One discussion this week involved the effects of octreotide.
Reference: Octreotide: a drug often used in the critical care setting but not well understood. Chest. 2013 Dec;144(6):1937-1945. doi:10.1378/chest.13-0382.
Summary: While a majority of octreotide is metabolized by the liver, 30-35% of octreotide acetate is excreted in the urine. Thus, octreotide accumulates in patients with moderate to severe renal or hepatic insufficiency.
Compared with SST-14, it exhibits 45-fold more potent inhibition of growth hormone, 11-fold more of glucagon, and 1.3-fold more insulin secretion.
Octreotide inhibits insulin secretion in the following ways (p.1943):
- Binds to SSTR-5 present on pancreatic B islet cells, inhibiting the formation of cAMP and reducing influx of calcium into the cytoplasm, thus preventing insulin secretion.
- Inhibition of direct phosphorylation of specific proteins required for secretion of insulin-containing vesicles.
Additional reading: Adabala M, et al. Severe hyperkalaemia resulting from octreotide use in a haemodioalysis patient. Nephrology, Dialysis, Transplantation. 2010 Oct;25(10):3439-3442. doi:10.1093/ndt/gfq381.