Octreotide Therapy for Nateglinide-Induced Hypoglycemia
Article Outline
To the Editor:
A 73-year-old female with a history of hypertension, Type 2 diabetes mellitus, and chronic anuric renal failure was transported to the emergency department (ED) by emergency medical services for complaints of low blood sugar. Her last hemodialysis was noted to be 1 day prior to presentation. An accucheck revealed a blood glucose of 20 mg/dL at which time she was administered one 50 mL ampule of 50% dextrose (D50) and observed for several hours prior to being discharged home in good condition. Instructions were to continue her current medications which included aspirin, minoxidil, and nateglinide (Starlix®).
The following morning, she took her normal dose of nateglinide. Within 2 hours, she experienced dizziness, diaphoresis, and nausea prior to calling emergency medical services for transport back to the ED. Her blood glucose was noted to be 25 mg/dL en route at which time she was subsequently treated with one ampule of D50. While in the ED, her glucose was noted to be 123 mg/dL. However, 1 hour later her glucose had decreased to 60 mg/dL. At this point, another ampule of D50 was administered in addition to octreotide 100 mcg subcutaneously per the regional poison center’s recommendations. The patient was admitted to the hospital and had no further hypoglycemic episodes or dextrose requirements prior to discharge the following day.
Nateglinide is a relatively newer hypoglycemic agent prescribed for the treatment of Type 2 diabetes mellitus. While nateglinide is chemically and pharmacologically distinct from sulfonylureas, its mechanism of action is quite similar. By binding to and inhibiting the potassium-adenosine triphosphate channel, depolarization of the pancreatic beta cell occurs resulting in the opening of voltage-gated calcium channels. This ultimately results in a cascade of phophorylation reactions leading to insulin release. Unlike sulfonylureas, however, which bind much more avidly, nateglinide binding is more rapidly reversed which results in quicker and shorter-lived hypoglycemic effects all the while lowering the risk of hypoglycemic events.1, 2
Overdose of nateglinide has been reported once in the medical literature.3 The patient had hypoglycemic effects early (1 hour post ingestion) after poisoning and required 4 boluses of dextrose in addition to a 10% glucose drip infusion in order to treat the relatively short-lived 6 hour course of hypoglycemia.3 Because of poor insulin clearance and an active metabolite of nateglinide, patients with chronic renal failure who take nateglinide therapeutically are at risk of hypoglycemia.4
Our patient had several hypoglycemic events that were treated with dextrose and octreotide. Octreotide has been reported to be useful in hypoglycemia secondary to sulfonylurea overdose by binding to its own receptor on the pancreatic beta cell and inhibiting calcium entry into the cell and subsequent insulin release. It is safe, inexpensive, and decreases the number and severity of hypoglycemic events associated with sulfonylurea-induced hypoglycemia.5 We are the first to report the utilization of octreotide therapy in nateglinide-induced hypoglycemia in chronic renal failure. Octreotide may also minimize the number and severity of hypoglycemic events associated with massive nateglinide overdose.
References
- Pancreatic beta-cell K-ATP channel activity and membrane-binding studies with nateglinide: a comparison with sulfonylureas and repaglinide. J Pharmacol Exp Ther. 2000;293:444–452
- Hypoglycemic potential of nateglinide versus glyburide in patients with Type 2 diabetes mellitus. Metabolism. 2004;53:1331–1335
- Hypoglycemia following a nateglinide overdose in a suicide attempt. Diabetes Care. 2005;28:227–228
- Hypoglycemia due to nateglinide administration in a diabetic patient with chronic renal failure. Diabetes Research and Clinical Practice. 2003;59:191–194
- . Octreotide: an antidote for sulfonylurea-induced hypoglycemia. Ann Emerg Med. 2000;36:133–138
PII: S0196-0644(07)01260-7
doi:10.1016/j.annemergmed.2007.06.490
© 2007 American College of Emergency Physicians. Published by Elsevier Inc. All rights reserved.
