pituitrin and End-Stage-Liver-Disease

Gastroesophageal variceal hemorrhage is a major complication of portal hypertension in 50% to 60% of patients with liver cirrhosis and is a frequent cause of mortality in these patients. The prevalence of variceal hemorrhage is approximately 5% to 15% yearly, and early variceal rebleeding has a rate of occurrence of 30% to 40% within the first 6 weeks. More than 50% of patients who survive after the first bleeding episode will experience recurrent bleeding within 1 year. Management of gastroesophageal varices should include prevention of initial and recurrent bleeding episodes and control of active hemorrhage. Therapies used in the management of gastroesophageal variceal hemorrhage may include pharmacologic therapy (vasoactive agents, nonselective b-blockers, and antibiotic prophylaxis), endoscopic therapy, transjugular intrahepatic portosystemic shunt, and shunt surgery. This article focuses primarily on pharmacologic management of acute variceal hemorrhage.

Topics: End Stage Liver Disease; Esophageal and Gastric Varices; Gastrointestinal Agents; Gastrointestinal Hemorrhage; Humans; Liver Cirrhosis; Octreotide; Primary Prevention; Prognosis; Proton Pump Inhibitors; Recurrence; Risk Factors; Sclerotherapy; Severity of Illness Index; Vasoconstrictor Agents; Vasopressins

Relative vasopressin deficiency, a contributor to vasodilatory septic shock, also may be a cause of the vasodilatory state in liver disease. This study assessed endogenous vasopressin levels in patients with liver disease and their hemodynamic response to exogenous vasopressin.. A prospective, observational study.. A single-center, tertiary hospital.. Human subjects undergoing liver transplantation or major surgery.. Vasopressin levels were measured in 28 patients with liver disease undergoing liver transplantation and 7 control patients with normal liver function. Additionally, intravenous vasopressin was administered to 20 liver transplant recipients, and the hemodynamic response was observed.. Patients with liver disease had significantly lower baseline vasopressin levels than controls (19.3 ± 27.1 pg/mL v 50.9 ± 36.7 pg/mL, p = 0.015). Patients with low vasopressin levels (≤20 pg/mL) were more likely to have lower baseline mean blood pressure (≤80 mmHg) than patients with high vasopressin levels (11/16 v 0/4, p = 0.013). Systemic vascular resistance increased by 33% 3 minutes after intravenous vasopressin. Thirteen of 16 patients with low vasopressin levels compared with 1 of 4 patients with high vasopressin levels responded to exogenous vasopressin, with an increase of mean blood pressure by more than 20% (p = 0.028).. Patients with liver disease have lower vasopressin levels than controls and respond with a brisk vasoconstrictor response to exogenous vasopressin. Therefore, relative endogenous vasopressin deficiency may contribute to vasodilatory shock in liver disease similar to what has been observed in septic shock.

Topics: Adult; Aged; End Stage Liver Disease; Female; Humans; Liver Transplantation; Male; Middle Aged; Prospective Studies; Shock, Septic; Vascular Resistance; Vasodilation; Vasopressins