The effect of terlipressin acetate in the treatment of decompensated liver cirrhosis

2018-08-18

Introduction 

Somatostatin is the main hemostatic drug in the clinic, and its derivative octreotide has been confirmed by many studies that it has a significant effect in treating upper gastrointestinal hemorrhage of cirrhosis. Terlipressin is a synthetic bioactive triglycine-lysine-vasopressin. It has been studied for the treatment of upper gastrointestinal hemorrhage of cirrhosis and has achieved good results.

Pharmacologic action

Ascites is one of the common complications in patients with decompensated cirrhosis. Patients with ascites have a high power circulation characterized by peripheral and visceral vasodilation, decreased arterial blood pressure, and increased systemic vascular resistance. Portal hypertension and visceral vasodilation are major factors in the development of ascites. Vasoactive substances such as the renin angiotensin aldosterone system and the sympathetic nervous system are activated. The new generation of vasoactive drug terlipressin is a synthetic pituitrin analog, which can effectively reduce the portal pressure and improve clinical symptoms and prognosis. Terlipressin, which is combined with traditional Chinese medicine enema to eliminate endotoxin, can improve hemodynamic changes Terlipressin can also reduce the activation of endogenous vasoactive substances, increase the efficacy and help the recovery of liver function.

Function

Terlipressin has a half-life of 6 hours and a clear half-life of 50 minutes. Terlipressin can reduce portal blood pressure, portal blood flow, spleen and mesenteric blood flow, and the formation of ascites by contracting visceral blood vessels. It can also redistribute the splanchnic blood flow after vasoconstriction, which increases renal perfusion and inactivates the renin-angiotensin-aldosterone system (RAAS system) and the sympathetic nervous system (SNS system), making plasma aldosterone, renin, etc. The concentration of vasoactive substances is reduced, which increases the excretion of water and sodium in the kidney and reduces ascites. Therefore, terlipressin can effectively address the important links of ascites and reduce the formation of ascites.

Pharmacokinetics and metabolism

Animal experiments with terlipressin showed that after intravenous administration, portal blood flow and hepatic blood flow were reduced by 30% in a few minutes, and umbilical vein low blood flow and hepatic venous pressure gradient were reduced by 20%. The increase in volume is not affected. In patients with cirrhosis, after treatment with terlipressin, the hemostatic effect is obvious and the safety is high. The total incidence of adverse reactions is 4.65%.

References:

1. Qi Huchang, Ling Jing, Lu Fangfang. Progress in clinical research of terlipressin. Pharm J Chin PLA, Vol. 28, No. 2, Apr 20, 2012.

2. Li Dongyue, Wu Bo. Therapeutic effect of terlipressin on decompensated liver cirrhosis. J Clin Hepatol,Feb. 2012.Vol.15No.1.

3. Cardenas A,Arroyo V. Refractory ascites. Dig Dis, 2005, 23 (1):30-38.

4. Wang Guocai, Zhang Guo. The effect of vasopressin and vasopressin on portal hemodynamics in normal and portal hypertension rabbits. Chinese Journal of Digestion, 2002, 22(10): 595-597.

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