Octreotide is a synthetic analog of the hormone somatostatin which exerts its effects through binding to somatostatin receptors subtype 2 and, to a lesser extent, 3 and 5. In carcinoid tumours, long-term administration of octreotide can control clinical symptoms due to hypersecretion of hormones. In addition, it may have some anti-proliferative effects. Patients who benefit from octreotide include those with functioning NETs of the gut or pancreas. Octreotide is guideline recommended to control symptoms associated with carcinoid tumours and neuroendocrine tumors. The guidelines says: “.
Because the mechanism of action and the pathophysiology of other secretory neuroendocrine tumours are similar to that of carcinoid tumours, it is reasonable to recommend octreotide to control symptoms associated with secretory neuroendocrine tumours. ” The recommended dose is in a subcutaneous dose of 100 micrograms three times daily, or 200 micrograms twice daily, with an increase in the dose of 50 to 100 micrograms every eight or twelve hours until symptom control is achieved. Although initially it had to be dosed more frequenlty, monthly formulations are now available. Sandostatin LAR is one such formulation. Sandostatin LAR Depot 10 mg, 20 mg and 30 mg is indicated in patients in whom initial treatment with Sandostatin Injection has been shown to be effective and tolerated.
Generally, patients are started on the short acting drug and switched to the long acting version (some people empirically use Long Acting (LAR) formulation right away). Patients currently receiving Sandostatin Injection can be switched to Sandostatin LAR Depot in a dosage of 20 mg given IM intragluteally at 4-week intervals for 2 months. Because of the need for serum octreotide to reach therapeutically effective levels following initial injection of Sandostatin LAR Depot, carcinoid tumor and VIPoma patients should continue to receive Sandostatin Injection subcutaneously for at least 2 weeks in the same dosage they were taking before the switch. Failure to continue subcutaneous injections for this period may result in exacerbation of symptoms. (Some patients may require 3 or 4 weeks of such therapy.)
After 2 months, dosage may be adjusted as follows:
•If symptoms are adequately controlled, consider a dose reduction to 10 mg for a trial period. If symptoms recur, dosage should then be increased to 20 mg every 4 weeks. Many patients can, however, be satisfactorily maintained at a 10-mg dosage every 4 weeks.
•If symptoms are not adequately controlled, increase Sandostatin LAR Depot to 30 mg every 4 weeks if symptoms are not adequately controlled. Patients who achieve good control on a 20-mg dose may have their dose lowered to 10 mg for a trial period. If symptoms recur, dosage should then be increased to 20 mg every 4 weeks.
•Dosages higher than 30 mg are not recommended.
On the other hand, Uptodate cites newer evidence to octreotide actually retarding tumor growth and recommends it use even in asymptomatic patient with high volume, unresectable disease. The same would apply to the very similar drug Lanreotide. Lanreotide also shows activity against non-endocrine tumors, including in a 2014 phase III trial, and, along with other somatostatin analogues, is being studied as a possible general antitumor agent.
Sandostatin LAR, Prescribing Information, 2014
Holger Petersen, Jean-Claude Bizec, Helmut Schuetz and Marie-Laure Delporte Pharmacokinetic and technical comparison of Sandostatin® LAR® and other formulations of long-acting octreotide, BMC Research Notes 2011, 4:344
Systemic Treatment Disease Site Group. Major P, Figueredo A, Tandan V, Bramwell V, Charette M, Oliver T. The role of octreotide in the management of patients with cancer [full report]. Toronto (ON): Cancer Care Ontario (CCO); 2004 Aug [online update]. 30 p. (Practice guideline report; no. 12-7). [57 references]
Ruszniewski P, Ducreux M, Chayvialle JA, Blumberg J, Cloarec D et al. Treatment of the carcinoid syndrome with the long-acting somatostatin analogue lanreotide: a prospective study in 39 patients. Gut 1996; 39: 279-283.
Kvols L, Woltering E (2006). “Role of somatostatin analogs in the clinical management of non-neuroendocrine solid tumors”. Anticancer Drugs 17 (6): 601–8.
Susini C, Buscail L (2006). “Rationale for the use of somatostatin analogs as antitumor agents”. Ann Oncol 17 (12): 1733–42.
K. Öberg et al, Consensus report on the use of somatostatin analogs for the management of neuroendocrine tumors of the gastroenteropancreatic system Ann Oncol (2004) 15 (6): 966-973.
Uptodate, Neuroendocrine, 2014
NCCN, Neuroendocrine , 2014
Kvols L, Woltering E (2006). “Role of somatostatin analogs in the clinical management of non-neuroendocrine solid tumors”. Anticancer Drugs. 17 (6): 6018. PMID 16917205. doi:10.1097/01.cad.0000210335.95828.ed.
Jump up ^ Susini C, Buscail L (2006). “Rationale for the use of somatostatin analogs as antitumor agents”. Ann Oncol. 17 (12): 173342.
Martín-Richard M, Massutí B, Pineda E, et al. Antiproliferative effects of lanreotide autogel in patients with progressive, well-differentiated neuroendocrine tumours: a Spanish, multicentre, open-label, single arm phase II study. BMC Cancer. 2013;13:427.