 0.22 mmol/L) and frequent hypoglycaemic episodes. The gliclazide was stopped but, despite good oral dietary intake, hypoglycaemia worsened and failed to respond to vigorous intravenous glucose therapy. He suffered a hypoglycaemic seizure (blood sugar level, 0.8 mmol/L). Over the next day, he received more than 300 g of glucose in the form of a 10% glucose intravenous infusion, but, despite this, went into hypoglycaemic coma. Blood results were: insulin, 472 pmol/L (reference range [RR], 15–60 pmol/L); C-peptide, 7616 pmol/L (RR, 300–800 pmol/L); and gliclazide, 9.4 mg/L (steady state average, 2.5 mg/L). He was given an intravenous infusion (30 ng/kg per minute) of octreotide.2 Within an hour, his blood sugar level rose to 7.9 mmol/L and continued to rise. Dextrose and octreotide infusions were ceased within 13 hours, with no further episodes of hypoglycaemia. He was discharged home 2 days later.

A 75-year-old man with type 2 diabetes was taking glibenclamide 2.5 mg each morning. He was transferred from a rural hospital with acute on chronic renal failure (serum creatinine level, 0.4 mmol/L), as well as recurrent hypoglycaemia. The glibenclamide was stopped, but blood sugar levels remained low, and he became comatose despite boluses of 50% dextrose and a continuous infusion of 10% dextrose. The high volume of intravenous fluid precipitated cardiac failure and pulmonary oedema, requiring inotropic support. Blood results were: blood sugar, 1.5 mmol/L; insulin, 1250 pmol/L; C-peptide, 20 949 pmol/L. As an alternative to the high-dose, continuous infusion of octreotide used in our first patient, we administered a single subcutaneous injection of octreotide 50 μg. One hour later, the patient’s blood sugar level had risen to 9.0 mmol/L. He had no further episodes of hypoglycaemia. Eight hours later, insulin and C-peptide levels had fallen markedly (insulin, 153 pmol/L; C-peptide, 5654 pmol/L). He made a full recovery.

Octreotide is a somatostatin analogue that inhibits the secretion of a number of neuropeptides, including insulin. It is a safe and effective therapy for sulfonylurea-induced hypoglycaemia when initial therapy with oral or intravenous glucose fails.2-5 It is particularly useful in elderly patients with renal or cardiac complications, in whom fluid overload may be a limiting factor in intravenous dextrose therapy. Octreotide may also break the vicious circle that can occur in sulfonylurea-induced hypoglycaemia in which repeated dextrose boluses further stimulate insulin release.