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Terlipressin is frequently used in acute variceal bleeding due to its powerful effect on vasopressin V1 receptors. Although terlipressin is also a partial agonist of renal vasopressin V2 receptors, its effects on serum sodium concentration have not been specifically investigated. To examine the effects of terlipressin on serum sodium concentration in patients with acute portal-hypertensive bleeding, 58 consecutive patients with severe portal-hypertensive bleeding treated with terlipressin were investigated. In the whole population, serum sodium decreased from 134.9 6 6.6 mEq/L to 130.5 6 7.7 mEq/L (P 5 0.002). Thirty-nine patients (67%) had a decrease in serum sodium ! 5 mEq/L during treatment: in 18 patients (31%), between 5 and 10 mEq/L and in 21 patients (36%), greater than 10 mEq/L. In this latter group, serum sodium decreased from 137.2 6 5 to 120.5 6 5 mEq/L (P < 0.001). In multivariate analysis, the reduction in serum sodium was related to baseline serum sodium and Model for End-Stage Liver Disease (MELD) score; patients with low MELD and normal or near-normal baseline serum sodium had the highest risk of hyponatremia. Serum sodium returned to baseline values in most patients shortly after cessation of therapy. Three of the 21 patients with marked reduction in serum sodium developed neurological manifestations, including osmotic demyelination syndrome in one patient due to a rapid recovery of serum sodium (serum sodium in these three patients decreased from 135, 130, and 136 to 117, 114, and 109 mEq/L, respectively). Conclusion: An acute reduction in serum sodium concentration is common during treatment with terlipressin for severe portal-hypertensive bleeding. It develops rapidly after start of therapy, may be severe in some patients and is associated with neurological complications, and is usually reversible after terlipressin withdrawal. (HEPATOLOGY 2010;52:1783-1790 T erlipressin is a prodrug that releases vasopressin in the circulation and is highly effective in the management of variceal bleeding in patients with portal hypertension.1-4 Its efficacy is due to a powerful agonistic activity on vasopressin V1 receptors, which are very abundant in the splanchnic circulation. Activation of V1 receptors causes splanchnic vasoconstriction with subsequent reduction in portal and variceal pressure. [5][6][7] In addition to its activity on the V1 receptors, in vitro studies have shown that terlipressin also has activity on the V2 vasopressin receptors present in the renal collecting ducts that are responsible for the antidiuretic effect of vasopressin.8 Moreover, there is also evidence for an in vivo activity of terlipressin on renal vasopressin V2 receptors. In fact, the administration of a single dose of terlipressin to patients with cirrhosis is Abbreviations: CI, confidence interval; MELD, Model for End-Stage Liver Disease.From the