Baseline Renal Function Predicts Hyponatremia in Liver Cirrhosis Patients Treated with Terlipressin for Variceal Bleeding

Kim, Sung Eun; Jung, Dong Min; Park, Ji Won; Ju, Yeonmi; Lee, Bohyun; Kim, Hyoung Su; Suk, Ki Tae; Jang, Myoung Kuk; Park, Sang Hoon; Kang, Jun Goo; Soh, Jae Seung; Lim, Hyun; Kang, Ho Suk; Moon, Sung Hoon; Kim, ChulSik; Lee, SeongJin; Kim, Jong Hyeok; Lee, Myung Seok; Kim, Dong Joon; Ihm, Sung-Hee; Park, ChoongKee

doi:10.1155/2017/7610374

Cited by 6 publications

(5 citation statements)

References 26 publications

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“…Moreover, mild or moderate neurological symptoms resulting from hyponatraemia may simply be misdiagnosed as hepatic encephalopathy, meaning that changes in serum sodium levels can be overlooked . Normally, serum sodium levels will recover rapidly after the discontinuation of terlipressin . The serum sodium levels of the two patients returned to normal range 1 day and 4 days after the end of treatment, respectively.…”

Section: Discussionmentioning

confidence: 98%

“…However, hyponatraemia as a side effect of terlipressin has been reported in recent studies, and the incidence of hyponatraemia is not the same in different studies. Two large‐sample retrospective studies by Sola et al and by Yim et al reported that the prevalence of hyponatraemia was 67%, but the incidence of hyponatremia ranged between 35% and 54% in other randomized studies . Differences in the definitions and methods used to diagnose hyponatraemia and differences in the study populations may have led to this discrepancy.…”

Section: Discussionmentioning

confidence: 99%

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

Qing-bo

Dang

et al. 2019

J Clin Pharm Ther

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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

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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

Qing-bo

Dang

et al. 2019

J Clin Pharm Ther

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“…In 2015, Yim et al [12] found that younger age, lower Child-Pugh score, higher baseline serum sodium, and long-term use of terlipressin (>5 days) were independent risk factors for hyponatremia and that lower body mass index and Child-Pugh score and higher baseline serum sodium were independent risk factors for rapid and severe hyponatremia. In 2017, Kim et al [9] found that hepatitis B, diabetes mellitus, baseline serum sodium and creatinine levels, and shock at admission were independent risk factors for hyponatremia. Taken together, higher baseline serum sodium level and better liver function (low MELD or Child-Pugh score) are risk factors for hyponatremia during the treatment with terlipressin.…”

Section: Discussionmentioning

confidence: 99%

“…This V2 receptor-mediated antidiuretic effect may result in dilutional hyponatremia. Mild to severe hyponatremia has been reported in a proportion of patients receiving terlipressin [9][10][11][12]. More notably, scattered case reports have also shown that patients with hyponatremia related to terlipressin develop the seizure [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Serum Sodium Concentration in Patients with Portal Hypertension and Acute Gastrointestinal Bleeding Treated with Terlipressin: A Retrospective Observational Study

Zhou¹,

Shao²,

Song³

et al. 2020

Digestive System - Recent Advances

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This retrospective observational study aimed to investigate the risk of serum sodium concentration in patients treated with terlipressin and attempted to explore the factors associated with serum sodium concentration. We included 17 patients with portal hypertension treated with terlipressin (Group 1), 7 with portal hypertension treated with somatostatin/octreotide (Group 2), 20 with acute non-variceal gastrointestinal bleeding treated with somatostatin/octreotide (Group 3), and 19 with acute pancreatitis treated with somatostatin/octreotide (Group 4). In all groups, serum sodium concentration at baseline was not significantly different from the lowest value during the infusion of terlipressin, somatostatin, or octreotide (Group 1: 136.95 AE 4.68 versus 135.52 AE 4.79, p = 0.426; Group 2: 139.64 AE 3.86 versus 138.41 AE 5.34, p =0.813; Group 3: 138.02 AE 4.08 versus 137.69 AE 3.11, p = 0.630; Group 4: 135.96 AE 6.87 versus 134.60 AE 3.40, p = 0.098). The rate of serum sodium concentration reduction in Group 1 (8/17) was not significantly different from Group 2 (3/7, p =1.000),Group3 (11/20, p = 0.746), or Group 4 (14/19, p = 0.171). Age, sex, baseline MELD and Child-Pugh scores, cDDD value and duration of terlipressin, blood transfusion, and diuretics and paracentesis during terlipressin were not significantly associated with serum sodium concentration reduction in Group 1. In conclusion, serum sodium concentration is often reduced in patients treated with terlipressin. However, the association of sodium concentration reduction with terlipressin should be clarified.

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“…The rationale for using VP is the relative/absolute insufficiency in septic shock and the vasoconstriction effect mainly through V1 receptor in the vascular smooth muscle, thus restoring vascular tone, achieving a pre-determined MAP goal, and reducing the requirements of catecholamines [ 8 , 9 ]. Terlipressin (TP) is a V1-selective synthetic analog of VP, thereby decreasing the need of NE and meanwhile avoiding the side effects of V2 activation partly [ 10 ]. Selepressin, a novel pure VP V1a agonist, may benefit patients with septic shock in the coming years due to the lack of V2 activity [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Non-catecholamine vasopressors in the treatment of adult patients with septic shock—evidence from meta-analysis and trial sequential analysis of randomized clinical trials

et al. 2020

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Background Norepinephrine (NE) has currently been the first-choice vasopressor in treating septic shock despite generally insufficient for patients with refractory septic shock. The aim of this update meta-analysis was to assess the safety and efficacy of a combination of non-catecholamine vasopressors (vasopressin/pituitrin/terlipressin/selepressin/angiotensin II) and NE versus NE in managing adult septic shock patients. Methods We conducted this study of literatures published from the inception to April 30, 2020, using PubMed, Embase, and the Cochrane Library databases without language restriction. Randomized controlled trials comparing NE with non-catecholamine vasopressors among adult septic shock patients were included in this meta-analysis. Pooled effects of relative risk (RR) or standard mean difference (SMD) and corresponding 95% confidence interval (CI) were calculated using a random-effects model. Results Twenty-three studies covering 4380 participants were finally enrolled. The combined analysis of non-catecholamine vasopressors resulted in a nonsignificant reduction in 90-day/ICU/hospital mortality except for a decreased in 28-day mortality (n = 4217; RR, 0.92; 95% CI 0.86–0.99; P = 0.02). This favorable result was subsequently verified by the subgroup analyses of low risk of bias studies (RR = 0.91, 95% CI = 0.84 to 0.98; P = 0.02) and catecholamine-resistant refractory shock patients group (RR, 0.84; 95% CI = 0.70–1.00; P = 0.048). The pooled analysis of non-catecholamine vasopressors showed a 14% higher success rate of shock reversal at 6 h, a 29% decreased risk of continuous renal replacement therapy, but a 51% increased risk of hyponatremia and a 2.43 times higher risk of digital ischemia. Besides, the pooled data showed that non-catecholamine vasopressors decreased heart rate (HR) (SMD, − 0.43; 95% CI − 0.66 – − 0.19; P < 0.001), serum creatinine (− 0.15; 95% CI − 0.29 – − 0.01; P = 0.04), and the length of mechanical ventilation (MV) (− 0.19; 95% CI − 0.31 – − 0.07; P < 0.01, but there was no significant difference in other parameters. Conclusions Current pooled results suggest that the addition of NE to non-catecholamine vasopressors was associated with a marginally significant reduction in 28-day mortality. Moreover, they were able to shorten the length of MV, improved renal function, decreased HR, and increased the 6-h shock reversal success rate at the expense of increased the risk of hyponatremia and digital ischemia.

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Baseline Renal Function Predicts Hyponatremia in Liver Cirrhosis Patients Treated with Terlipressin for Variceal Bleeding

Cited by 6 publications

References 26 publications

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

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

Serum Sodium Concentration in Patients with Portal Hypertension and Acute Gastrointestinal Bleeding Treated with Terlipressin: A Retrospective Observational Study

Non-catecholamine vasopressors in the treatment of adult patients with septic shock—evidence from meta-analysis and trial sequential analysis of randomized clinical trials

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