Application of a novel electrochemical sensor containing organo-modified sericite for the detection of low-level arsenic.

A simple cyclic voltammetry (CV) analytical method with organo-modified sericite for the working electrode was investigated to detect As(III) in an aquatic environment, and optimal conditions for the reliable measurement of trace amounts of As(III) were studied. A distinct, specific peak was clearly observed at 0.8 V due to the reduction of H3AsO4 to H3AsO3. The specific peak current of arsenic increased with increasing the concentration of As(III) and initially increased proportionally to the scan rates. However, it disappeared as the scan rate increased over 400 mV/s. Because the surface of the organo-modified sericite electrode rapidly became saturated with As(III) when the deposition time increased, an optimal deposition time was determined as 60 s. Pb(2+) had no significant influence on the peak signal of As(III), whereas it was reduced as the ratio of Cu/As increased. Considering the detection limit of arsenic (1 ppb), this system can be used to detect low levels of As(III) in water systems.

Diagnostic and Prognostic Values of Noninvasive Predictors of Portal Hypertension in Patients with Alcoholic Cirrhosis.

Portal hypertension is a direct consequence of hepatic fibrosis, and several hepatic fibrosis markers have been evaluated as a noninvasive alternative to the detection of portal hypertension and esophageal varices. In the present study, we compared the diagnostic and prognostic values of the noninvasive fibrosis markers in patients with alcoholic cirrhosis. A total of 219 consecutive alcoholic cirrhosis patients were included. Biochemical scores and liver stiffness (LS) were compared with hepatic venous pressure gradient (HVPG). For the detection of clinically significant portal hypertension (CSPH; HVPG≥10 mmHg) in compensated patients, LS and LS-spleen diameter to platelet ratio score (LSPS) showed significantly better performance with area under the curves (AUCs) of 0.85 and 0.82, respectively, than aspartate aminotransferase-to-platelet ratio index, FIB-4, Forns' index, Lok index, (platelet count)2/[monocyte fraction (%) × segmented neutrophil fraction (%)], and platelet count-to-spleen diameter ratio (all P<0.001). However, for the detection of high-risk varices, none of the non-invasive tests showed reliable performance (AUCs of all investigated tests < 0.70). During a median follow-up period of 42.6 months, 46 patients with decompensated cirrhosis died. Lok index (hazard ratio [HR], 1.13; 95% confidence interval [CI], 1.05-1.22; P = 0.001) and FIB-4 (HR, 1.06; 95% CI, 1.01-1.10; P = 0.009) were independently associated with all-cause death in decompensated patients. Among the tested noninvasive markers, only Lok index significantly improved discrimination function of MELD score in predicting overall survival. In conclusion, LS and LSPS most accurately predict CSPH in patients with compensated alcoholic cirrhosis. In the prediction of overall survival in decompensated patients, however, Lok index is an independent prognostic factor and improves the predictive performance of MELD score.

Is microsatellite instability (MSI) associated with multiplicity in early stage gastric neoplasias?

BACKGROUND/AIMS: The aim of this study was to investigate the relationship between microsatellite instability (MSI) and clinicopathologic features including multiplicity in early stage gastric neoplasias (ESGN). METHODS: From November 2004 until September 2009, 372 patients with consecutive resected gastric neoplasias were retrospectively enrolled. The gastric neoplasias were composed of 117 advanced gastric cancers (AGCs) and 255 ESGNs including 31 gastric dysplasias (including low and high grade dysplasia) and 224 early gastric cancers (EGCs). RESULTS: Based on microsatellite markers, high MSI (MSI-H) was observed in 61 cases (16.4%) and low MSI (MSI-L) in 14 cases (3.8%) of 372 cases. There was a positive correlation between the presence of MSI-H and progression of gastric adenoma to gastric tumor. We compared ESGNs with microsatellite stable (MSS; 223 cases, 87.5%) and ESGNs with MSI-H (24 cases, 9.4%). The ESGNs with MSI-H were only associated with older age and female gender. There were no association with Helicobacter pylori infection, intestinal metaplasia, and distal location in contrast with EGCs with MSI-H. Furthermore, multiplicity of ESGNs was not associated with MSI status. CONCLUSIONS: The clinicopatholgic features of MSI-H phenotype were different according to the progression of gastric neoplasias from ESGNs to AGCs. ESGNs with MSI-H were only associated with old age, female sex. In addition ESGNs with MSI-H were not associated with an increased risk of multifocal tumors.

Clinical outcomes and risk factors of rebleeding following endoscopic therapy for nonvariceal upper gastrointestinal hemorrhage.

BACKGROUND/AIMS: Rebleeding after endoscopic therapy for non-variceal upper gastrointestinal hemorrhage (NGIH) is the most important predictive factor of mortality. We evaluated the risk factors of rebleeding in patients undergoing endoscopic therapy for the NGIH. METHODS: Between January 2003 and January 2007, 554 bleeding events in 487 patients who underwent endoscopic therapy for NGIH were retrospectively enrolled. We reviewed the clinicoendoscopical characteristics of patients with rebleeding and compared them with those of patients without rebleeding. RESULTS: The incidence of rebleeding was 21.7% (n=120). In the multivariate analysis, initial hemoglobin level ≤9 g/dL (p=0.002; odds ratio [OR], 2.433), inexperienced endoscopist with less than 2 years of experience in therapeutic endoscopy (p=0.001; OR, 2.418), the need for more 15 cc of epinephrine (p=0.001; OR, 2.570), injection therapy compared to thermal and injection therapy (p=0.001; OR, 2.840), and comorbidity with chronic renal disease (p=0.004; OR, 2.908) or liver cirrhosis (p=0.010; OR, 2.870) were risk factors for rebleeding following endoscopic therapy. CONCLUSIONS: Together with patients with low hemoglobin level at presentation, chronic renal disease, liver cirrhosis, the need for more 15 cc of epinephrine, or therapy done by inexperienced endoscopist were risk factors for the development of rebleeding.

Hepatic venous pressure gradient can predict the development of hepatocellular carcinoma and hyponatremia in decompensated alcoholic cirrhosis.

OBJECTIVE: Portal hypertension is closely associated with serious complications of cirrhosis, which contribute to bad prognosis. Hepatocellular carcinoma (HCC) and low serum sodium (SNa) are manifestations of end-stage liver disease and are associated with poor survival in decompensated cirrhosis patients. We aimed to determine the relationship between hepatic venous pressure gradient (HVPG) and the development of HCC or low SNa in decompensated alcoholic cirrhosis patients. METHODS: Child-Pugh scores, Model for End-Stage Liver Disease scores, and HVPG at baseline, and the development of HCC or low SNa (SNa <130 mEq/l) during follow-up were analyzed prospectively in 170 patients with decompensated alcoholic cirrhosis from December 1999 to January 2008 (mean follow-up period of 33.9+/-27.9 months). The predictive value of different risk factors for the development of HCC and low SNa and survival were investigated. RESULTS: Twenty-four patients developed HCC during the follow-up period. In the multivariate analysis, only baseline HVPG greater than 15 mmHg was an independent predictive factor for the development of HCC (relative risk=1.128, P<0.05) and which showed a significantly shorter time for the development of HCC on the Kaplan-Meier analysis. Twenty patients developed low SNa during follow-up. Initial HVPG was also an independent predictive factor for the new development of low SNa in the multivariate analysis (relative risk=1.169, P<0.05) and which also showed significantly shorter times for the development of low SNa on the Kaplan-Meier analysis. CONCLUSION: In decompensated alcoholic cirrhosis, HVPG may be a useful predictive factor for the development of HCC and low SNa.

Angiotensin receptor blockers are superior to angiotensin-converting enzyme inhibitors in the suppression of hepatic fibrosis in a bile duct-ligated rat model.

BACKGROUND: Angiotensin blockade such as with an angiotensin II receptor blocker (ARB) or angiotensinconverting enzyme inhibitor (ACEI) has antifibrotic properties. The aim of this study was to evaluate and compare the antifibrotic effect between ARBs and ACEIs. METHODS: Common bile duct-ligated (BDL) adult Sprague-Dawley rats were allocated to five groups (each group, n = 8) as follows: G1, BDL without drug; G2, BDL + captopril 100 mg/kg per day; G3, BDL + ramipril 10 mg/kg per day; G4, BDL + losartan 10 mg/kg per day; G5, BDL + irbesartan 15 mg/kg per day. Four weeks post-BDL, hepatic fibrosis was analyzed histomorphologically using Batts and Ludwig scores. alpha-Smooth muscle actin (alpha-SMA) expression by immunohistochemical staining, hydroxyproline contents of liver tissue by spectrophotometry, and angiotensin receptor, collagen, procollagen, and transforming growth factor beta (TGF-beta) expressions were evaluated by real-time reverse transcriptase-polymerase chain reaction. Angiotensin receptor expression was also determined by Western blotting. RESULTS: Batts and Ludwig scores were 3.8, 2.6, 2.4, 1.8, and 1.6 in G1, G2, G3, G4, and G5, respectively. Histologically, ARB groups (G4, G5) showed significant suppression of hepatic fibrosis compared with ACEI groups or the control. Expressions of alpha-SMA (%) and the content of hydroxyproline (microg liver tissue) were significantly lower in ARB groups (G4, G5) than in ACEI groups (G2, G3) (P < 0.05). Also, ARB reduced the expression of angiotensin receptor, collagen, procollagen, and TGF-beta1 compared with ACEI. Western blot analysis showed that the expression of angiotensin receptor was inhibited in both ARB and ACEI groups. CONCLUSIONS: Both ARB and ACEI attenuate hepatic fibrosis through inhibiting hepatic stellate cell activation, and the inhibitory effect of ARBs on hepatic fibrosis is superior to that of ACEIs in the BDL rat model.

[Measurement of hepatic venous pressure gradient in liver cirrhosis: relationship with the status of cirrhosis, varices, and ascites in Korea].

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.