Gadobenate dimeglumine-enhanced magnetic resonance imaging can accurately predict the severity of esophageal varices and portal vein pressure in patients with hepatitis B cirrhosis.

OBJECTIVE: To explore the effectiveness of gadobenate dimeglumine (Gd-BOPTA)-enhanced magnetic resonance imaging (MRI) in predicting portal hypertension and high-risk esophageal varices (EV) in patients with hepatitis B cirrhosis. METHODS: In total, 71 and 30 patients comprising the training and validation groups, respectively, were enrolled in the study. Univariate and multivariate analyses were performed to detect their risk of developing high-risk EV to generate a formula for scoring EV. The relationships between the relative enhancement ratio (RE) of Gd-BOPTA-enhanced MRI and portal vein pressure were explored. RESULTS: Platelet count, portal vein width and RE were identified as independent predictors of high-risk EV. Based on these parameters, the EV score model were calculated as: -6.483 + 15.612 × portal vein width + 2.251 × RE - 0.176 × platelet count. The area under the receiver operating characteristic curve was 0.903. At a cut-off value of ≤ -2.74, the negative predictive value was 94.00%, while the positive predictive value was as high as 93.80% when the cut-off was set at > 4.00. Gd-BOPTA-enhanced MRI was effective in predicting portal pressure. Its accuracy was confirmed with the validation set. CONCLUSIONS: Gd-BOPTA-enhanced MRI was successfully applied to evaluate high-risk EV and portal hypertension. These results represent an accurate, non-invasive model for detecting high-risk EV, based on which we propose a cost-effective algorithm for EV management, eliminating the need to perform an endoscopy in all patients with cirrhosis.

Hepatic venous pressure gradient is a useful predictor in guiding treatment on prevention of variceal rebleeding in cirrhosis.

BACKGROUND: The best therapy to prevent esophageal variceal (EV) rebleeding in cirrhotic patients who are non-responsive to pharmacological therapy have not been determined. AIMS: To evaluate efficacy of a strategy to assign different treatments according to hepatic vein pressure gradient (HVPG) values to prevent EV rebleeding in non-responders. METHODS: This study is a non-randomized controlled prospective study. 109 cirrhotic patients with EV bleeding who were non-responders based on two HVPG measurements were enrolled and divided two groups: 55 patients (EVL+ß-blocker group) were treated with endoscopic variceal ligation (EVL) and nonselective ß-blocker; 54 patients (HVPG-guided group) were treated with EVL and nonselective ß-blocker if HVPG ≤ 16 mmHg (low-HVPG), with percutaneous transhepatic variceal embolization (PTVE) if HVPG > 16 mmHg and ≤ 20 mmHg (medium-HVPG), or with transjugular intrahepatic portosystemic shunt (TIPS) if HVPG > 20 mmHg (high-HVPG). Patients were followed up for rebleeding and mortality. RESULTS: The mean follow-up period was 17.0 months; rebleeding was higher in the EVL+ß-blocker group than HVPG-guided group (25.5%, 9.3%, P = 0.026); 3-year probability of rebleeding in the EVL+Beta-blocker group increased with elevated levels of HVPG (12.5% vs 46.4% vs 64.9%, χ(2) = 11.551, P = 0.003), and 3-year probability of survival was no difference (96.6% vs 85.7% vs 90.9%, χ(2) = 2.638, P = 0.267). Rebleeding rate in PTVE group (7.7%) was lower than that in EVL+ß-blockergroup with medium-HVPG (35.7%), but there was no difference. Rebleeding rate in TIPS group (7.7%) was lower than that in EVL+ß-blockergroup with high-HVPG (45.5%), but there was no difference. CONCLUSIONS: HVPG measurement was useful for making decisions to select EVL and Beta-blocker, PTVE or TIPS in secondary prophylaxis. HVPG-guided treatment is feasible and effective in preventing esophageal varices rebleeding.

Risk factors for early rebleeding and mortality in acute variceal hemorrhage.

AIM: To investigate the risk factors for 6-wk rebleeding and mortality in acute variceal hemorrhage (AVH) patients treated by percutaneous transhepatic variceal embolization (PTVE). METHODS: A retrospective cohort study of AVH patients who had undergone PTVE treatment was conducted between January 2010 and December 2012. Demographic information, medical histories, physical examination findings, and laboratory test results were collected. The PTVE procedure was performed as a rescue therapy for patients who failed endoscopic and pharmacologic treatment. Survival analysis was estimated using the Kaplan-Meier method and compared using the log-rank test. The multivariate analysis was performed using the Cox regression test to identify independent risk factors for rebleeding and mortality. RESULTS: One hundred and one patients were included; 71 were males and the average age was 51 years. Twenty-one patients rebled within 6 wk. Patients with high-risk stigmata, PTVE with trunk obliteration, and a hepatic vein pressure gradient (HVPG) ≥ 20 mmHg were at increased risk for rebleeding (OR = 5.279, 95%CI: 2.782-38.454, P = 0.003; OR = 4.309, 95%CI: = 2.144-11.793, P < 0.001; and OR = 1.534, 95%CI: 1.062-2.216, P = 0.022, respectively). Thirteen patients died within 6 wk. A model for end-stage liver disease (MELD) score ≥ 18 and an HVPG ≥ 20 mmHg were associated with 6-wk mortality (OR = 2.162, 95%CI: 1.145-4.084, P = 0.017 and OR = 1.423, 95%CI: 1.222-1.657, P < 0.001, respectively). CONCLUSION: MELD score and HVPG in combination allow for early identification of patients with AVH who are at substantially increased risk of death over the short term.

Increased expression of matrix metalloproteinase-9 associated with gastric ulcer recurrence.

AIM: To compare matrix metalloproteinase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)-1 in gastric ulcer (GU) and chronic superficial gastritis (CSG). METHODS: This study enrolled 63 patients with GU and 25 patients with CSG. During upper gastroduodenal endoscopy, we took samples of gastric mucosa from the antrum and ulcer site from patients with GU, and samples of antral mucosa from patients with CSG. Mucosal biopsy tissues were cultured for 24 h, and the culture supernatant was measured for levels of MMP-9 and TIMP-1. After receiving eradication therapy for Helicobacter pylori (H. pylori) and 8 wk proton-pump inhibitor therapy for GU, follow-up endoscopy examination was performed after 6 mo and whenever severe symptoms occurred. RESULTS: Levels of MMP-9 and TIMP-1 at the ulcer site or in the antrum were significantly higher in GU than CSG patients. MMP-9 levels at the ulcer site were significantly higher than in the antrum in GU patients, and had a significantly positive correlation with TIMP-1. MMP-9 levels were significantly higher in H. pylori-positive than H. pylori-negative GU and CSG patients. Levels of MMP-9 or TIMP-1 at the ulcer site were associated with the histological severity of activity and inflammation. About 57 GU patients were followed up, and seven had GU recurrence. H. pyloriinfection and MMP-9 levels were risk factors for the recurrence of GU adjusted for age and sex by multiple logistic regression analysis. CONCLUSION: MMP-9 may perform an important function in gastric ulcer formation and recurrence.

[An improved method for the isolation of rat hepatic stellate cells].

OBJECTIVE: To present an improved method to obtain pure, viable, freshly isolated hepatic stellate cells. METHODS: Adult male SD rats were used. All procedures were performed with the animals under sodium pentobarbital anesthesia. Three days after the single intravenous administration of 1 ml liposome-encapsulated CL2MDP, which has selective cytotoxicity of Kupffer cells, livers were perfused with D-Hank's solution containing 100 U/ml heparin for 10 to 15 minutes, and then with 0.05% collagenase dissolved in D-Hank's solution for 25 to 30 minutes. The liver was then gently homogenized and further incubated in 0.025% collagenase, and 0.005% DNAase I for 30 minutes at 37 degrees C under constant stirring. This suspension was filtered through stainless steel gauze and centrifuged for 2 minutes at 50 x g to remove parenchymal cells. Sinusoidal cells in the supernatant were recovered by centrifugation for 10 minutes at 300 x g. The cells were resuspended in the presence of 28.7% Nycodenz stock solution. The final concentration of Nycodenz at this stage was 11.5%. Following centrifugation for 17 minutes at 1400 x g, The cells at the top of this Nycodenz solution were collected. Cells were resuspended in Dulbecco's modified Eagle medium supplemented with 10% fetal calf serum, The cells were seeded in 50 ml culture flask at a density of 500,000 cells/ml, The cell viability was determined by trypan blue exclusion staining, the purity of hepatic stellate cells was identified by the expression of Desmin using immunocytochemistry method. Endogenous peroxidase staining was used to detect Kupffer cells. RESULTS: The yield rate of hepatic stellate cells was 3 x 10(7) per rat, the cell viability was more than 95%, the desmin positive cell rate was 90%, no endogenous peroxidase positive cells were detected. CONCLUSION: The method for the isolation of hepatic stellate cells was developed without Kupffer cells confusion. The availability of highly purified stellate cells will facilitate the investigation of their functions in primary culture.