No abstract available.
Hepatic Veins/*physiopathology ; Humans ; Liver Cirrhosis/complications/*diagnosis ; Predictive Value of Tests ; Prognosis ; Severity of Illness Index ; Venous Pressure

Portal hypertension is a severe consequence of chronic liver diseases and is responsible for the main clinical complications of liver cirrhosis. Hepatic venous pressure gradient (HVPG) measurement is the best available method to evaluate the presence and severity of portal hypertension. Clinically significant portal hypertension is defined as an increase in HVPG to >10 mmHg. In this condition, the complications of portal hypertension might begin to appear. HVPG measurement is increasingly used in the clinical fields, and the HVPG is a robust surrogate marker in many clinical applications such as diagnosis, risk stratification, identification of patients with hepatocellular carcinoma who are candidates for liver resection, monitoring of the efficacy of medical treatment, and assessment of progression of portal hypertension. Patients who had a reduction in HVPG of > or =20% or to < or =12 mmHg in response to drug therapy are defined as responders. Responders have a markedly decreased risk of bleeding/rebleeding, ascites, and spontaneous bacterial peritonitis, which results in improved survival. This review provides clinical use of HVPG measurement in the field of liver disease.
Chronic Disease ; Hemodynamics ; Hemorrhage/etiology ; Hepatic Veins/physiology ; Humans ; Hypertension, Portal/complications ; Liver Cirrhosis/diagnosis ; Liver Diseases/complications/*physiopathology ; Portal Pressure

Portal hypertension as a consequence of liver cirrhosis is responsible for serious complications such as variceal bleeding, ascites and hepatic encephalopathy. Successful pharmacological treatment of portal hypertension can prevent the risk of the variceal bleeding, and contribute to reduce the morbidity and mortality in patients with liver cirrhosis. To identify the effect of drugs on portal hypertension, portal pressure was evaluated accurately before and after the drug administration. The hepatic venous pressure gradient has been accepted as the gold-standard method for assessing the severity of portal hypertension and the response to drug treatment. The mean hepatic venous pressure gradient was 15.1+/-5.4 mmHg in Korean cirrhotic patients who had experienced variceal bleeding. Non-selective beta blockers are the treatment of choice for primary and secondary prevention of variceal bleeding. The dose of propranolol should be subsequently adjusted until the resting heart rate had been reduced by 25% or less than 55 beats per minute. It has been reported that the optimal dose of propranolol is variable due to racial differences in cardiovascular receptor sensitivity. In Korean patients with portal hypertension and liver cirrhosis, the mean required dose of propranolol to reach target heart rate was 165 mg (range; 80-280 mg). This review covers mainly the results of the pharmacological therapy of portal hypertension in Korean cirrhotic patients.
Adrenergic beta-Antagonists/administration & dosage ; Hepatic Veins ; Humans ; Hypertension, Portal/diagnosis/*drug therapy/physiopathology ; Korea ; Liver Cirrhosis/complications/physiopathology ; Propranolol/administration & dosage ; Venous Pressure/drug effects

Blood Gas Analysis ; Echocardiography ; Hepatopulmonary Syndrome ; diagnosis ; physiopathology ; therapy ; Humans ; Hypoxia ; diagnosis ; etiology ; therapy ; Liver Cirrhosis ; complications ; Liver Transplantation ; Lung ; pathology ; physiopathology ; Oxygen ; therapeutic use ; Radiography, Thoracic ; Respiratory Function Tests

OBJECTIVETo evaluate the predictive value of portal vein flow rate preoperative for portal vein thrombosis (PVT) after periesophagastric devascularization in hepatitis B cirrhosis-related portal hypertension.

METHODSFrom January 2007 to July 2008, 45 patients with portal hypertension caused by hepatitis B cirrhosis were performed splenectomy with peri-esophagogastric devascularization in the same medical group in West China Hospital of Sichuan University. The portal vein flow rate and the diameter of portal vein were measured with doppler sonography respectively before and after the operation. At the same time, the level of PT and PLT were detected. The weight of spleens were measured after operation.

RESULTSThirteen cases suffered from PVT postoperatively. Portal vein flow rate was significantly lower in patients with PVT postoperation than that in patients without PVT (P < 0.01). In patients with PVT (n = 13) postoperation, the preoperative portal vein flow rate was (19.5 +/- 5.3) cm/s. Among the 13 cases, there were 12 cases whose flow rate were lower than 25 cm/s, and 1 case whose flow rate was 32. 3 cm/s; In patients without PVT (n = 32), the preoperative portal vein flow rate was (9.6 +/- 8.0) cm/s. In patients with lower rate (n = 17), the incidence rate of PVT was 70.6%; in patients with higher rate (n = 28), the incidence rate of PVT was 3.6%. The incidence rate of PVT in patients with lower rate was significantly lower than patients with higher rate (P < 0.01). The diameter of portal vein in patients with PVT was significantly wider than patients without PVT. The diameter of portal vein was negative correlative with the portal vein flow rate. The value 25 cm/s was of diagnostic efficiency, the sensitivity was 92.3%, and specificity was 70.6%.

CONCLUSIONSThe portal vein flow rate preoperative can be used as an early predictor of portal vein thrombosis after periesophagastric devascularization in hepatitis B cirrhosis-related portal hypertension to give a guide to clinical work.

Adult ; Aged ; Blood Flow Velocity ; Female ; Humans ; Hypertension, Portal ; etiology ; physiopathology ; surgery ; Liver Cirrhosis ; complications ; Male ; Middle Aged ; Portal Vein ; diagnostic imaging ; physiopathology ; Postoperative Complications ; diagnosis ; etiology ; Preoperative Care ; Risk Factors ; Splenectomy ; Ultrasonography ; Venous Thrombosis ; diagnosis ; etiology

OBJECTIVETo investigate the risk factors for and the prognosis of acute kidney injury (AKI) in decompensated cirrhotic patients.

METHODSA total of 126 patients with decompensated cirrhosis and with (n =60) or without (n =66, control group) AKI were enrolled in this retrospective analysis. Follow-up was carried out on all patients, with durations ranging from less than 1 year to up to 4 years. Blood biochemistry, liver and renal functional parameters and prognosis of these patients were recorded. Logistic regression analysis was used to evaluate possible risk factors for decompensated cirrhotic patients developing AKI.

RESULTSThe patients with AKI had a significantly lower survival rate than the patients without AKI (55.0% vs.83.3%, x2 =13.270, p =0.001). Unconditional multivariate logistic regression analysis identified risk factors of AKI development in decompensated cirrhotic patients as increased serum creatinine (odds ratio (OR):1034), increased total bilirubin (OR:1.005), increased international normalized ratio (INR; OR:2.471), decreased plasma sodium concentration (OR:0.910), decreased serum cholinesterase (OR:0.999), and decreased glomerular filtration rate (GFR; OR:0.972) (all P less than 0.05).

CONCLUSIONThe development of acute kidney injury represents an adverse prognosis in decompensated cirrhotic patients. An increase in serum creatinine, total bilirubin or INR or a decrease in plasma sodium concentration, serum cholinesterase or GFR may be early-warning factors of development of AKI in decompensated cirrhotic patients.

Acute Kidney Injury ; diagnosis ; etiology ; Adult ; Case-Control Studies ; Female ; Humans ; Kidney Function Tests ; Liver Cirrhosis ; complications ; physiopathology ; Male ; Middle Aged ; Prognosis ; Retrospective Studies ; Risk Factors

The survival of a recent series of 823 cirrhosis patients who were followed up for a mean of 48 months was analyzed. Cirrhosis was ascribed to alcohol (26%), hepatitis virus B (58%), hepatitis virus C (11%) or both (2%), or was cryptogenic (3%). Features of decompensation were observed in 51% of the patients at entry, and newly developed in 44% of compensated patients within 5 yr. The 5-yr survival after decompensation was 25%. The leading causes of death were liver failure (53%), hepatocellular carcinoma (HCC, 23%), and variceal bleeding (10%). Early detection of HCC significantly improved the survival of cirrhosis patients. Biannual ultrasonography increased the detection rate of small HCC. Mortality of variceal hemorrhage was much lower in patients with Child-Pugh scores from 5 to 8 than in those with scores above 8 (5% vs. 52%). Endoscopic prophylaxis significantly decreased the incidence of first variceal hemorrhage, but the effect was insufficient to improve the rate of survival. Mortality of first spontaneous bacterial peritonitis was 18%. These data suggest that the mortality of major complications of liver cirrhosis has considerably decreased during the last two decades, while there was no remarkable improvement in long-term survival. More efficient management of etiologic factors would be required.
Adult ; Aged ; Carcinoma, Hepatocellular/etiology/physiopathology ; Female ; Gastrointestinal Hemorrhage ; Human ; Korea ; Liver Cirrhosis/complications/*diagnosis/mortality/*physiopathology ; Liver Neoplasms/etiology/pathology ; Male ; Middle Aged ; Peritonitis ; Prognosis ; Retrospective Studies ; *Survival Analysis ; Survival Rate

High prevalence of diabetes mellitus in patients with liver cirrhosis has been reported in many studies. The aim of our study was to evaluate the relationship of hepatic fibrosis and steatosis assessed by transient elastography with diabetes in patients with chronic liver disease. The study population consisted of 979 chronic liver disease patients. Liver fibrosis and steatosis were assessed by liver stiffness measurement (LSM) and controlled attenuation parameter (CAP) on transient elastography. Diabetes was diagnosed in 165 (16.9%) of 979 patients. The prevalence of diabetes had significant difference among the etiologies of chronic liver disease. Higher degrees of liver fibrosis and steatosis, assessed by LSM and CAP score, showed higher prevalence of diabetes (F0/1 [14%], F2/3 [18%], F4 [31%], P<0.001; S0/1 [15%], S2 [17%], S3 [26%], P=0.021). Multivariate analysis showed that the independent predictive risk factors for diabetes were hypertension (OR, 1.98; P=0.001), LSM F4 (OR, 1.86; P=0.010), male gender (OR, 1.60; P=0.027), and age>50 yr (OR, 1.52; P=0.046). The degree of hepatic fibrosis but not steatosis assessed by transient elastography has significant relationship with the prevalence of diabetes in patients with chronic liver disease.
Causality ; Comorbidity ; Diabetes Complications/diagnosis/epidemiology/physiopathology ; Elastic Modulus ; Elasticity Imaging Techniques/methods/statistics & numerical data ; End Stage Liver Disease/*epidemiology/physiopathology/*ultrasonography ; Fatty Liver/*epidemiology/physiopathology/*ultrasonography ; Female ; Humans ; Image Interpretation, Computer-Assisted/methods ; Incidence ; Liver/physiopathology/ultrasonography ; Liver Cirrhosis/*epidemiology/physiopathology/*ultrasonography ; Male ; Middle Aged ; Reproducibility of Results ; Republic of Korea/epidemiology ; Risk Factors ; Sensitivity and Specificity

High prevalence of diabetes mellitus in patients with liver cirrhosis has been reported in many studies. The aim of our study was to evaluate the relationship of hepatic fibrosis and steatosis assessed by transient elastography with diabetes in patients with chronic liver disease. The study population consisted of 979 chronic liver disease patients. Liver fibrosis and steatosis were assessed by liver stiffness measurement (LSM) and controlled attenuation parameter (CAP) on transient elastography. Diabetes was diagnosed in 165 (16.9%) of 979 patients. The prevalence of diabetes had significant difference among the etiologies of chronic liver disease. Higher degrees of liver fibrosis and steatosis, assessed by LSM and CAP score, showed higher prevalence of diabetes (F0/1 [14%], F2/3 [18%], F4 [31%], P<0.001; S0/1 [15%], S2 [17%], S3 [26%], P=0.021). Multivariate analysis showed that the independent predictive risk factors for diabetes were hypertension (OR, 1.98; P=0.001), LSM F4 (OR, 1.86; P=0.010), male gender (OR, 1.60; P=0.027), and age>50 yr (OR, 1.52; P=0.046). The degree of hepatic fibrosis but not steatosis assessed by transient elastography has significant relationship with the prevalence of diabetes in patients with chronic liver disease.
Causality ; Comorbidity ; Diabetes Complications/diagnosis/epidemiology/physiopathology ; Elastic Modulus ; Elasticity Imaging Techniques/methods/statistics & numerical data ; End Stage Liver Disease/*epidemiology/physiopathology/*ultrasonography ; Fatty Liver/*epidemiology/physiopathology/*ultrasonography ; Female ; Humans ; Image Interpretation, Computer-Assisted/methods ; Incidence ; Liver/physiopathology/ultrasonography ; Liver Cirrhosis/*epidemiology/physiopathology/*ultrasonography ; Male ; Middle Aged ; Reproducibility of Results ; Republic of Korea/epidemiology ; Risk Factors ; Sensitivity and Specificity

BACKGROUND/AIMS: The relationships between the hepatic venous pressure gradient (HVPG) and the status of cirrhosis, complications of portal hypertension and the severity of cirrhosis are not clear. The aim of this study was to determine the relationships between HVPG and the complications or status of cirrhosis. METHODS: The HVPG, gastroesophageal varices, Child-Pugh score, Model for End-Stage Liver Disease (MELD) score, presence of ascites, recent bleeding history and the status of cirrhosis were assessed in a cohort of 172 patients (156 males, 16 females) with liver cirrhosis. RESULTS: The HVPG was 15.6+/-5.1 (mean+/-SD) mmHg (4-33 mmHg) and was significantly higher in patients in the decompensated stage than in those in the compensated stage (16.6+/-4.3 vs. 10.8+/-6.1 mmHg, respectively; P<0.01). HVPG was higher in bleeders than in nonbleeders (16.9+/-4.5 vs. 12.8+/-5.3 mmHg, respectively; P<0.01), and in patients with ascites than in those without ascites (16.4+/-4.1 vs. 14.5+/-6.2 mmHg, respectively; P<0.05). HVPG was significantly lower in the presence of gastric varices than in their absence (14.0+/-3.4 vs. 16.0+/-5.3 mmHg, respectively; P<0.05); however, no significant correlation was detected between HVPG and the grade of esophageal varices (P>0.05). HVPG was significantly higher in Child's B cirrhosis (n=87, 15.6+/-4.7 mmHg) and Child's C cirrhosis (n=36, 18.4+/-4.7 mmHg) than in Child's A cirrhosis (n=49, 13.7+/-5.1 mmHg; P<0.01). HVPG also was strongly correlated with the MELD score (P<0.01). The time required to measure the HVPG was 11.2+/-6.4 min, and only three cases of minor complication occurred during the procedure. CONCLUSIONS: HVPG was correlated with the severity of liver cirrhosis, presence of ascites, and risk of variceal bleeding in patients with liver cirrhosis.
Adult ; Ascites/*complications ; Cohort Studies ; Data Interpretation, Statistical ; Esophageal and Gastric Varices/*complications/diagnosis ; Female ; Hepatic Veins/*physiopathology ; Humans ; Hypertension, Portal/complications/*physiopathology ; Korea ; Liver Cirrhosis/complications/*diagnosis/physiopathology ; Male ; Middle Aged ; Predictive Value of Tests ; ROC Curve ; Severity of Illness Index ; Venous Pressure