Liver cirrhosis is a major global health burden worldwide due to its high risk of morbidity and mortality. Role of terlipressin for the management of liver cirrhosis related complications has been recognized during recent years. This paper aims to develop evidence-based clinical practice guidance on the use of terlipressin for liver cirrhosis related complications. Hepatobiliary Study Group of Chinese Society of Gastroenterology of Chinese Medical Association and Hepatology Committee of Chinese Research Hospital Association have invited gastroenterologists, hepatologists, infectious disease specialists, surgeons, and clinical pharmacists to formulate the clinical practice guidance based on comprehensive literature review and experts' clinical experiences. Overall, 10 major statements regarding efficacy and safety of terlipressin in liver cirrhosis were proposed. Terlipressin can be beneficial for the management of cirrhotic patients with acute variceal bleeding and hepatorenal syndrome (HRS). However, the evidence regarding the use of terlipressin in cirrhotic patients with ascites, post-paracentesis circulatory dysfunction, and bacterial infections and in those undergoing hepatic resection and liver transplantation remains insufficient. Terlipressin-related adverse events, mainly including gastrointestinal symptoms, electrolyte disturbance, and cardiovascular and respiratory adverse events, should be closely monitored. The current clinical practice guidance supports the use of terlipressin for gastroesophageal variceal bleeding and HRS in liver cirrhosis. High-quality studies are needed to further clarify its potential effects in other liver cirrhosis related complications.
Electrolytes ; Esophageal and Gastric Varices/drug therapy* ; Gastrointestinal Hemorrhage/etiology* ; Hepatorenal Syndrome/etiology* ; Humans ; Liver Cirrhosis/drug therapy* ; Lypressin/adverse effects* ; Terlipressin/adverse effects* ; Vasoconstrictor Agents/adverse effects*

BACKGROUND/AIMS: Data on the epidemiology of alcoholic cirrhosis, especially in Asian countries, are limited. We compared the temporal evolution of patterns of alcoholic and nonalcoholic cirrhosis over the last decade. METHODS: We retrospectively examined the inpatient datasets of five referral centers during 2002 and 2011. The study included patients who were admitted due to specific complications of liver cirrhosis. We compared the causes of hospital admissions and in-hospital deaths between patients with alcoholic and nonalcoholic cirrhosis. RESULTS: Among the included 2,799 hospitalizations (2,165 patients), 1,496 (1,143 patients) were from 2002, and 1,303 (1,022 patients) were from 2011. Over time, there was a reduction in the rate of hepatic encephalopathy (HE) as a cause of hospitalization and an increase in the rate of hepatocellular carcinoma. Deaths that were attributable to HE or spontaneous bacterial peritonitis (SBP) significantly decreased, whereas those due to hepatorenal syndrome (HRS) significantly increased over time in patients with alcoholic cirrhosis. However, in patients with nonalcoholic cirrhosis, hepatic failure and HRS remained the principal causes of in-hospital death during both time periods. CONCLUSIONS: The major causes of in-hospital deaths have evolved from acute cirrhotic complications, including HE or SBP to HRS in alcoholic cirrhosis, whereas those have remained unchanged in nonalcoholic cirrhosis during the last decade.
Aged ; Asia/epidemiology ; Bacterial Infections/etiology/mortality ; Carcinoma, Hepatocellular/etiology/mortality ; Cause of Death ; Female ; Hepatic Encephalopathy/etiology/mortality ; Hepatorenal Syndrome/etiology/mortality ; Hospital Mortality/*trends ; Hospitalization/*trends ; Humans ; Liver Cirrhosis/*complications/mortality ; Liver Cirrhosis, Alcoholic/*complications/mortality ; Liver Neoplasms/etiology/mortality ; Male ; Middle Aged ; Peritonitis/microbiology/mortality ; Retrospective Studies ; Risk Factors ; Time Factors

OBJECTIVETo investigate the clinical application, indication, timing and prognosis of blood purification (artificial liver, BP) in treatment of acute liver failure in children.

METHODArtificial liver was used to treat 30 cases of pediatric acute liver failure (PALF), who were hospitalized in pediatric intensive care unit of Bayi Children's Hospital Affiliated to Beijing Military Command General Hospital, during March 2010 to July 2013. Simple plasma exchange (PE) mode was used for PALF without complications, while PE combined with continuous veno-venous hemodiafiltration (CVVHDF) mode was used for PALF with cerebral edema and/or hepatorenal syndrome and/or serious abnormality of electrolyte and acid-base balance.

RESULTSixteen cases survived and restored hepatic function, with a survival rate of 53.3%. Single PE therapy could significantly decrease total bilirubin (TBIL) from (293.96 ± 214.52) µmol/L to (155.64 ± 140.97) µmol/L (P = 0.033), increase prothrombin time activity (PTA) from (34.50 ± 18.34) % to (60.50 ± 33.97) % (P = 0.013), while it did not significantly influence ammonia from (156.43 ± 67.23) µmol/L to (124.03 ± 62.58) µmol/L (P = 0.156) and alanine transarninase (ALT) from (752.53 ± 1 291.84) U/L to (132.00 ± 98.57) U/L (P = 0.066). PE + CVVHDF therapy could significantly ameliorate TBIL from (326.90 ± 233.85) µmol/L to (157.53 ± 125.31) µmol/L (P = 0.033), ALT from (1 476.64 ± 1 728.18) U/L to (169.38 ± 207.18) U/L (P = 0.019), ammonia from (215.83 ± 83.92) µmol/L to (141.25 ± 63.09) µmol/L (P = 0.022) and PTA from (36.68 ± 23.13)% to (71.75 ± 50.50) % (P = 0.044). Prothrombin time (PT) from (29.71 ± 17.75)s to (16.27 ± 6.38)s (P = 0.008) , ALT from (1 574.11 ± 1 775.96) U/L to (145.81 ± 113.89 ) U/L (P = 0.003) , TBIL from (233.16 ± 219.70) µmol/L to (75.19 ± 86.07) µmol/L (P = 0.012) , ammonia from (182.75 ± 90.07) µmol/L to (101.81 ± 37.14) µmol/L (P = 0.002) and PTA from (38.38 ± 20.39)% to (83.13 ± 41.68)% (P = 0.001) in survived cases significantly ameliorated after BP therapy. TBIL from (394.04 ± 192.80) µmol/L to (249.34 ± 113.97) µmol/L (P = 0.023) in died cases declined significantly after BP therapy, while alteration of PT, ALT, ammonia , and PTA had no statistical significance (P > 0.10) after BP therapy.

CONCLUSIONPE + CVVHDF therapy could significantly ameliorate not only TBIL and PTA but also ammonia and ALT compared with single PE therapy. The decline of only an index like TBIL or ALT after BP therapy could not improve the prognosis. The inconsistency between serum bilirubin and ALT levels was an important factor that suggested poor prognosis of ALF, and it might increase survival rate to use BP therapy before that inconsistency emerged.

Adolescent ; Bilirubin ; blood ; Biomarkers ; blood ; Brain Edema ; etiology ; therapy ; Child ; Child, Preschool ; Female ; Hemodiafiltration ; methods ; Heparin ; pharmacology ; Hepatorenal Syndrome ; etiology ; therapy ; Humans ; Infant ; Liver Failure, Acute ; blood ; complications ; mortality ; therapy ; Liver Function Tests ; Male ; Plasma Exchange ; Prothrombin Time ; Survival Rate ; Treatment Outcome

OBJECTIVETo perform an analysis and comparative study of the clinical data for patients with cirrhosis and type 1 hepatorenal syndrome (HRS) who received treatment with terlipressin using high-or low-dose regimens.

METHODSA total of 56 patients with cirrhosis and type 1 HRS who presented for treatment to the Wuhan Medical Treatment Center and Taizhou Central Hospital between March 2010 and October 2012 were enrolled in the study. The patients were randomly assigned to the terlipressin treatment groups for receipt of the high-dose regimen (1 mg/6-8 h;n =27) or low-dose regimen (1 mg/12 h;n =29). All patients were assessed for 24-hour urine volume, serum blood urea nitrogen (BUN) and creatinine (Cr) levels, therapeutic effect and prognosis, and adverse reactions. Measurements were made before and after the treatment, and on post-treatment days 3, 7 and 14. Inter-group differences were assessed by statistical analyses.

RESULTSThe high-dose group showed an increase in 24-hour urine volumes from post-treatment day 3 (1112 ± 262 ml) to day 7 (1938 ± 312 ml), and the volumes on both days were significantly better than those of the low-dose group (day 3:986 ± 162 ml and day 7:1760 ± 300 ml, t =1.500, 1.830, P=0.038, 0.041). The high-dose group also showed a significantly better decreases in serum BUN levels (35.1 ± 8.6 to 30.2 ± 6.3 mmol/L vs.low-dose group: 43.2 ± 10.9 to 35.1 ± 7.6 mmol/L, t =3.200, 5.901, P =0.043, 0.047) and in serum Cr values (219.0 ± 35.1 to 128.2 ± 41.6 vs.low-dose group: 230.3 ± 82.1 to 151.5 ± 38.7, t =2.997, 5.765, P =0.036, 0.046).On post-treatment day 14 the 24-hour urine volume of patients in the high-dose group decreased (to 720+/-136 ml), but the difference from that of the low-dose group was not significant (vs. 620 ± 164 ml, t =1.855, P =0.069). The serum BUN level increased in the high-dose group (to 54.4 ± 15.0 mmol/L), which was statistically different from that in the low-dose group (vs .57.7 ± 17.3 mmol/L, t=5.166, P =0.022); the same trend was seen for the serum Cr value (397.8 ± 127.4 mumol/L vs. 480.3 ± 179.8 mumol/L, t =5.638, P =0.047). No statistically significant differences were observed for the groups in regard to significant efficiency, efficiency or 2-week survival rate (x2 =2.314, 1.767, 0.678, P =0.128, 0.128, 0.410 respectively), but the total efficiency was significantly different between the two groups (x² =5.793, P =0.016). In addition, no serious adverse reactions (including precordial pain, myocardial infarction or intestinal necrosis) were observed in either group.

CONCLUSIONTerlipressin therapy at both high and low dosages can lead to significant beneficial effects within as little as 3 days after the treatment; however, the high-dose appears to produce a better lasting efficacy (at day 14 after the treatment). The difference in doses does not appear to markedly affect significant efficiency, efficiency, nor the 2-week survival rate.

Adolescent ; Adult ; Aged ; Dose-Response Relationship, Drug ; Female ; Hepatorenal Syndrome ; drug therapy ; etiology ; Humans ; Liver Cirrhosis ; complications ; drug therapy ; Lypressin ; administration & dosage ; analogs & derivatives ; therapeutic use ; Male ; Middle Aged ; Retrospective Studies ; Treatment Outcome ; Young Adult

Acute Kidney Injury ; etiology ; End Stage Liver Disease ; complications ; Hepatorenal Syndrome ; etiology ; Humans

OBJECTIVETo identify the risk factors of hepatorenal syndrome in patients with hepatitis B virus (HBV)-related acute-on-chronic liver failure(ACLF).

METHODSA total of 726 hospitalized patients with HBV-ACLF were retrospectively analyzed. Data of demographic and clinical parameters (sex, age, family history, and presence of liver cirrhosis and diabetes), common complications (spontaneous bacterial peritonitis, pulmonary infection, hepatic encephalopathy, and upper gastrointestinal hemorrhage), and baseline biochemical parameters (albumin, globulin, total bilirubin, direct bilirubin, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, alkaline phosphatase, cholesterol, cholinesterase, K+, Na+, plasma thromboplastin antecedent, alpha-fetoprotein, HBV DNA, white blood cell count, hemoglobin, and platelet count) were collected from the medical records database. Univariate and multiple regression analyses were performed to determine the risk factors of hepatorenal syndrome.

RESULTSMultiple logistic regression analysis indicated that upper gastrointestinal hemorrhage [risk (R) = 1.313, relative hazard (RH) = 3.716, 95% confidence interval (CI): 2.156-6.404], hepatic encephalopathy (R = 1.120, RH = 3.065, 95% CI: 1.900-4.945), spontaneous bacterial peritonitis (R = 1.005, RH = 2.733, 95% CI: 1.379-5.417), pulmonary infection (R = 1.051, RH = 2.862, 95% CI: 1.783-4.592), and white blood cell count (R = 0.056, RH = 1.058, 95% CI: 1.010-1.107) were independent risk factors for hepatorenal syndrome development in patients with HBV-ACLF.

CONCLUSIONSeveral risk factors were significantly associated with the development of hepatorenal syndrome in HBV-ACLF, including upper gastrointestinal hemorrhage, hepatic encephalopathy, spontaneous bacterial peritonitis, pulmonary infection, and elevated white blood cell count.

Adult ; Causality ; End Stage Liver Disease ; complications ; Female ; Hepatitis B, Chronic ; complications ; Hepatorenal Syndrome ; etiology ; Humans ; Liver Failure ; complications ; etiology ; Male ; Middle Aged ; Retrospective Studies ; Risk Factors

Ascites, hepatic encephalopathy and variceal hemorrhage are three major complications of portal hypertension. The diagnostic evaluation of ascites involves an assessment of its etiology by determining the serum-ascites albumin gradient and the exclusion of spontaneous bacterial peritonitis. Ascites is primarily related to an inability to excrete an adequate amount of sodium into urine, leading to a positive sodium balance. Sodium restriction and diuretic therapy are keys of ascites control. But, with the case of refractory ascites, large volume paracentesis and transjugular portosystemic shunts are required. In hepatorenal syndrome, splanchnic vasodilatation with reduction in effective arterial volume causes intense renal vasoconstriction. Splanchnic and/or peripheral vasoconstrictors with albumin infusion, and renal replacement therapy are only bridging therapy. Liver transplantation is the only definitive modality of improving the long term prognosis.
Anti-Bacterial Agents/therapeutic use ; Ascites/complications/*diagnosis/therapy ; Bacterial Infections/*diagnosis ; Hepatic Encephalopathy/complications ; Hepatorenal Syndrome/complications/*diagnosis/therapy ; Humans ; Hypertension, Portal/*complications ; Liver Transplantation ; Peritonitis/*diagnosis/drug therapy/etiology ; Serum Albumin/administration & dosage

OBJECTIVETo analyze the relationship between hepatorenal syndrome (HRS) and plasma ammonia.

METHODSPlasma ammonia, liver and renal function of 465 patients with liver cirrhosis in our hospital, from June 2007 to March 2009, were analyzed. 80 renal dysfunction patients and 80 healthy controls were recruited in the control group. In addition, 40 patients with HRS were followed up.

RESULTSUsing urea as the diagnosis standard of HRS, the morbidity rate of HRS was 39.6%, which was higher than that using creatinine as the diagnosis standard of HRS (Chi-square test = 97.33, P less than 0.01). using urea and creatinine as the diagnosis standard of HRS, the ammonia level of HRS groups was (57.39+/-48.83)mumol/L, (64.80+/-47.25)mumol/L, which were higher than that in the non-HRS groups (t = -3.07, t = -3.67, P less than 0.01). The ammonia level of patients with renal dysfunction was (26.59+/-14.34)mumol/L, which was lower than that in HRS group, non-HRS group (P less than 0.01), but there was no statistical significance between the patients with renal dysfunction and the healthy peoples [(22.36+/-8.72)mumol/L] (t = 1.52, P more than 0.05). The followed-up analysis of 40 patients with HRS indicated that plasma ammonia level was positively correlated with urea and creatinine, and correlation coefficients were 0.874 and 0.834 (P less than 0.05).

CONCLUSIONHepatic encephalopathy is liver-kidney-intestine-brain syndrome. HRS plays an important role in the development of hepatic encephalopathy.

Adult ; Aged ; Ammonia ; blood ; Biomarkers ; blood ; Blood Urea Nitrogen ; Case-Control Studies ; Creatinine ; blood ; Female ; Hepatic Encephalopathy ; etiology ; prevention & control ; Hepatorenal Syndrome ; blood ; diagnosis ; epidemiology ; Humans ; Liver Cirrhosis ; blood ; complications ; Liver Function Tests ; Male ; Middle Aged ; Retrospective Studies

Liver cirrhosis represents the final common pathway of virtually all chronic liver diseases, and is characterized by an accumulation of extracellular matrix rich in fibrillar collagens. Patients with cirrhosis are at risk of developing many potential complications. The most common complication seen in patients with liver cirrhosis is ascites, and the most lethal one is bleeding varices. Other intermediate and late stage complications include spontaneous bacterial peritonitis, hepatic encephalopathy, and hepatorenal syndrome. The mortality and morbidity attributable to liver disease in Korea have decreased continuously over the past decades, probably due to the implementation of universal vaccination and potent antiviral therapies. In addition, recent advances in the understanding of the pathophysiology of cirrhosis and in various management approaches to cirrhosis complications will contribute to the steady improvement in patient outcomes in this country. This review article outlines recent changes in etiologies and prognosis, and the advances in management of cirrhosis in Korea.
Ascites/etiology ; Esophageal and Gastric Varices/etiology ; Gastrointestinal Hemorrhage/etiology ; Hepatic Encephalopathy/etiology ; Hepatorenal Syndrome/etiology ; Humans ; Hypertension, Portal/etiology ; Korea/epidemiology ; *Liver Cirrhosis/complications/epidemiology/therapy ; Peritonitis/etiology ; Prognosis ; Risk Factors

Liver cirrhosis represents the final common pathway of virtually all chronic liver diseases, and is characterized by an accumulation of extracellular matrix rich in fibrillar collagens. Patients with cirrhosis are at risk of developing many potential complications. The most common complication seen in patients with liver cirrhosis is ascites, and the most lethal one is bleeding varices. Other intermediate and late stage complications include spontaneous bacterial peritonitis, hepatic encephalopathy, and hepatorenal syndrome. The mortality and morbidity attributable to liver disease in Korea have decreased continuously over the past decades, probably due to the implementation of universal vaccination and potent antiviral therapies. In addition, recent advances in the understanding of the pathophysiology of cirrhosis and in various management approaches to cirrhosis complications will contribute to the steady improvement in patient outcomes in this country. This review article outlines recent changes in etiologies and prognosis, and the advances in management of cirrhosis in Korea.
Ascites/etiology ; Esophageal and Gastric Varices/etiology ; Gastrointestinal Hemorrhage/etiology ; Hepatic Encephalopathy/etiology ; Hepatorenal Syndrome/etiology ; Humans ; Hypertension, Portal/etiology ; Korea/epidemiology ; *Liver Cirrhosis/complications/epidemiology/therapy ; Peritonitis/etiology ; Prognosis ; Risk Factors