Severe hyponatraemia with neurological manifestations in patients treated with terlipressin: Two case reports

Terlipressin has been shown to be effective in controlling variceal bleeding and decreasing associated mortality. Terlipressin is a synthetic analogue of vasopressin and is safer than arginine vasopressin; it induces selective vasoconstriction by stimulating the vasopressin V1 receptors that are predominantly located in the splanchnic tissues. However, severe hyponatraemia may occur during terlipressin treatment, resulting in neurological manifestations.

We describe two patients who presented a marked decrease in serum sodium levels and developed obvious neurological manifestations after receiving terlipressin therapy. Although the two patients were given sodium supplementation, their serum sodium levels continually declined. After the discontinuation of terlipressin, their serum sodium levels rapidly recovered to normal limits, and the neurological manifestations subsequently disappeared in both patients.

Some studies have reported hyponatraemia as a side effect of terlipressin; however, severe hyponatraemia with neurological manifestations has rarely been reported. We presented the cases of 2 patients with obvious neurological manifestations after receiving terlipressin therapy. Severe hyponatraemia may develop in patients treated with terlipressin, resulting in associated neurological symptoms. Therefore, the close monitoring of serum sodium is necessary.