Background: Terlipressin can effectively control acute gastrointestinal bleeding (GIB) in cirrhotic patients by acting on the V1 receptors, but may lead to the development of dilutional hyponatremia by acting on the V2 receptors.Research design and methods: This retrospective multicenter study enrolled 674 cirrhotic patients with acute GIB in whom serum sodium concentrations were tested before and during the use of terlipressin. ΔSodium reduction ≥5 mmol/L, hyponatremia (sodium <130 mmol/L), and severe hyponatremia (sodium <125 mmol/L) during the use of terlipressin were evaluated. Logistic regression analyses were employed to identify the risk factors.Results: The incidence of Δsodium reduction ≥5 mmol/L, hyponatremia, and severe hyponatremia was 37.1%, 26.3%, and 13.0%, respectively. All of them were not significantly associated with in-hospital mortality (p = 0.973; p = 0.789; p = 0.887). In multivariate logistic regression analyses, the independent risk factors of Δsodium reduction ≥5 mmol/L were higher baseline sodium concentration, lower serum creatinine and prothrombin time, and larger dosage of terlipressin; those of hyponatremia were lower baseline sodium concentration and longer duration of terlipressin; those of severe hyponatremia were lower baseline sodium concentration and prothrombin time and longer duration of terlipressin.Conclusions: Hyponatremia was common in cirrhotic patients with acute GIB treated with terlipressin, but might not significantly increase the in-hospital mortality.
Keywords: Terlipressin; gastrointestinal bleeding; hyponatremia; liver cirrhosis; mortality.