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

Abstract

Gastroesophageal varices are present in 50% of patients with liver cirrhosis, and the annual incidence of variceal bleeding is 5%-15%. 1 Acute variceal bleeding is the most serious complication of portal hypertension, and mortality during the first episode ranges from 15% to 25%; variceal bleeding remains the major cause of death in cirrhotic patients. 2 Therefore, it is recommended that vasoactive drugs be started early in patients with advanced cirrhosis and known variceal bleeding and in those at risk of bleeding. 3 Terlipressin, a synthetic analogue of vasopressin, is highly effective in controlling acute variceal bleeding and is obviously correlated with decreased mortality. 4 Furthermore, a strong preference for the vasopressin V1 receptor makes terlipressin safer than vasopressin. However, some studies have demonstrated that patients receiving terlipressin treatment can develop varying degrees of hyponatraemia. 5,6 In this study, we report two cases of severe hyponatraemia with neurological manifestations during terlipressin treatment. AbstractWhat is known and objective: 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. Case summary: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. What is new and conclusion: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. K E Y W O R D Shyponatremia, neurological manifestations, portal hypertension, terlipressin

Vasopressin and Its Analogues: From Natural Hormones to Multitasking Peptides

“…These effects have been exploited in studies exploring its role in the management of HRS and variceal bleeding [ 207 , 223 ]. In recent years, as the physiological effects of terlipressin became better understood, roles of the drug in the setting of refractory ascites and cirrhotic hyponatremia have been proposed [ 224 , 225 , 226 ]. Despite the fact that terlipressin has been used for over 20 years, research on this drug is still continued.…”

Practice guidance for the use of terlipressin for liver cirrhosis–related complications

“…The incidence of serum sodium concentration <130 mmol/L was 0-6%, 162,163 and a decrease in serum sodium concentration of >5 mmol/L was observed in 30-60% of patients treated with terlipressin. [164][165][166][167] Patients with better liver function, higher baseline sodium concentration, and longer duration of terlipressin treatment had a higher risk of developing hyponatremia. 168,169 In addition, non-steroidal anti-inflammatory drugs can enhance the reabsorption of water by vasopressin receptors located in the renal tubules by inhibiting prostaglandin synthesis, thereby increasing the risk of terlipressin-induced hyponatremia.…”