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| Names | |
|---|---|
| Trade names | Sandostatin, Bynfezia Pen, Mycapssa, others |
| |
| Clinical data | |
| Drug class | Somatostatin[1] |
| Main uses | Carcinoid syndrome,acromegaly,congenital hyperinsulinism,gastrointestinal bleeding due toesophageal varices[1] |
| Side effects | Nausea, slow heart rate, abdominal discomfort[1] |
| Pregnancy category | |
| Routes of use | Subcutaneous,intramuscular,intravenous,by mouth |
| External links | |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a693049 |
| Legal | |
| License data | |
| Legal status | |
| Pharmacokinetics | |
| Bioavailability | 60% (IM), 100% (SC) |
| Protein binding | 40–65% |
| Metabolism | Liver |
| Eliminationhalf-life | 1.7–1.9 hours |
| Excretion | Urine (32%) |
| Chemical and physical data | |
| Formula | C49H66N10O10S2 |
| Molar mass | 1019.25 g·mol−1 |
| 3D model (JSmol) | |
| |
| |
Octreotide, sold under the brand nameSandostatin among others, is a medication used to treatcarcinoid syndrome,acromegaly,congenital hyperinsulinism, andgastrointestinal bleeding due toesophageal varices.[1][2] It can be given by injection into a vein or muscle.[1] The immediate release form may be effective up to 12 hours.[1]
Common side effects include nausea, a slow heart rate, and abdominal discomfort.[1] Other side effects may include low or high blood sugar,gall bladder problems, andanaphylaxis.[1] It is unclear if use during pregnancy is safe.[3] Use is not recommended when breastfeeding.[4] It mimics the effects of naturalsomatostatin and inhibits the release ofgrowth hormone,serotonin,insulin, andglucagon.[1]
Octreotide was first made in 1979, by the chemist Wilfried Bauer.[5] It is on theWorld Health Organization's List of Essential Medicines.[6] It was approved for medical use in the United States in 1988.[7] It is available as ageneric medication.[4] In the United Kingdom it costs about 3 pounds per 50 ug dose as of 2020.[4] In the United States this amount costs about 5.30 USD as of 2020.[8]
Octreotide is used for the treatment ofgrowth hormone producing tumors (acromegaly andgigantism), when surgery is contraindicated, pituitary tumors that secretethyroid-stimulating hormone (thyrotropinoma),[citation needed]diarrhea andflushing episodes associated withcarcinoid syndrome, and diarrhea in people withvasoactive intestinal peptide-secreting tumors (VIPomas). Octreotide is also used in mild cases ofglucagonoma when surgery is not an option.[9][10]
Octreotide is often given as an infusion for management of acutehemorrhage fromesophageal varices in livercirrhosis on the basis that it reducesportal venous pressure, though current evidence suggests that this effect is transient and does not improve survival.[11]
The recommended dose for this purpose is often a 50 ug bolus followed by 50 ug per hour for five days.[2]
Octreotide is used innuclear medicine imaging by labeling withindium-111 (Octreoscan) to noninvasively image neuroendocrine and other tumours expressing somatostatin receptors.[12] More recently,[when?] it has been radiolabeled withcarbon-11[13] as well asgallium-68, enabling imaging withpositron emission tomography (PET), which provides higher resolution and sensitivity.
Octreotide can also be labeled with a variety of radionuclides, such asyttrium-90 orlutetium-177, to enablepeptide receptor radionuclide therapy (PRRT) for the treatment of unresectable neuroendocrine tumours.
Octreotide can also be used in the treatment ofacromegaly, a disorder of excessive growth hormone (GH). Octreotide, being a somatostatin analog, inhibits the release of GH from the pituitary gland through a process normally involved in negative feedback.
In June 2020, Mycapssa (octreotide) was approved for medical use in the United States with an indication for the long-term maintenance treatment in acromegaly patients who have responded to and tolerated treatment with octreotide orlanreotide.[14][15] Mycapssa is the first and only oral somatostatin analog (SSA) approved by the FDA.[15]
Octreotide helps in management of the fistula by reducing gastrointestinal secretions and inhibiting gastrointestinal motility, thus controlling and reducing its output.[citation needed] The value in healing intestinal fistulas is yet to be proven and routine use is limited because of the side effects.
Octreotide is also used in the treatment of refractory hypoglycemia in neonates andsulphonylurea-induced hypoglycemia in adults.
The dose of octreotide in those withvarices andupper gastrointestinal bleeding is an intravenous bolus of 20 mcg to 50 mcg, followed by a continuous infusion at a rate of 25 mcg to 50 mcg per hour.[16]
Octreotide has not been adequately studied for the treatment of children as well as pregnant and lactating women. The drug is given to these groups only if arisk-benefit analysis is positive.[17][18]
The most common side effects are headache,hypothyroidism,cardiac conduction changes,gastrointestinal reactions (including cramps, nausea/vomiting and diarrhoea or constipation),gallstones, reduction ofinsulin release,hyperglycemia[19] or sometimeshypoglycemia, and (usually transient) injection site reactions.Slow heart rate, skin reactions such aspruritus,hyperbilirubinemia,hypothyroidism,dizziness anddyspnoea are also fairly common (more than 1%). Rare side effects include acuteanaphylactic reactions,pancreatitis andhepatitis.[17][18]
Some studies reportedalopecia in those who were treated by octreotide.[20] Rats which were treated by octreotide experiencederectile dysfunction in a 1998 study.[21]
A prolongedQT interval has been observed, but it is uncertain whether this is a reaction to the drug or the result of an existing illness.[17]
Octreotide is useful in overdose management of sulfonylurea type hypoglycemic medications, when recurrent or refractory to parenteral dextrose. Mechanism of action is the suppression of insulin secretion.[medical citation needed]
Octreotide can reduce the intestinal reabsorption ofciclosporin, possibly making it necessary to increase the dose.[22] People withdiabetes mellitus might need lessinsulin ororal antidiabetics when treated with octreotide, as it inhibits glucagon secretion more strongly and for a longer time span than insulin secretion.[17] Thebioavailability ofbromocriptine is increased;[18] besides being anantiparkinsonian, bromocriptine is also used for the treatment of acromegaly.
| Identifiers | |
|---|---|
| Symbol | N/A |
| OPM superfamily | 158 |
| OPM protein | 1soc |
Since octreotide resembles somatostatin in physiological activities, it can:
It has also been shown to produceanalgesic effects, most probably acting as apartial agonist at themu opioid receptor.[23][24]
Octreotide is absorbed quickly and completely aftersubcutaneous application. Maximal plasma concentration is reached after 30 minutes. Theelimination half-life is 100 minutes (1.7 hours) on average when applied subcutaneously; afterintravenous injection, the substance is eliminated in two phases with half-lives of 10 and 90 minutes, respectively.[17][18]
Octreotide acetate was approved for use in the United States in 1988.[25][26]
In January 2020, approval of octreotide acetate in the United States was granted to Sun Pharmaceutical under the brand name Bynfezia Pen for the treatment of:[26][27]
Octreotide has also been usedoff-label for the treatment of severe, refractory diarrhea from other causes. It is used in toxicology for the treatment of prolonged recurrent hypoglycemia aftersulfonylurea and possiblymeglitinide overdose. It has also been used with varying degrees of success in infants withnesidioblastosis to help decrease insulin hypersecretion. Several clinical trials have demonstrated the effect of octreotide as acute treatment (abortive agent) incluster headache, where it has been shown that administration of subcutaneous octreotide is effective when compared with placebo.[28]
Octreotide has also been investigated in people with pain fromchronic pancreatitis.[29]
It has been used in the treatment of malignant bowel obstruction.[30]
Octreotide may be used in conjunction withmidodrine to partially reverse peripheral vasodilation in thehepatorenal syndrome. By increasing systemic vascular resistance, these drugs reduce shunting and improve renal perfusion, prolonging survival until definitive treatment with liver transplant.[31] Similarly, octreotide can be used to treat refractorychronic hypotension.[32]
While successful treatment has been demonstrated in case reports,[33][34] larger studies have failed to demonstrate efficacy in treatingchylothorax.[35]
A small study has shown[when?] that octreotide may be effective in the treatment ofidiopathic intracranial hypertension.[36][37]
Octreotide has been used experimentally to treatobesity, particularly obesity caused by lesions in the hunger and satiety centers of thehypothalamus, a region of the brain central to the regulation of food intake and energy expenditure.[38] The circuit begins with an area of the hypothalamus, thearcuate nucleus, that has outputs to thelateral hypothalamus (LH) andventromedial hypothalamus (VMH), the brain's feeding and satiety centers, respectively.[39][40] The VMH is sometimes injured by ongoing treatment foracute lymphoblastic leukemia (ALL) or surgery or radiation to treatposterior cranial fossa tumors.[38] With the VMH disabled and no longer responding to peripheral energy balance signals, "Efferent sympathetic activity drops, resulting in malaise and reduced energy expenditure, andvagal activity increases, resulting in increasedinsulin secretion andadipogenesis."[41] "VMH dysfunction promotes excessive caloric intake and decreased caloric expenditure, leading to continuous and unrelenting weight gain. Attempts at caloric restriction or pharmacotherapy with adrenergic or serotonergic agents have previously met with little or only brief success in treating this syndrome."[38] In this context, octreotide suppresses the excessive release of insulin and may increase its action, thereby inhibiting excessive adipose storage. In a smallclinical trial in eighteen pediatric subjects with intractable weight gain following therapy for ALL or brain tumors and other evidence of hypothalamic dysfunction, octreotide reducedbody mass index (BMI) and insulin response duringglucose tolerance test, while increasing parent-reported physical activity andquality of life (QoL) relative toplacebo.[38] In a separate placebo-controlled trial of obese adults without known hypothalamic lesions, obese subjects who received long-acting octreotide lost weight and reduced their BMI compared to subjects receiving placebo; post hoc analysis suggested greater effects in patients receiving the higher dose of the drug, and among "Caucasian subjects having insulin secretion greater than the median of the cohort." "There were no statistically significant changes in QoL scores, body fat, leptin concentration,Beck Depression Inventory, or macronutrient intake", although subjects taking octreotide had higher blood glucose after a glucose tolerance test than those receiving placebo.[42]
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