Octreotide is a synthetic analogue of somatostatin. An understanding of the biologic and pharmacologic principles surrounding this agent is important, as it has recently seen increasing use for a diversity of indications in hospitalized patients. Following are a few points of interest from the review.
Somatostatin (SST) is a hypothalamic hormone best known for its inhibition of growth hormone secretion. However, it has other actions less well appreciated. For example, from the review:
SST is synthesized not only in the hypothalamus but also by δ cells of the pancreatic islets, the myenteric neural plexi, and the epithelial lining of the stomach and intestines. Based on the sites where it is found, it is not surprising that SST can influence numerous endocrine and exocrine functions of the GI tract and pancreas, including inhibition of the secretion of insulin, glucagon, cholecystokinin, gastrin, secretin, serotonin, vasoactive intestinal peptide, motilin, and pancreatic polypeptide.3,4 Thus, SST and its synthetic analogs are able to inhibit gastric acid production, gastric emptying, and GI motility, pancreatic exocrine and endocrine secretion, nutrient absorption (eg, glucose, fats, amino acids), and biliary flow and contractility. These functional effects of SST provide the rationale for the use of SST analogs in various GI and non-GI endocrine disorders such as carcinoid syndrome, islet cell tumors, β-islet cell hyperplasia (nesidioblastosis), and acromegaly.4,5 In addition, SST and octreotide can induce vasoconstriction of the splanchnic vessels, thereby reducing blood flow in the splanchnic and portal venous systems.3,4
Clinical uses in hospitalized patients:
Octreotide induces splanchnic vasoconstriction which reduces splanchnic flow thereby reducing portal venous pressure.
The splanchnic vasodilation characteristic of cirrhosis reduces effective blood volume in turn activating a neurohumoral response. These factors are adverse to renal perfusion. By inducing splanchnic vasoconstriction octreotide may help reverse these effects. However, it is not effective as monotherapy and for treatment of HRS is combined with another vasoconstrictor, typically midodrine. The level of supporting evidence is low.
Hypoglycemia from sulfonylureas
The hypoglycemia associated with sulfonylurea therapy can be profound and prolonged. Glucose therapy is necessary as part of the treatment but when used alone may associated with rebound hypoglycemia since sulfonylurea agents are insulin secretagogues and a glucose load stimulates insulin release. Octreotide is a useful adjunct and is now favored over glucagon for sulfonylurea induced hypoglycemia.
Chylous pleural effusion
Octreotide reduces intestinal chyle production thus improving the chances for resolution.