Octreotide Injection 100 Mcg

Octreotide Injection 100 mcg, as an artificially synthesized somatostatin analog, plays an important role in clinical emergency treatment due to its long-lasting effect, strong selectivity, and mild side effects. Especially in the emergency treatment of esophageal and gastric variceal bleeding caused by portal hypertension in cirrhosis, it plays an irreplaceable core role. Esophageal and gastric variceal rupture and bleeding are the most dangerous acute complications of portal hypertension in the middle and late stages of liver cirrhosis.

The onset is sudden and the amount of bleeding is huge, which can easily lead to serious consequences such as hemorrhagic shock and hepatic encephalopathy. The clinical mortality rate is as high as 30% -50%, posing great challenges to clinical emergency treatment. By precisely targeting the pathogenesis, it can quickly achieve the effect of reducing portal pressure and emergency hemostasis, while creating safe conditions for subsequent endoscopic radical treatment, making it one of the preferred emergency drugs for dealing with this emergency. This article will focus on the specific therapeutic effects of this in this disease, and provide a detailed explanation based on its pathophysiological mechanisms and clinical application characteristics.

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Octreotide COA

Certificate of Analysis
Compound name	Octreotide
Grade	Pharmaceutical grade
CAS No.	79517-01-4
Quantity	35g
Packaging standard	PE bag+Al foil bag
Manufacturer	Shaanxi BLOOM TECH Co., Ltd
Lot No.	202501090096
MFG	Jan 9th 2025
EXP	Jan 8th 2028
Structure
Item	Enterprise standard	Analysis result
Appearance	White or almost white powder	Conformed
Water content	≤5.0%	0.54%
Loss on drying	≤1.0%	0.42%
Heavy Metals	Pb≤0.5ppm	N.D.
	As≤0.5ppm	N.D.
	Hg≤0.5ppm	N.D.
	Cd≤0.5ppm	N.D.
Purity (HPLC)	≥99.0%	99.90%
Single impurity	<0.8%	0.52%
Total microbial count	≤750cfu/g	95
E. Coli	≤2MPN/g	N.D.
Salmonella	N.D.	N.D.
Ethanol (by GC)	≤5000ppm	500ppm
Storage	Store in a sealed, dark, and dry place below -20°C

Esophageal and gastric variceal bleeding is one of the most serious and dangerous acute complications of portal hypertension in the middle and late stages of liver cirrhosis. Its onset is sudden and progresses rapidly, often manifested as massive vomiting of blood and black stool in a short period of time. Some patients may rapidly develop hemorrhagic shock. If not intervened in time, the clinical mortality rate is high, up to 30% -50%. Octreotide injection, as an artificially synthesized somatostatin analog, has the advantages of longer action time, stronger selectivity, and milder side effects compared to natural somatostatin. Therefore, it has become one of the core emergency drugs for treating this emergency. Based on clinical treatment logic, its core role always revolves around three dimensions: "rapidly reducing portal pressure, urgently controlling bleeding, and creating safe conditions for subsequent endoscopic radical treatment". The specific points are explained in detail in the following text.

(I)Core Role: Reducing Portal Venous Pressure (The Fundamental Prerequisite for Hemostasis)

 

Mechanism of Action: Octreotide powerfully and selectively constricts the splanchnic blood vessels (especially the arterial vessels of the gastrointestinal tract and spleen), reducing blood flow to the splanchnic region.

Advantages: It acts rapidly and mildly, taking effect within 10–15 minutes after intravenous injection. It can quickly reduce portal pressure while having a minimal impact on systemic blood pressure (compared to other vasoconstrictors, it is safer and more suitable for patients with cirrhosis to tolerate).

Specific Principle: In cirrhosis, hepatic fibrosis leads to obstructed portal venous blood return, causing blood to accumulate in the portal venous system. This results in abnormally elevated portal venous pressure (portal hypertension), which in turn causes compensatory dilation and varicose veins in the esophageal and gastric fundus. By constricting the splanchnic arteries, it reduces the blood flow into the portal vein, lowering the pressure in the portal vein and its branches at the source, thereby alleviating the congested state of the varicose veins.

Hemostatic Mechanism

Based on the reduction in portal pressure, blood flow in the varicose veins decreases, and intravascular pressure drops. This slows the blood flow at the rupture site, facilitating platelet aggregation and the action of coagulation factors, thereby forming a thrombus to seal the rupture and achieve emergency hemostasis.

Key Usage Points

Requires intravenous administration (subcutaneous injection has a slower onset and is unsuitable for emergencies). It typically involves a "loading dose + maintenance dose" approach to rapidly achieve effective blood concentrations and sustain bleeding control.

Clinical Application

Primarily used for acute-phase emergency treatment of esophageal and gastric fundal variceal bleeding. It can quickly control the amount of bleeding, reduce the frequency and volume of hematemesis and melena, and prevent severe complications such as shock or hepatic encephalopathy caused by acute massive bleeding.

(III)Important Auxiliary Role: Preparing for Endoscopic Treatment (Improving Treatment Success Rate)

 

Role of Endoscopic Treatment: Endoscopic hemostasis (e.g., ligation, sclerotherapy) is the "definitive" treatment for esophageal and gastric fundal variceal bleeding, directly addressing the varicose veins and preventing rebleeding. However, it requires stable vital signs and preliminary control of bleeding.

Note: This is only an "auxiliary emergency + preoperative preparation" medication and cannot replace endoscopic treatment. After hemostasis, timely endoscopic treatment is necessary to fundamentally prevent rebleeding.

Auxiliary Value of Octreotide injection: (I)Controls acute bleeding, reducing blood loss during endoscopic procedures and avoiding operational difficulties or missed rupture sites due to obscured vision. (II)Stabilizes the patient's vital signs (e.g., blood pressure, heart rate), reducing risks during endoscopic procedures (e.g., shock, arrhythmias). (III)Buys time for endoscopic treatment. Typically, after using it to control bleeding, endoscopic treatment is scheduled within 24–48 hours, significantly improving the success rate of endoscopic hemostasis.

Based on the pathological characteristics of cirrhosis-induced portal hypertension and the pharmacological properties of this, this critical process can be divided into three interconnected cause-and-effect steps, detailed as follows:

Step 1: Clarify the Core Relationship-The Splanchnic Arteries Are the "Blood Supply Source" of the Portal Vein.
The majority of blood flow in the portal venous system originates from splanchnic arteries in areas such as the gastrointestinal tract and spleen (e.g., gastric arteries, intestinal arteries, splenic arteries). After passing through these organs, blood from these arteries converges into the portal vein and then enters the liver for metabolism.

Step 2: The Direct Effect of Octreotide-Constriction of Splanchnic Arteries Reduces Blood Supply.
This has a potent and selective constrictive effect on splanchnic arteries (with minimal impact on arteries in other parts of the body). When these arteries constrict, their lumens narrow, significantly reducing the volume of blood flowing through them per unit of time. This, in turn, leads to a synchronous decrease in the "total blood flow entering the portal vein" (equivalent to reducing the portal vein's blood input at the "supply source").

Step 3: The Final Outcome-Reduced Blood Flow → Decreased Pressure → Alleviated Congestion.
In cirrhosis, hepatic fibrosis obstructs portal venous blood return and causes blood accumulation, which is the core mechanism of portal hypertension. By reducing portal venous blood flow, octreotide injection directly lessens the "blood congestion burden" in the portal venous system, lowering the intravascular pressure in the portal vein and its branches from the source. As vascular pressure decreases, the passive dilation and congestion in esophageal and gastric fundal varices-initially caused by high pressure-gradually improve, and vascular tension reduces accordingly, laying the foundation for subsequent hemostasis.

Octreotide coagulates platelets for emergency hemostasis

 

The hemostatic mechanism of it involves a series of interconnected pathophysiological changes following the reduction of portal pressure, rather than a single isolated step. Based on clinical and pathological characteristics, this process can be detailed in the following four points:

01

Core Prerequisite: Reduction in Portal Pressure (Continuing from the Previous Core Mechanism).

Octreotide reduces the intravascular pressure in the portal vein and esophageal-gastric varices by constricting splanchnic arteries and decreasing portal venous blood flow. This serves as the foundation for hemostasis. Without alleviating portal hypertension, variceal veins remain under high pressure and congestion, making it difficult to form stable clots and leading to persistent bleeding, even with coagulative effects.

02

Direct Changes: Simultaneous Decrease in Blood Flow and Pressure Within Variceal Veins.

After portal pressure is lowered, the blood flow through esophageal and gastric varices significantly decreases, reducing intravascular pressure to a safer range and avoiding continuous high-pressure impact on the rupture site. Additionally, reduced blood flow slows the velocity of blood within the vessels, breaking the vicious cycle of "high-speed blood flow scouring the rupture site and impeding coagulation," which is a critical turning point for hemostasis.

03

Initiation of Coagulation: Platelet Aggregation and Activation of Coagulation Factors.

As blood flow slows at the rupture site, platelets in the blood more easily adhere to the damaged vascular endothelium, gradually aggregating to form a "platelet thrombus." This provides initial temporary hemostasis by partially sealing the rupture. Simultaneously, the slowed blood flow allows sufficient time for coagulation factors (such as thrombin and fibrinogen) to act. Once activated, these factors promote fibrin production, which binds the aggregated platelets and blood cells together, forming a more stable "fibrin thrombus."

04

Final Outcome: Stable Thrombus Formation, Sealing the Rupture Site and Achieving Hemostasis.

The fibrin thrombus adheres tightly to the rupture site in the variceal vein, completely blocking blood leakage. As the thrombus gradually organizes and the vascular endothelium slowly repairs, bleeding ceases entirely, achieving the clinical goal of emergency hemostasis. This process typically becomes evident within 30 minutes to 1 hour after octreotide takes effect (i.e., after portal pressure is reduced), with the exact timing depending on factors such as the severity of bleeding and the patient's coagulation function.

• What is octreotide used for in GI bleed?

This is used in gastrointestinal (GI) bleeding, primarily for variceal bleeds (from enlarged veins, often in the esophagus) by reducing portal blood flow and pressure, and also shows promise in controlling certain non-variceal bleeds like angiodysplasia, by constricting blood vessels, inhibiting acid, and stabilizing clots, though it's often an adjunct to endoscopic treatments

• Why is octreotide used in pancreatitis?

A potential role of somatostatin (SST) or its analogs such as it in the treatment of pancreatitis has been postulated since they were found to inhibit pancreatic secretion in a dose- and time-dependent manner. Many experiments have demonstrated the efficacy of this in the treatment of AP in animals.

• Who should not take octreotide?

Pancreatic disease. Thyroid disease. An unusual or allergic reaction to it, other medications, foods, dyes, or preservatives. Pregnant or trying to get pregnant.

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