Sandostatin injection solution 0.1 mg/ml, 5 pcs.: instructions, price, reviews, analogues. Buy Sandostatin injection solution 0.1 mg/ml, 5 pcs. from Novartis in Ukraine: Kyiv, Kharkov, Odessa

Pharmacological properties of the drug Sandostatin

Pharmacodynamics . Sandostatin is a synthetic octapeptide, a derivative of the natural hormone somatostatin and has similar pharmacological effects, but a much longer duration of action. The drug suppresses the pathologically increased secretion of growth hormone, as well as peptides and serotonin produced in the gastroenteropancreatic endocrine system. In healthy individuals, Sandostatin suppresses:

secretion of growth hormone caused by arginine, exercise and insulin hypoglycemia;
secretion of insulin, glucagon, gastrin and other peptides of the gastroenteropancreatic endocrine system caused by food intake, as well as secretion of insulin and glucagon stimulated by arginine;
secretion of thyrotropin caused by thyrotropin-releasing hormone.

Unlike somatostatin, octreotide suppresses growth hormone more than insulin; its administration is not accompanied by rebound hypersecretion of hormones (that is, growth hormone in patients with acromegaly). In patients with acromegaly, Sandostatin reduces the concentration of growth hormone and insulin-like growth factor (IGF-1) in the blood plasma. Inhibition of growth hormone by 50% or more is observed in 90% of patients; a decrease in the level of growth hormone in the blood plasma of ≤5 ng/ml is achieved in approximately 50% of patients. In most patients with acromegaly, Sandostatin significantly reduces the severity of symptoms such as headache, swelling of the skin and soft tissues, hyperhidrosis, joint pain and paresthesia. In patients with a large pituitary adenoma, treatment with Sandostatin may result in a reduction in tumor size. In patients with functional endocrine tumors of the gastrointestinal tract and pancreas, Sandostatin, due to its various endocrine effects, affects a number of clinical signs of the disease. Clinical and symptomatic improvement is observed in patients who have tumor-related symptoms despite previous treatment, including surgery, hepatic artery embolization, and various chemotherapy, such as streptozocin and fluorouracil. In carcinoma tumors, the use of Sandostatin can reduce the severity of symptoms such as hot flashes and diarrhea, which in many cases is accompanied by a decrease in the concentration of serotonin in the blood plasma and a decrease in the excretion of 5-hydroxyindoleacetic acid in the urine. For tumors characterized by overproduction of vasoactive intestinal peptide (VIP), the use of Sandostatin in most patients leads to a decrease in the severity of secretory diarrhea characteristic of this condition, which in turn improves the patient’s quality of life. At the same time, there is a decrease in the number of concomitant electrolyte imbalances, such as hypokalemia, which makes it possible to cancel enteral and parenteral administration of fluids and electrolytes. In some patients, tumor progression slows or stops and even shrinks in size, especially liver metastases. Clinical improvement is usually accompanied by a decrease (down to normal values) in the concentration of VIP in the blood plasma. In glucagonomas , the use of Sandostatin in most cases leads to a noticeable decrease in the severity of the necrotizing migratory rash characteristic of this condition. Sandostatin does not have any significant effect on the severity of diabetes mellitus, which is often noted in glucagonomas and usually does not lead to a decrease in the need for insulin or oral hypoglycemic drugs. In patients with diarrhea, Sandostatin causes a decrease in its severity, which is accompanied by an increase in body weight. When using Sandostatin, a rapid decrease in the concentration of glucagon in the blood plasma is often noted, but with long-term treatment this effect does not persist. At the same time, symptomatic improvement remains stable over a long period of time. In gastrinomas/Zollinger-Ellison syndrome, Sandostatin, used as monotherapy or in combination with proton pump inhibitors or H2 receptor blockers, can reduce gastric acid secretion and lead to clinical improvement, including diarrhea. There may also be a decrease in the severity of other symptoms, probably caused by the synthesis of peptides by the tumor, including hot flashes. In some cases, a decrease in the concentration of gastrin in the blood plasma is noted. In patients with insulinomas , Sandostatin reduces the level of immunoreactive insulin in the blood (this effect, however, can be short-term - about 2 hours). In patients with a resectable tumor, Sandostatin can restore and maintain normoglycemia in the preoperative period. In patients with inoperable benign and malignant tumors, glycemic control may improve without a simultaneous prolonged decrease in blood insulin levels. In patients with a tumor that produces growth hormone RF (somatoliberinomas), Sandostatin reduces the severity of symptoms of acromegaly. This is apparently due to the suppression of RF secretion of growth hormone and growth hormone itself. In the future, pituitary hypertrophy may decrease. For refractory diarrhea AIDS patients, the use of Sandostatin leads to complete or partial normalization of stool in approximately 1/3 of AIDS patients with concomitant diarrhea that is not controlled by adequate therapy with antimicrobial and/or antidiarrheal agents. In patients undergoing pancreatic surgery , the use of Sandostatin during and after surgery reduces the incidence of typical postoperative complications (for example, pancreatic fistulas, abscesses, sepsis, postoperative acute pancreatitis). When bleeding from varicose veins of the esophagus and stomach in patients with liver cirrhosis, the use of Sandostatin in combination with specific treatment (for example, sclerotherapy) led to more effective stoppage of bleeding and early rebleeding, a reduction in the volume of transfusions and an increase in 5-day survival. Although the mechanism of action of Sandostatin is not clearly established, the drug is believed to reduce organ blood flow through the suppression of vasoactive hormones such as VIP and glucagon. Pharmacokinetics . After subcutaneous administration, Sandostatin is quickly and completely absorbed. The maximum concentration of the drug in the blood plasma is achieved after 30 minutes. Plasma protein binding is 65%. The binding of Sandostatin to blood cells is extremely insignificant. The volume of distribution is 0.27 l/kg, total clearance is 160 ml/min. The half-life of the drug after subcutaneous injection is 100 minutes. After intravenous administration, the drug is excreted in two phases with half-periods of 10 and 90 minutes, respectively. Most of the administered dose of the peptide is excreted in the feces, approximately 32% is excreted unchanged in the urine. Impaired renal function does not affect the total exposure (AUC) of octreotide administered subcutaneously. The ability to eliminate may be reduced in patients with liver cirrhosis.

Sandostatin®

The active substance of the drug Sandostatin®, octreotide, is a synthetic octapeptide, a derivative of the natural hormone somatostatin, which has similar pharmacological effects, but a significantly longer duration of action. Octreotide suppresses growth hormone (GH) secretion, both pathologically elevated and induced by arginine, exercise, and insulin hypoglycemia. Octreotide also suppresses the secretion of insulin, glucagon, gastritis, serotonin, both pathologically increased and caused by food intake; also suppresses the secretion of insulin and glucagon stimulated by arginine. Octreotide suppresses the secretion of thyrotropin caused by thyrotropin-releasing hormone.

Unlike somatostatin, octreotide suppresses GH secretion to a greater extent than insulin secretion, and its administration is not accompanied by subsequent hypersecretion of hormones (for example, GH in patients with acromegaly).

In patients with acromegaly, octreotide reduces plasma concentrations of GH and insulin-like growth factor (IGF-1). A decrease in GH concentration by 50% or more is observed in 90% of patients, while a GH concentration of less than 5 mg/ml is achieved in approximately half of the patients. In most patients with acromegaly, Sandostatin® reduces the severity of headache, soft tissue swelling, hyperhidrosis, joint pain and paresthesia. In patients with large pituitary adenomas, treatment with the drug may lead to a slight reduction in tumor size.

For secreting endocrine tumors of the gastrointestinal tract (GIT) and pancreas in cases of insufficient effectiveness of the therapy (surgery, embolization of the hepatic artery, chemotherapy, including streptozotocin and 5-fluorouracil), the use of the drug Sandostatin® can lead to an improvement in the course of the disease. Thus, in case of carcinoid tumors, the use of the drug Sandostatin® can lead to a decrease in the severity of the sensation of “flushing” of blood to the face, diarrhea, which in many cases is accompanied by a decrease in the concentration of serotonin in the blood plasma and the excretion of 5-hydroxyindoleacetic acid by the kidneys.

For tumors characterized by overproduction of vasoactive intestinal peptide (VIPoma), the use of the drug Sandostatin® leads in most patients to a decrease in severe secretory diarrhea, and, accordingly, to an improvement in the quality of life. At the same time, there is a decrease in concomitant electrolyte imbalances, for example, hypokalemia, which makes it possible to cancel enteral and parenteral administration of fluids and electrolytes. In some patients, tumor progression slows down or stops, its size decreases, as does the size of liver metastases. Clinical improvement is usually accompanied by a decrease in the concentration of vasoactive intestinal peptide (VIP) in the blood plasma or its normalization.

For glucagonomas, the use of the drug Sandostatin® leads to a decrease in erythema migrans. The drug Sandostatin® does not have any significant effect on the severity of hyperglycemia in diabetes mellitus, while the need for insulin or oral hypoglycemic drugs usually remains unchanged. The drug causes a decrease in the severity of diarrhea, which is accompanied by an increase in body weight. Although the decrease in plasma glucagon concentration under the influence of Sandostatin® is transient, the clinical improvement remains stable throughout the entire period of drug use.

In patients with gastrinomas/Zollinger-Ellison syndrome, when using the drug Sandostatin® in monotherapy or in combination with proton pump inhibitors or H2-histamine receptor blockers, it is possible to reduce the hypersecretion of hydrochloric acid in the stomach, reduce the concentration of gastrin in the blood plasma, as well as reduce the severity of diarrhea and tides

In patients with insulinomas, the drug Sandostatin® reduces the concentration of immunoreactive insulin in the blood (this effect can be short-term - about 2 hours). In patients with operable tumors, Sandostatin® can restore and maintain normoglycemia in the preoperative period. In patients with inoperable benign and malignant tumors, glycemic control may improve without a simultaneous prolonged decrease in blood insulin concentrations.

In patients with rare tumors that overproduce growth hormone releasing factor (somatoliberinomas), Sandostatin® reduces the severity of symptoms of acromegaly. This is due to the suppression of the secretion of growth hormone releasing factor and GH itself. In the future, pituitary hypertrophy may decrease.

For refractory diarrhea in patients with acquired immunodeficiency syndrome (AIDS), the use of Sandostatin® leads to complete or partial normalization of stool in approximately 1/3 of patients with diarrhea not controlled by adequate therapy with antimicrobial and/or antidiarrheal agents,

In patients undergoing pancreatic surgery, the use of Sandostatin® during and after surgery reduces the incidence of typical postoperative complications (for example, pancreatic fistulas, abscesses, sepsis, postoperative acute pancreatitis).

When bleeding from varices of the esophagus and stomach in patients with cirrhosis of the liver, the use of Sandostatin® in combination with specific treatment (for example, sclerotherapy) leads to more effective control of bleeding and early rebleeding, a reduction in the volume of transfusions and an improvement in 5-day survival. It is believed that the mechanism of action of octreotide is associated with a decrease in organ blood flow through the suppression of vasoactive hormones such as VIP and glucagon.

Indications for use of the drug Sandostatin

Acromegaly : to control the main manifestations of the disease and reduce the level of growth hormone and IGF-1 in the blood plasma in cases where the effect of surgery, radiation therapy and dopamine agonist treatment is insufficient. Sandostatin is also indicated for the treatment of patients with acromegaly who refuse surgery or have contraindications to it, as well as for short-term treatment in the intervals between courses of radiation therapy until its effect is fully manifested. Relief of symptoms of endocrine tumors of the gastrointestinal tract and pancreas :

carcinoid tumors with the presence of carcinoid syndrome;
VIPomas (tumors characterized by hyperproduction of VIP);
glucagonomas; gastrinomas/Zollinger-Ellison syndrome - usually in combination with H2-histamine receptor blockers or proton pump inhibitors;
insulinomas (to control hypoglycemia in the preoperative period, as well as for maintenance therapy);
somatoliberinomas (tumors characterized by hyperproduction of RF growth hormone).

Sandostatin is not an antitumor drug and its use cannot lead to a cure for this category of patients. Refractory diarrhea in patients with AIDS . Prevention of complications after pancreatic surgery . Stopping bleeding and preventing re-bleeding from varicose veins of the esophagus in patients with cirrhosis of the liver (in combination with specific therapeutic measures, for example, endoscopic sclerotherapy).

Instructions for use SANDOSTATIN

Somatostatin analogue. A drug for intensive therapy in gastroenterology. It is a synthetic octapeptide, which is a derivative of the natural hormone somatostatin and has pharmacological effects similar to it, but a much longer duration of action. The drug suppresses the pathologically increased secretion of growth hormone (GH), as well as peptides and serotonin produced in the gastroenteropancreatic endocrine system.

In healthy individuals, Sandostatin suppresses growth hormone secretion induced by arginine, exercise, and insulin hypoglycemia; secretion of insulin, glucagon, gastrin and other peptides of the gastro-enteropancreatic endocrine system caused by food intake, as well as secretion of insulin and glucagon stimulated by arginine; secretion of thyrotropin caused by thyrotropin-releasing hormone.

In patients with acromegaly (including those in whom surgery, radiation therapy and dopamine antagonist treatment were ineffective), Sandostatin reduces the concentration of GH and/or somatomedin C in the blood plasma. A clinically significant decrease in GH concentration (by 50% or more) is observed in almost all patients; normalization of the level of growth hormone in plasma (less than 5 ng/ml) is achieved in approximately half of the patients. In most patients with acromegaly, Sandostatin significantly reduces the severity of symptoms such as headache, swelling of the skin and soft tissues, increased sweating, joint pain and paresthesia. In patients with large pituitary adenomas, treatment with Sandostatin may lead to some reduction in tumor size.

In carcinoid tumors, the use of Sandostatin may lead to a decrease in the severity of symptoms such as flushing and diarrhea, which in many cases is accompanied by a decrease in plasma serotonin concentrations and urinary excretion of 5-hydroxyindoleacetic acid. If the desired treatment effect is not observed, then the duration of Sandostatin use should not exceed 1 week.

For tumors characterized by overproduction of vasoactive intestinal peptide (VIP), the use of Sandostatin leads in most patients to a decrease in severe secretory diarrhea, which is characteristic of this condition, which, in turn, leads to an improvement in the patient’s quality of life. At the same time, there is a decrease in concomitant electrolyte imbalances (for example, hypokalemia), which makes it possible to cancel enteral and parenteral administration of fluids and electrolytes. In some patients, tumor progression slows or stops and even reduces its size, especially liver metastases. Clinical improvement is usually accompanied by a decrease (down to normal values) in plasma VIP concentrations.

In glucagonomas, the use of Sandostatin in most cases leads to a noticeable reduction in the necrotizing migratory rash that is characteristic of this condition. Sandostatin does not have any significant effect on the severity of diabetes mellitus, which is often observed in glucagonomas, and usually does not lead to a decrease in the need for insulin or oral hypoglycemic drugs. In patients suffering from diarrhea, Sandostatin causes its reduction, which is accompanied by an increase in body weight. When using Sandostatin, a rapid decrease in plasma glucagon concentrations is often observed, but this effect does not persist with long-term treatment. At the same time, symptomatic improvement remains stable for a long time.

In gastrinomas/Zollinger-Ellison syndrome, Sandostatin, used as monotherapy or in combination with histamine H2 receptor blockers, can reduce acid production in the stomach and lead to clinical improvement (including diarrhea). It is also possible to reduce the severity of other symptoms (probably related to the synthesis of peptides by the tumor, including hot flashes). In some cases, there is a decrease in plasma gastrin concentration.

In patients with insulinomas, Sandostatin reduces the level of immunoreactive insulin in the blood (this effect, however, can be short-term - about 2 hours). In patients with operable tumors, Sandostatin can restore and maintain normoglycemia in the preoperative period. In patients with inoperable benign and malignant tumors, glycemic control may improve without a simultaneous prolonged decrease in blood insulin levels.

In patients with rare tumors that overproduce growth hormone releasing factor (somatoliberinomas), Sandostatin reduces the severity of symptoms of acromegaly. This appears to be due to suppression of the secretion of growth hormone releasing factor and growth hormone itself. In the future, pituitary hypertrophy may decrease.

For refractory diarrhea in patients with AIDS, the use of Sandostatin leads to complete or partial normalization of stool in approximately 1/3 of patients suffering from diarrhea not controlled by adequate therapy with antimicrobial and/or antidiarrheal agents.

In patients undergoing pancreatic surgery, the use of Sandostatin during and after surgery reduces the incidence of typical postoperative complications (for example, pancreatic fistulas, abscesses, sepsis, postoperative acute pancreatitis).

When bleeding from varices of the esophagus and stomach in patients with cirrhosis of the liver, the use of Sandostatin in combination with specific treatment (for example, sclerotherapy) led to more effective control of bleeding and early rebleeding, a reduction in the volume of transfusions and an improvement in 5-day survival. Although the mechanism of action of Sandostatin is not precisely established, the drug is believed to reduce organ blood flow through the suppression of vasoactive hormones such as VIP and glucagon.

Use of the drug Sandostatin

For acromegaly , the drug is initially administered at 0.05–0.1 mg subcutaneously at intervals of 8 or 12 hours. Subsequently, the dose is set based on monthly determinations of the concentration of growth hormone and IGF-1 in the blood, analysis of clinical symptoms and tolerability of the drug (target concentrations of hormones in the blood are: growth hormone ≤2.5 ng/ml, IGF-1 - within normal limits). For most patients, the optimal daily dose is 0.2–0.3 mg. The maximum daily dose of 1.5 mg should not be exceeded. If after 3 months of treatment with Sandostatin there is no sufficient reduction in growth hormone levels and improvement in the clinical picture of the disease, therapy should be discontinued. For endocrine tumors of the digestive tract and pancreas, the drug is administered subcutaneously at an initial dose of 0.05 mg 1–2 times a day. In the future, depending on the achieved clinical effect, the effect on the levels of hormones produced by the tumor (in the case of carcinoid tumors - on the excretion of 5-hydroxyindoleacetic acid in the urine), and tolerability, the dose of the drug can be gradually increased to 0.1–0.2 mg 3 times per day. In exceptional cases, it may be necessary to use the drug in higher doses. Maintenance doses of the drug should be set individually. If no improvement occurs within 1 week of treatment with Sandostatin at the maximum tolerated dose, therapy should be discontinued. For refractory diarrhea in patients with AIDS, the drug is administered subcutaneously at an initial dose of 0.1 mg 3 times a day. If after 1 week of treatment the symptoms of diarrhea do not disappear, the dose of the drug should be increased individually up to 0.25 mg 3 times a day. Dose adjustment is carried out taking into account the dynamics of bowel movements and tolerability of the drug. If no improvement occurs within 1 week of treatment with Sandostatin at a dose of 0.25 mg 3 times a day, therapy should be discontinued. To prevent complications after pancreatic surgery, 0.1 mg is administered subcutaneously 3 times a day for 7 days in a row, starting from the day of surgery (at least 1 hour before laparotomy). For bleeding from varicose veins of the esophagus, the drug is administered at a dose of 25 mcg/hour by continuous intravenous infusion for 5 days. Sandostatin can be diluted with isotonic sodium chloride solution. Patients with liver cirrhosis showed good tolerability of Sandostatin, used for 5 days at a dose of 50 mcg/h as a continuous IV infusion due to bleeding from esophageal varices.

Sandostatin amp 0.1 mg 1 ml N5 (Novartis)

Pharmacodynamics Sandostatin is a synthetic octapeptide that is a derivative of the natural hormone somatostatin and has pharmacological effects similar to it, but a significantly longer duration of action. Sandostatin suppresses the secretion of growth hormone (GH), both pathologically increased and caused by arginine, exercise and insulin hypoglycemia. The drug also suppresses the secretion of insulin, glucagon, gastrin, serotonin, both pathologically increased and caused by food intake; also suppresses the secretion of insulin and glucagon stimulated by arginine. Sandostatin suppresses the secretion of thyrotropin caused by thyrotropin-releasing hormone. Unlike somatostatin, octreotide suppresses the secretion of GH to a greater extent than the secretion of insulin, and its administration is not accompanied by subsequent hypersecretion of hormones (for example, GH in patients with acromegaly). In patients with acromegaly, Sandostatin reduces the concentration of GH and insulin-like growth factor (IGF-1) in blood plasma. A decrease in GH concentration by 50% or more is observed in 90% of patients, while a GH concentration of less than 5 ng/ml is achieved in approximately half of the patients. In most patients with acromegaly, Sandostatin reduces the severity of headache, soft tissue swelling, hyperhidrosis, joint pain and paresthesia. In patients with large pituitary adenomas, treatment with Sandostatin may lead to a slight reduction in tumor size. For secreting endocrine tumors of the gastrointestinal tract and pancreas, in cases of insufficient effectiveness of the therapy (surgery, hepatic artery embolism, chemotherapy, including streptozotocin and 5-fluorouracil), prescription Sandostatin may improve the course of the disease. Thus, in case of carcinoid tumors, the use of Sandostatin helps to reduce the severity of the sensation of flushing and diarrhea, which in many cases is accompanied by a decrease in the concentration of serotonin in plasma and the excretion of 5-hydroxyindoleacetic acid in the urine. For tumors characterized by overproduction of vasoactive intestinal peptide (VIP), the use of Sandostatin leads in most patients to a decrease in severe secretory diarrhea, and, accordingly, to an improvement in the patient’s quality of life. At the same time, there is a decrease in concomitant electrolyte imbalances, for example, hypokalemia, which makes it possible to cancel enteral and parenteral administration of fluids and electrolytes. In some patients, tumor progression slows down or stops, its size decreases, as does the size of liver metastases. Clinical improvement is usually accompanied by a decrease in the concentration of vasoactive intestinal peptide (VIP) in plasma or its normalization. In glucagonomas, the use of Sandostatin leads to a decrease in erythema migrans. Sandostatin does not have a significant effect on the severity of hyperglycemia in diabetes mellitus, while the need for insulin or oral hypoglycemic drugs usually remains unchanged. The drug causes a decrease in diarrhea, which is accompanied by an increase in body weight. Although the decrease in the concentration of glucagon in the blood plasma under the influence of Sandostatin is transient, the clinical improvement remains stable throughout the entire period of use of the drug. In patients with gastrinomas/Zollinger-Ellison syndrome, when using Sandostatin as monotherapy or in combination with proton pump inhibitors or histamine blockers H2 receptors may reduce the hypersecretion of hydrochloric acid in the stomach, reduce the concentration of gastrin in the blood plasma, as well as reduce the severity of diarrhea and hot flashes. In patients with insulinomas, Sandostatin reduces the level of immunoreactive insulin in the blood (this effect can be short-term - about 2 hours). In patients with operable tumors, Sandostatin can restore and maintain normoglycemia in the preoperative period. In patients with inoperable benign and malignant tumors, glycemic control can improve without a simultaneous prolonged decrease in blood insulin levels. In patients with rare tumors that overproduce growth hormone releasing factor (somatoliberinomas), Sandostatin reduces the severity of symptoms of acromegaly. This is due to the suppression of the secretion of growth hormone releasing factor and growth hormone itself. In the future, pituitary hypertrophy may decrease. With refractory diarrhea in patients with AIDS, the use of Sandostatin leads to complete or partial normalization of stool in approximately 1/3 of patients suffering from diarrhea that is not controlled by adequate therapy with antimicrobial and/or antidiarrheal agents. In patients who are planning to undergo operations on the pancreas, the use of Sandostatin during and after surgery reduces the incidence of typical postoperative complications (for example, pancreatic fistulas, abscesses, sepsis, postoperative acute pancreatitis). For bleeding from varices of the esophagus and stomach in patients with liver cirrhosis, the use of Sandostatin in combination with specific treatment (eg, sclerosing therapy) leads to more effective control of bleeding and early rebleeding, reduced transfusion volume and improved 5-day survival. It is believed that the mechanism of action of Sandostatin is associated with a decrease in organ blood flow through the suppression of vasoactive hormones such as VIP and glucagon. Pharmacokinetics Absorption After subcutaneous administration, Sandostatin is quickly and completely absorbed. Cmax of octreotide in plasma is achieved within 30 minutes. Distribution: Plasma protein binding is 65%. The binding of Sandostatin to blood cells is extremely insignificant. Vd is 0.27 l/kg. Elimination T1/2 after subcutaneous injection of the drug is 100 minutes. After intravenous administration, the drug is eliminated in 2 phases, with T1/2 of 10 and 90 minutes, respectively. Most of the drug is excreted in feces, about 32% is excreted unchanged in urine. The total clearance is 160 ml/min.

Side effects of the drug Sandostatin

The most common adverse reactions during treatment with octreotide include disorders of the gastrointestinal tract, central nervous system, liver and gallbladder, metabolism and trophism. The adverse reactions most commonly reported during clinical trials of octreotide were diarrhea, abdominal pain, nausea, flatulence, headache, cholelithiasis, hyperglycemia, and constipation. Other frequently reported adverse reactions were dizziness, localized pain, gallstones, thyroid dysfunction (eg, decreased thyroid-stimulating hormone, decreased total T4 and decreased free T4), decreased glucose tolerance, vomiting, asthenia, and hypoglycemia. In isolated cases, adverse reactions from the gastrointestinal tract may resemble acute intestinal obstruction - progressive bloating, severe epigastric pain, abdominal tenderness and muscle tension. The feeling of acute pain, tingling or burning at the site of subcutaneous injection with redness and swelling rarely lasts 15 minutes. To reduce the sensation of local discomfort or pain at the injection site, the solution for administration should be at room temperature or a smaller volume of a more concentrated solution should be administered. Although fat excretion in the feces may be increased, there is no indication that long-term treatment with Sandostatin may lead to the development of nutritional deficiencies due to malabsorption. The incidence of side effects from the digestive tract can be reduced by increasing the time between meals and the administration of Sandostatin; it is recommended to administer the drug between meals or before bedtime. In rare cases, the development of acute pancreatitis has been reported. This phenomenon is usually observed in the first hours or days of treatment with Sandostatin and disappears after discontinuation of the drug. In addition, long-term use of Sandostatin may lead to the formation of gallstones. Patients receiving Sandostatin in the form of subcutaneous injections for a long time may develop pancreatitis caused by cholelithiasis. In patients with acromegaly and carcinoid syndrome, ECG changes were observed such as prolongation of the Q–T , axis shift, early repolarization, low wave voltage, R/S transition, early increase in the R ST–T wave . The relationship between these phenomena and the use of octreotide acetate has not been established, since most of these patients had a history of cardiovascular disease (see SPECIAL INSTRUCTIONS). The adverse reactions listed below were obtained during clinical trials of octreotide. Adverse reactions that occur as a result of taking the drug are classified by frequency using the following gradation: very often (≥1/10); often (≥1/100, ≤1/10); uncommon (≥1/1000, ≤1/100); rare (≥1/10,000, ≤1/1000); very rare (≤1/10,000), including isolated reports. Within each frequency group, adverse reactions are arranged in order of decreasing severity. From the digestive tract, pancreas, liver and gall bladder : very often - diarrhea, abdominal pain, nausea, constipation, flatulence; often - dyspepsia, vomiting, bloating, steatorrhea, frequent loose stools, discoloration of stool. From the side of the central nervous system : very often - headache; often - dizziness. From the endocrine system : often - hypothyroidism, thyroid dysfunction (for example, reduced levels of thyroid-stimulating hormone, reduced levels of total T4 and free T4). From the hepatobiliary system : very often - cholelithiasis; often - cholecystitis, gallstones, hyperbilirubinemia. From the side of metabolism : very often - hyperglycemia; often - hypoglycemia, impaired glucose tolerance, anorexia; infrequently - dehydration. General disorders and disorders at the injection site : very often - pain at the injection site. From the skin and subcutaneous tissue : often - itching, skin rash, alopecia. From the respiratory system : often - dyspnea. From the cardiovascular system : often - bradycardia; infrequently - tachycardia. From laboratory parameters : often - increased levels of transaminases. Post-marketing studies . The following side effects to the drug are described in spontaneous reports. The following adverse reactions were reported voluntarily, and it is not always possible to reliably establish the frequency or cause-and-effect relationship with the use of the drug. From the immune system : anaphylaxis, allergy/hypersensitivity reactions. From the skin and subcutaneous tissue : urticaria. From the hepatobiliary system : acute hepatitis, acute pancreatitis without cholestasis, cholestatic hepatitis; cholestasis, jaundice, cholestatic jaundice. From the cardiovascular system : arrhythmia. Laboratory indicators : increased levels of alkaline phosphatase, gamma-glutamyl transferase.

Sandostatin

A synthetic derivative of the hormone somatostatin, which has similar pharmacological effects and a significantly longer duration of action. Reduces the secretion of growth hormone, TSH, has an antithyroid, antispasmodic effect. Reduces acid production and gastrointestinal motility. Suppresses pathologically increased secretion of growth hormone, peptides and serotonin produced in the gastroenteropancreatic endocrine system.

Normally, it reduces the secretion of growth hormone caused by arginine, stress and insulin hypoglycemia; secretion of insulin, glucagon, gastrin and other peptides of the gastroenteropancreatic endocrine system caused by food intake, as well as secretion of insulin and glucagon stimulated by arginine; secretion of thyrotropin caused by thyrotropin-releasing hormone.

Suppression of growth hormone secretion by octreotide (as opposed to somatostatin) occurs to a much greater extent than by insulin. The administration of octreotide is not accompanied by the phenomenon of hypersecretion of hormones through the “negative feedback” mechanism. In patients with acromegaly, it reduces the concentration of growth hormone and/or somatomedin A in plasma. A clinically significant decrease in the concentration of growth hormone (by 50% or more) is observed in almost all patients, while normalization of the content of growth hormone in plasma (less than 5 ng/ml) is achieved in approximately half of the patients.

For carcinoid tumors, the administration of octreotide can lead to a decrease in the severity of symptoms of the disease, primarily such as flushing of the face and diarrhea; clinical improvement is accompanied by a decrease in the concentration of serotonin in plasma and the excretion of 5-hydroxyindoleacetic acid in the urine.

For tumors characterized by overproduction of vasoactive intestinal peptide (VIP), a decrease in severe secretory diarrhea, which is characteristic of this condition, which in turn leads to an improvement in the patient’s quality of life. At the same time, there is a decrease in concomitant electrolyte imbalances, such as hypokalemia, which makes it possible to cancel enteral and parenteral administration of fluids and electrolytes. It is possible to slow down or stop the progression of the tumor and even reduce its size and especially liver metastases. Clinical improvement is usually accompanied by a decrease (down to normal values) in plasma VIP concentrations.

In glucagonomas, despite a marked reduction in the necrotizing migratory rash, it does not have any significant effect on the severity of diabetes mellitus (often observed in glucagonomas) and usually does not lead to a decrease in the need for insulin or oral hypoglycemic drugs. In patients suffering from diarrhea, it causes a decrease in it, which is accompanied by an increase in body weight; there is often a rapid decrease in the concentration of glucagon in plasma, but with long-term treatment this effect does not persist. At the same time, symptomatic improvement remains stable for a long time.

In gastrinomas (Zollinger-Ellison syndrome), octreotide, used as monotherapy or in combination with H2 receptor blockers and proton pump inhibitors, can reduce the formation of HCl in the stomach, possibly reducing the severity and other symptoms, probably associated with the synthesis of peptides by the tumor, incl. "tides". In some cases, there is a decrease in plasma gastrin concentration.

In patients with insulinomas, it reduces the concentration of immunoreactive insulin in the blood (this effect, however, can be short-term - about 2 hours).

In patients with operable tumors, it can ensure the restoration and maintenance of normoglycemia in the preoperative period. In patients with inoperable benign and malignant tumors, normoglycemia can be achieved without a simultaneous prolonged decrease in insulin in the blood.

In patients with rare tumors that overproduce growth hormone releasing factor (somatoliberinomas), it reduces the severity of symptoms of acromegaly. This appears to be due to suppression of the secretion of growth hormone releasing factor and growth hormone itself. In the future, it is possible to reduce the size of the pituitary gland, which was enlarged before treatment.

In patients with acromegaly, administration of octreotide provides, in the vast majority of cases, a persistent decrease in growth hormone and normalization of the concentration of insulin-like growth factor 1/somatomedin C (IGF1). Significantly reduces the severity of symptoms such as headache, increased sweating, paresthesia, fatigue, pain in bones and joints, peripheral neuropathy. In patients with pituitary adenomas that secrete growth hormone, a reduction in tumor size is possible.

Sandostatin is a long-acting dosage form of octreotide intended for administration at 4-week intervals to maintain stable therapeutic octreotide serum concentrations. The microspheres include a polymer matrix that serves as a carrier of the active substance. After intramuscular administration, as a result of the destruction of microspheres in muscle tissue, a long-term and gradual release of the active substance occurs.

Special instructions for the use of the drug Sandostatin

Subcutaneous administration Patients who self-administer the drug by subcutaneous injection should receive specific instructions from a doctor or nurse. In order to reduce discomfort at the injection site, it is recommended to bring the solution to room temperature before injection. Repeated injections in the same place over a short period of time should be avoided. Ampoules must be opened only before administration; any remaining drug must be disposed of. IV infusion The diluted solution remains physically and chemically stable for at least 24 hours at a temperature not exceeding 25 °C. General Because growth hormone-secreting pituitary tumors can sometimes enlarge, causing serious complications (eg, narrowing of the visual field), careful monitoring of the patient's condition is essential. If signs of tumor enlargement appear, alternative treatments should be considered. The therapeutic benefit of reducing growth hormone levels and normalizing IGF-1 concentrations in women with acromegaly may potentially restore fertility. During treatment with octreotide, women of reproductive age should be advised to use adequate methods of contraception. In patients receiving long-term therapy with octreotide, it is necessary to monitor thyroid function. Events related to the cardiovascular system: Cases of bradycardia have been reported occasionally. Dosage adjustments may be necessary for medications such as beta-blockers, calcium channel blockers, or medications that control fluid or electrolyte balance. Events associated with the gallbladder In 15–30% of patients receiving Sandostatin subcutaneously for a long time, the formation of gallstones is observed. The prevalence of this pathology in the general population is about 5–20%. In this regard, it is recommended to conduct an ultrasound of the gallbladder before starting Sandostatin therapy and every 6–12 months during the treatment period. The appearance of gallstones in patients treated with Sandostatin was in most cases not accompanied by the appearance of symptoms of cholelithiasis; in the presence of clinical manifestations of the latter, the use of bile acids is necessary to dissolve the stones; if conservative therapy is ineffective, the use of surgical treatment is necessary. Tumors of the gastroenteropancreatic endocrine system During treatment of tumors of the gastroenteropancreatic endocrine system, in rare cases, a sudden relapse of symptoms may occur. Glucose Metabolism Due to its inhibitory effect on growth hormone, glucagon and insulin, Sandostatin may impair the regulation of blood glucose levels. In some cases, there is impaired glucose tolerance, as a result of which persistent hyperglycemia may occur with prolonged administration of the drug after meals. In patients with insulinoma during treatment with Sandostatin, an increase in the severity and duration of hypoglycemia may be noted. This is due to a more pronounced inhibitory effect on the secretion of growth hormone and glucagon than on insulin secretion, as well as a shorter duration of the inhibitory effect on insulin secretion. Such patients should be carefully examined when starting treatment with Sandostatin, as well as whenever the dose of the drug is changed. Significant fluctuations in blood glucose levels can be reduced by administering Sandostatin more frequently. In diabetic patients receiving insulin, Sandostatin may reduce insulin requirements. The dependence of patients with type I diabetes mellitus on insulin can be reduced by administering Sandostatin. In patients without diabetes or with type II diabetes, the administration of Sandostatin may lead to an increase in blood glucose levels after meals. Careful monitoring of glucose tolerance and antidiabetic treatment is recommended. Esophageal varices During bleeding from esophageal varices, the risk of developing insulin-dependent diabetes mellitus is increased, and changes in insulin requirements in patients with diabetes mellitus are possible, so systematic monitoring of blood glucose levels is necessary. Local reactions There are no reports of tumors occurring at the injection site in patients treated with Sandostatin for up to 15 years. Trophics Octreotide may increase the absorption of dietary fats in some patients. Decreased vitamin B12 levels and abnormal Schilling test results have been observed in some patients treated with octreotide. In patients with a history of vitamin B12 deficiency, it is necessary to monitor the level of this vitamin during Sandostatin therapy. Elderly Patients There is no evidence regarding decreased tolerability or the need for dosage adjustment in elderly patients receiving Sandostatin therapy. Patients with impaired liver function In patients with liver cirrhosis, the half-life of the drug may increase, which leads to the need for adjustment of the maintenance dose. Patients with Renal Impairment Renal impairment does not affect the total exposure (AUC) of octreotide when administered by subcutaneous injection. Thus, there is no need to adjust the dose of Sandostatin. During pregnancy and breastfeeding . Adequate, well-controlled studies have not been conducted in women during pregnancy. There is post-marketing surveillance data for the treatment of a small number of pregnant women with acromegaly, but in half of the cases the pregnancy outcome was unknown. Most women received octreotide in the first trimester of pregnancy at a dose of 100–300 mcg/day in the form of Sandostatin subcutaneously. Based on the results of observation, most cases reported a normal completion of pregnancy, but there are also a few reports of spontaneous abortions in the first trimester of pregnancy. There are no reports of cases of congenital anomalies or malformations due to the use of octreotide during pregnancy. Thus, Sandostatin can be prescribed to women during pregnancy only for health reasons. It is not known whether octreotide passes into breast milk. If it is necessary to use the drug in women during breastfeeding, breastfeeding should be discontinued. Children . The use of Sandostatin in children is contraindicated due to lack of clinical experience. Influence on reaction speed when driving vehicles or while working with other mechanisms . Considering that sensitive patients may experience adverse reactions (dizziness and others) when using the drug, while taking the drug it is necessary to refrain from driving vehicles or performing work that requires concentration.

Sandostatin solution for injection 0.1 mg/ml, 5 pcs.

Sandostatin is a synthetic octapeptide that is a derivative of the natural hormone somatostatin and has similar pharmacological effects, but a significantly longer duration of action. The drug suppresses the pathologically increased secretion of growth hormone (GH), as well as peptides and serotonin produced in the gastroenteropancreatic endocrine system.

In animals, octreotide is a more potent inhibitor of growth hormone, glucagon, and insulin release than somatostatin, with greater selectivity for suppression of growth hormone and glucagon.

In healthy individuals, Sandostatin suppresses:

growth hormone secretion caused by arginine, exercise-induced hypoglycemia and insulin;
secretion of insulin, glucagon, gastrin and other peptides of the gastroenteropancreatic endocrine system caused by food intake, as well as secretion of insulin and glucagon, which is stimulated by arginine;
secretion of thyroid-stimulating hormone (TSH), which causes thyrotropin-releasing hormone.

Unlike somatostatin, octreotide suppresses growth hormone (GH) more than insulin; its administration is not accompanied by rebound hypersecretion of hormones (i.e. GH in patients with acromegaly).

In patients with acromegaly, Sandostatin reduces the concentration of GH and insulin-like growth factor 1 (IGF-1) in the blood plasma. Suppression of GH by 50% or more is observed in 90% of patients; a decrease in the level of GH in the blood plasma to less than 5 ng/ml is achieved in approximately half of the patients. In most patients with acromegaly, Sandostatin significantly reduces the severity of symptoms such as headache, swelling of the skin and soft tissues, increased sweating, joint pain, and paresthesia. In patients with large GH-secreting pituitary adenomas, treatment with sandostatin may result in some reduction in tumor size.

In patients with functional endocrine tumors of the gastrointestinal tract and pancreas, Sandostatin, due to its various endocrine effects, changes a number of clinical characteristics. Clinical and symptomatic improvement is observed in patients who still have tumor-related symptoms despite previous treatment, which may include surgery, hepatic artery embolization, and a variety of chemotherapy, such as streptozocin and 5-fluorouracil.

The effects of Sandostatin on various types of tumors are described below.

Carcinoid tumors

In carcinoid tumors, the use of Sandostatin can reduce the severity of symptoms such as hot flashes and diarrhea, in many cases accompanied by a decrease in the concentration of serotonin in the blood plasma and the excretion of 5-hydroxyindoleacetic acid in the urine.

VIPs

For tumors characterized by overproduction of vasoactive intestinal peptide (VIP), the use of Sandostatin in most patients reduces the severe secretory diarrhea that is characteristic of this condition, which, in turn, improves the patient's quality of life. At the same time, there is a decrease in concomitant electrolyte imbalances, such as hypokalemia, which makes it possible to cancel enteral and parenteral administration of fluids and electrolytes. As evidenced by computed tomography data, some patients experience a slowdown or cessation of tumor progression and even a decrease in its size, especially liver metastases. Clinical improvement is usually accompanied by a decrease (down to normal) in the concentration of vasoactive intestinal peptide (VIP) in the blood plasma.

Glucagonoma

In glucagonomas, the use of Sandostatin in most cases significantly reduces the necrolytic migratory rash that is characteristic of this condition. Sandostatin does not show any significant effect on mild diabetes mellitus, which is often observed in glucagonomas, and does not usually reduce the need for insulin or oral antidiabetic drugs. In patients suffering from diarrhea, Sandostatin helps reduce it, which is accompanied by an increase in body weight. When using Sandostatin, a rapid decrease in the concentration of glucagon in the blood plasma is often observed, but in most cases this effect does not persist with long-term treatment. At the same time, symptomatic improvement remains stable over a long period of time.

Gastrinoma/Zollinger-Ellison syndrome

Therapy with proton pump inhibitors or H2 receptor antagonists may reduce acid production in the stomach. However, diarrhea, also a major symptom, may not be sufficiently relieved by proton pump inhibitors or H2 blockers. In some patients, Sandostatin may further help reduce gastric acid hypersecretion and relieve symptoms, including diarrhea, by suppressing elevated gastrin levels.

Insulinomas

In patients with insulinomas, sandostatin reduces the level of immunoreactive insulin in the blood. This effect, however, may be short-lived - about 2 hours. In patients with operable tumors, Sandostatin can restore and maintain normoglycemia in the preoperative period. In patients with inoperable benign and malignant tumors, glycemic control may improve without a simultaneous sustained decrease in blood insulin levels.

Complications after pancreatic surgery

Bleeding from varicose veins of the stomach and esophagus

When bleeding from varices of the esophagus and stomach in patients with liver cirrhosis, the use of Sandostatin in combination with specific treatment (for example, sclerotherapy) led to more effective control of bleeding and early rebleeding, a reduction in the volume of transfusions and an improvement in 5-day survival. Although the mechanism of action of Sandostatin is not precisely established, it is believed that the drug reduces organ blood flow by suppressing vasoactive hormones such as VIP and glucagon.

In patients with tumors that overproduce growth hormone releasing factor (somatoliberinomas), Sandostatin reduces the severity of symptoms of acromegaly. This is obviously due to the suppression of the secretion of growth hormone releasing factor and GH itself. In the future, pituitary hypertrophy may decrease.

Interactions of the drug Sandostatin

It has been established that octreotide reduces the absorption of cyclosporine in the intestine and slows down the absorption of cimetidine. With simultaneous use of octreotide and bromocriptine, the bioavailability of the latter increases. There is evidence that somatostatin analogs may reduce the metabolism of drugs metabolized by cytochrome P450 enzymes, which may be due to growth hormone suppression. Since similar effects of ocreotide cannot be excluded, drugs metabolized by cytochrome P450 enzymes, mainly with the participation of CYP 3A4, and having a narrow therapeutic dose range (for example, quinidine, terfenadine) should be prescribed with caution.

Overdose of the drug Sandostatin, symptoms and treatment

The number of cases of Sandostatin overdose in adults and children is limited. In adults, doses ranged from 2400–6000 mcg/day when administered by continuous infusion (100–250 mcg/hour) or subcutaneously (1500 mcg three times daily). The following adverse events have been reported: arrhythmia, hypotension, cardiac arrest, cerebral hypoxia, pancreatitis, hepatic steatosis, diarrhea, weakness, drowsiness, weight loss, hepatomegaly and lactic acidosis. In children, doses ranged from 50–3000 mcg/day and were administered by continuous infusion (2.1–500 mcg/h) or subcutaneously (50–100 mcg). The only adverse event was mild hyperglycemia. No side effects were observed in cancer patients receiving Sandostatin doses of 3000–30,000 mcg/day in separate subcutaneous doses.