Journal of Gastroenterology and Hepatology (J GASTROEN HEPATOL)

Publications in this journal

• Article: The molecular epidemiology of Hepatitis B in the Indigenous people of northern Australia

  Davies J, Littlejohn M, Locarnini S, Whiting S, Haikowicz K, Cowie BC, Bowden DS, Tong SYC, Davis JS
  Journal of Gastroenterology and Hepatology 02/2013; In press.
• Article: Spigelian hernia; an uncommon cause of longstanding intermittent abdominal pain.

  N. Mustaffa,, R. Leong,, P.H. Katelaris
  Journal of Gastroenterology and Hepatology 01/2013;
• Article: Free cholesterol (FC) loading causes both apoptosis and necrosis to murine primary hepatocytes, while FC lipotoxicity predisposes hepatocytes to free fatty acid-mediated cellular injury

  Lay Gan, Derrick M Van Rooyen, Deborah Heydet, Vanessa Barn, Geoff Farrell
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  ABSTRACT: Background Hepatic accumulation of FC but not free fatty acids (FFA) distinguishes non-alcoholic steatohepatitis (NASH) from ‘non-NASH’ pathology in non-alcoholic fatty liver disease (NAFLD) [Puri, GE ‘08]. Further, hepatic FC but not FFA or triglycerides correlates with NASH severity in foz/foz mice [van Rooyen, GE ‘11]. While saturated palmitic acid [PA]-loading of primary hepatocytes has demonstrated lipotoxicity of this FFA, there are not similar in vitro experiments to test the hypothesis that FC contributes to lipotoxicity in NASH. Aims 1. To establish a method for loading primary hepatocytes with FC, determine whether such loading activates c-Jun N-terminal kinase (JNK) and causes apoptosis and necrosis, the pathways involved in lipotoxicity; 2. To test the hypothesis that FC accumulation sensitizes hepatocytes to saturated FFA-mediated lipotoxicity in interactive cytotoxicity. Methods Primary hepatocytes isolated from C57B6 female mice were cultured and exposed to 0–40 μM low density lipoprotein (LDL) with or without 0–850 μM of PA. After 24 h, FC content was assessed by fi lipin fl uorescence and biochemical assay, viability was determined by: lactate dehydrogenase (LDH) leakage, apoptosis (Hoechst 33342) and necrosis (propidium iodide). Harvested cells and supernatant were immunoblotted for JNK activation and high-mobility-group-box-1 (HMGB1). Results We obtained a dose-dependent increase in murine hepatocyte FC incubated with LDL for 24 h, with apparent maximal content at 40 μM LDL. Increased hepatocyte FC was associated with JNK activation and release of HMGB1 into supernatant, consistent with the proposed lipotoxic role of FC in NASH. Concomitant with the increased FC content, there were signifi cant increases (p < 0.05) in LDH release, apoptosis and necrosis indices that were clearly dose-related. Exposure of hepatocytes to PA produced similar, but more attenuated, JNK activation, HMGB1 effl ux, LDH release, and increased apoptosis and necrosis. Primary hepatocytes pre-loaded with 20 μM of LDL, a dose selected for minimal direct toxicity, showed signifi cant and substantial reductions in viability, particularly increased necrosis, when exposed to increasing concentration of PA. Conversely, primary hepatocytes pre-loaded with 250 μM of PA did not appear to exhibit increased susceptibility to increasing LDL loading over the consistent increase in apoptosis and necrosis caused by the same LDL concentrations added to naive hepatocytes. Conclusion FC is directly lipotoxic to primary hepatocytes by a process associated with JNK activation and release of HMGB1. While FC stimulates apoptosis, there is even more pronounced necrosis. Further, cholesterol- laden hepatocytes are more susceptible to PA lipotoxicity. These studies are the fi rst to show FC-mediated lipotoxicity directly in hepatocytes, and reveal synergistic liver toxicity between cholesterol and FFA in which the role of FC is essential.
  Journal of Gastroenterology and Hepatology 10/2012; 27(S4):4-5.
• Article: Alcohol, insulin resistance and the liver-brain axis

  Suzanne de la Monte, Zoltan Derdak, Jack R. Wands
  Journal of Gastroenterology and Hepatology 03/2012;
• Article: Single nucleotide polymorphism at exon 7 splice acceptor site of OAS1 gene determines response of hepatitis C virus patients to interferon therapy

  Mostafa K El Awady, Mohamed A Anany, Gamal Esmat, Naglaa Zayed, Ashraf A Tabll, Amr Helmy, Abdel Rahman El Zayady, Mohga S Abdalla, Hayat M Sharada, Maissa El Raziky, Wafaa El Akel, Shadia Abdalla, Noha G Bader El Din
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  ABSTRACT: Background and Aim: Response to interferon therapy and disease progression in hepatitis C virus (HCV) infected patients differs among individuals, suggesting a possibility of a contribution of host genetic factors. 2′-5′-oligoadenylate synthetase 1 (OAS1), an important component of the innate immune system with a proven antiviral function, may therefore have a relationship with the response to interferon therapy and clinical course of HCV disease. Our aim was to determine the frequency of single nucleotide polymorphism (SNP) at exon 7 splice acceptor site (SAS) of the OAS1 gene in relation to the interferon response and status of HCV infection. Methods: A 203 bp fragment containing exon 7 SAS was amplified in 70 HCV chronic patients and 50 healthy controls. SNP was examined using restriction fragment length polymorphism (RFLP) genotyping method. Correlations of SNP genotypes with response to interferon and clinical status of patients were statistically analyzed. Results: There was an increasing trend of response from AA to AG to GG genotypes (P = 0.007). Genotype AA was associated with non-response to interferon and higher degree of liver fibrosis (P = 0.05). Multivariate analysis showed this SNP as independent and a significant determinant of the outcome of interferon therapy (odds ratio 4.913 [95% confidence interval 1.365–8.2], P = 0.006). Conclusions: This is the first study to show a significant association between the functional SNP at exon 7 SAS of OAS1 gene and the viral response to interferon in chronic HCV patients. Patients with AA genotype were associated with progressive HCV disease and viral resistance to interferon therapy. This OAS SNP is a potential bio-marker to predict IFN response in chronic hepatitis C patients. Background and Aim: Response to interferon therapy and disease progression in hepatitis C virus (HCV) infected patients differs among individuals, suggesting a possibility of a contribution of host genetic factors. 2′-5′-oligoadenylate synthetase 1 (OAS1), an important component of the innate immune system with a proven antiviral function, may therefore have a relationship with the response to interferon therapy and clinical course of HCV disease. Our aim was to determine the frequency of single nucleotide polymorphism (SNP) at exon 7 splice acceptor site (SAS) of the OAS1 gene in relation to the interferon response and status of HCV infection. Methods: A 203 bp fragment containing exon 7 SAS was amplified in 70 HCV chronic patients and 50 healthy controls. SNP was examined using restriction fragment length polymorphism (RFLP) genotyping method. Correlations of SNP genotypes with response to interferon and clinical status of patients were statistically analyzed. Results: There was an increasing trend of response from AA to AG to GG genotypes (P = 0.007). Genotype AA was associated with non-response to interferon and higher degree of liver fibrosis (P = 0.05). Multivariate analysis showed this SNP as independent and a significant determinant of the outcome of interferon therapy (odds ratio 4.913 [95% confidence interval 1.365–8.2], P = 0.006). Conclusions: This is the first study to show a significant association between the functional SNP at exon 7 SAS of OAS1 gene and the viral response to interferon in chronic HCV patients. Patients with AA genotype were associated with progressive HCV disease and viral resistance to interferon therapy. This OAS SNP is a potential bio-marker to predict IFN response in chronic hepatitis C patients.
  Journal of Gastroenterology and Hepatology 01/2011; Volume 26:pages 843–850.
• Article: Ezetimibe and atorvastatin ameliorate liver injury in foz/foz mice with NASH

  Derrick M Van Rooyen, Claire Larter, Matthew Yeh, Geoff Haigh, Narci Teoh, Geoff Farrell
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  ABSTRACT: Background We previously demonstrated that hepatic cholesterol loading increases liver injury (serum ALT, cell death, macrophage infi ltration) in high fat (HF)-fed foz/foz (Alms1 mutant) mice with NASH (JGH. 2010; 25: A5). This is associated with NF-κB and c-Jun N-terminal kinase (JNK) activation, and fi brogenesis. We have now investigated whether pharmacological inhibition of cholesterol uptake and/or biosynthesis after the onset of NASH in this model reverses liver injury and infl ammation, and examined the pathways involved. Methods Female foz/foz and WT mice were fed HF diet containing 0.2% cholesterol for 16 wk, after which atorvastatin (20 mg/kg/day, corresponding to human doses adjusted for species differences in statin metabolism) and/or ezetimibe (5 mg/kg/day) was introduced into the diet (vehicle for positive controls); mice were then fed for an additional 8 wk. We determined serum cholesterol and alanine transaminase (ALT) (clinical chemistry, TCH) and hepatic protein expression (western blot) and localisation (IHC). Liver sections stained with H&E were blinded and ranked (by MMY) according to NAFLD activity score. Sirius red-stained sections were subjected to image analysis (ImageJ, NIH, Bethesda) to quantify fi brosis. Results Atorvastatin and/or ezetimibe for 8 wk after NASH onset (at 16 wk) lowered ALT substantially (P < 0.05) vs vehicle-treated foz/foz mice, in association with reduced serum total cholesterol and HDL; liver lipid analyses are in train. Likewise, hepatomegaly was reduced while peri-ovarian adipose wt and serum adiponectin levels increased in drugtreated foz/foz mice. Hepatocellular cell death (by M30 IHC), and expression of nuclear NF-κB p65, JNK, vascular cell adhesion molecule-1 and inter-cellular adhesion molecule-1 were all suppressed in drug treated foz/ foz mice, in addition to hepatic macrophage infi ltration. Drug treatment also lowered serum monocyte chemotactic protein-1 levels in foz/foz mice. Conclusions Inhibition of intestinal/tissue cholesterol uptake/redistribution and/or biosynthesis lowers serum cholesterol and reduces liver injury and infl ammation in foz/foz mice with NASH. These fi ndings support the hypothesis that hepatic cholesterol acts as a lipotoxic mediator of profi brotic liver injury and infl ammation in experimental NASH.
  Journal of Gastroenterology and Hepatology 01/2011; 24(S4):2.
• Article: Dietary cholesterol modulates severity of liver injury in mice with metabolic-syndrome related NASH

  Derrick M Van Rooyen, Claire Larter, Matthew Yeh, Geoff Haigh, Narci Teoh, Geoff Farrell
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  ABSTRACT: Background Foz/foz mice develop metabolic syndrome and fi brotic nonalcoholic steatohepatitis (NASH) after 24 weeks on high-fat (HF)-diet. HF-fed wildtype (WT) and chow-fed foz/foz mice only develop simple steatosis. HF-fed foz/foz mice with NASH exhibit hepatic cholesterol accumulation attributable to increased hepatic uptake and decreased biotransformation and elimination of cholesterol. In the present study, we tested the hypothesis that dietary cholesterol contributes to cholesterol accumulation in foz/foz mice and thereby to NASH pathogenesis. Methods Female foz/foz and WT mice were fed HF diet (containing 0.2% cholesterol, wt/wt) or chow (0% cholesterol) for 24 weeks. Separate groups were fed HF diet with varying cholesterol content (0, 0.2 and 2.0% by wt). Gene expression (real-time PCR), protein expression (western blot) and localisation (immunohistochemistry, IHC), enzyme activity (radiometric), hepatic cholesterol and cholesteryl content (HPLC), hepatocyte cell death (M30 IHC) and infl ammatory recruitment (F4/80 IHC) were determined. Cholesterol regulation was examined in murine primary hepatocytes. Results By 24 weeks, HF-fed foz/foz mice with NASH showed signifi - cant increases in hepatic cholesterol, cholesteryl esters (~fi vefold and ~250-fold, respectively) and LDL receptor (which mediates cholesterol uptake). HMG-CoA reductase activity, the rate limiting step in cholesterol biosynthesis, as well as biotransformation genes, including cytochrome P450 7a (Cyp7a) and Cyp27a, cholesterol and bile export pathways (ABCG8, BSEP) were all down-regulated. In cultured hepatocytes, concentrations of insulin that circulate in HF-fed foz/foz mice activated both sterol regulatory element binding protein-2 (SREBP2) and LDL receptor. Reducing dietary cholesterol in HF-fed-foz/foz mice ameliorated liver injury by serum ALT, M30 and F4/80 IHC, while high (2%) cholesterol greatly accentuated liver injury (ALT: 0% cholesterol, 259 ± 37; 0.2% cholesterol, 430 ± 26; 2% cholesterol, 534 ± 58, P < 0.05). Conclusions Dietary cholesterol contributes to hepatic cholesterol accumulation in foz/foz mice with NASH, most likely attributable to increased LDL receptor-mediated uptake of dietary cholesterol with concomitant down-regulation of cholesterol biotransformation and export. Insulininduced activation of SREBP2 is a key mediator of altered hepatic cholesterol homeostasis in NASH. The substantial modulation of disease severity exerted by dietary cholesterol content provides strong, direct evidence to support our proposal that cholesterol plays an important lipotoxic role in the pathogenesis of NASH.
  Journal of Gastroenterology and Hepatology 01/2010; 25(S3):A5.
• Article: Reduced immunostaining for c-kit receptors in mucosal mast cells in inflammatory bowel disease.

  Ashkan Farhadi, Ali Keshavarzian, Jeremy Z Fields, Shriram Jakate, Maliha Shaikh, Ali Banan
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  ABSTRACT: The deleterious effects of stress in inflammatory bowel disease (IBD) have been attributed to activation of the brain-gut axis (BGA) and its end effectors, mast cells (MC). We previously showed that cold pressor stress test (CPT) results in increased activation and degranulation (but not increased proliferation) of mucosal MC, mitochondrial damage to epithelial cells and mucosal protein oxidation in both healthy controls and IBD patients. These changes are more marked in IBD patients. This increased activation of MC in IBD could be due to (i) greater activation of the BGA or (ii) inherited or acquired abnormalities in mucosal MC. In the current study we investigated the latter possibility. To assess the effects of stress on mucosal MC in patients with IBD, seven controls and 15 subjects with inactive IBD underwent 5 consecutive days of CPT to activate the BGA. Endoscopic mucosal biopsies of the distal sigmoid colon were taken during unprepared sigmoidoscopy before the first CPT and after the last CPT, and formalin-fixed samples were stained for both MC granules (MCg) and for the c-kit receptor, which is present on MC membranes (MCm). Mast cell degranulation was assessed using electron microscopy. Mast cell granule staining suggested that IBD subjects do not have a significantly different number of MC compared with controls, either before or after stress. Mast cell membrane staining, in contrast, suggested that MC c-kit immunostaining was significantly reduced - at both baseline (P = 0.01) and post stress (P = 0.04) samples - in IBD patients compared to controls. MC c-kit immunostaining was independent of stress-induced MC degranulation. There was no significant change in MC number as a result of the stress intervention using either staining method in both groups. These data support our previous report that the size of the mucosal MC population in patients with inactive IBD is not altered by disease or by stress, yet MC in IBD are different (fewer c-kit receptors) and respond differently (greater activation) than MC in control subjects. It remains to be seen whether this abnormality is an inherited or acquired one and to identify its role and mechanism in tissue injury in the pathogenesis of IBD.
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2338-43.
• Article: Consent for direct access endoscopy.

  Anthony C Clarke
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2051-2.
• Article: Education and imaging. Hepatobiliary and pancreatic: choledochal cyst.

  K K Leung, T E Yusuf
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2358.
• Article: Mechanism of impaired regeneration of fatty liver in mouse partial hepatectomy model.

  Hiroshi Murata, Takahito Yagi, Hiromi Iwagaki, Tetsuya Ogino, Hiroshi Sadamori, Hiroyoshi Matsukawa, Yuzoh Umeda, Sanae Haga, Noriaki Takaka, Michitaka Ozaki
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  ABSTRACT: The mechanism of injury in steatotic liver under pathological conditions been extensively examined. However, the mechanism of an impaired regeneration is still not well understood. The aim of this study was to analyze the mechanism of impaired regeneration of steatotic liver after partial hepatectomy (PH). db/db fatty mice and lean littermates were used for the experiments. Following 70% PH, the survival rate and recovery of liver mass were examined. Liver tissue was histologically examined and analyzed by western blotting and RT-PCR. Of 35 db/db mice, 25 died within 48 h of PH, while all of the control mice survived. Liver regeneration of surviving db/db mice was largely impaired. In db/db mice, mitosis of hepatocytes after PH was disturbed, even though proliferating cell nuclear antigen (PCNA) expression (G1 to S phase marker) in hepatocytes was equally observed in both mice groups. Interestingly, phosphorylation of Cdc2 in db/db mice was suppressed by reduced expression of Wee1 and Myt1, which phosphorylate Cdc2 in S to G2 phase. In steatotic liver, cell-cycle-related proliferative disorders occurred at mid-S phase after PCNA expression. Reduced expression of Wee1 and Myt1 kinases may therefore maintain Cdc2 in an unphosphorylated state and block cell cycle progression in mid-S phase. These kinases may be critical factors involved in the impaired liver regeneration in fatty liver.
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2173-80.
• Article: Differentiation of gastric surface mucous cells (GSM06) induced by air-liquid interface is regulated partly through mitogen-activated protein kinase pathway.

  Fumie Yokoyama, Yasuhisa Sakata, Akifumi Ootani, Takahiro Fujise, Takashi Kakimoto, Sadahiro Amemori, Ryosuke Shiraishi, Tsukasa Kuroki, Seiji Tsunada, Ryuichi Iwakiri, Kazuma Fujimoto
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  ABSTRACT: The aim of the present study was to examine the role of mitogen-activated protein (MAP) kinase pathway on gastric surface epithelium using an established cell culture model in which differentiation is promoted in GSM06 cells by air-liquid interface. A double-dish culture system of mouse gastric surface mucous cell line GSM06 in Ham's F12 medium supplemented with 10% fetal calf serum and 50 microg/mL gentamicin at 37 degrees C in a humidified atmosphere of 5% CO(2) in air was used for an air-liquid interface. Culture cells were examined on histology, cell proliferation was evaluated by bromodeoxy-uridine (BrdU) uptake, and western blot analysis of extracellular signal-regulated kinase (ERK)1/2 and phosphate ERK1/2. On day 3, U0126, an inhibitor of MAP kinase kinase (MEK), was added to medium of incubated cells. GSM06 cells were differentiated with an air-liquid interface for 3 weeks. Compared to immersion control culture, phosphorylated ERK 1/2 expression increased significantly. This increase was completely suppressed with U0126, and tall columnar cells developed by air-liquid interface in GSM06 were not observed in U0126-treated cells. Increase in BrdU uptake with air-liquid interface was suppressed by U0126. These results suggested that MAP kinase signaling, activated by air-liquid interface, was, at least in part, related to cell differentiation in GSM06 cells induced by air-liquid interface.
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2310-5.
• Article: Pilot study on the correlation of optical coherence tomography with histology in celiac disease and normal subjects.

  Enzo Masci, Benedetto Mangiavillano, Luca Albarello, Alberto Mariani, Claudio Doglioni, Pier Alberto Testoni
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  ABSTRACT: Celiac disease (CD) is a common condition but often it goes unrecognized because characteristic histopathological abnormalities must be found to confirm the diagnosis. A way is needed to select patients who need biopsy of the duodenal mucosa to detect CD. No data are currently available on the use of in vivo optical coherence tomography (OCT), during real-time endoscopic imaging, in the small intestine and, particularly, in the diagnosis of CD. The aim of the present study was to test the utility of OCT in patients undergoing esophagogastroduodenoscopy (EGD) for histological diagnosis. Eighteen patients with suspected CD (positive for antigliadin, antiendomysial and antitransglutaminase antibodies) and 22 dyspeptic subjects (negative for these antibodies) who were also examined by EGD, were prospectively enrolled. OCT scans of descending duodenum were taken during diagnostic EGD, with biopsies of the same duodenal area. OCT images and histological specimens were evaluated blindly, analysis being done independently by a gastroenterologist and a pathologist. Three patterns of intestinal villous morphology were considered (1, no atrophy; 2, mild atrophy; 3, marked atrophy). Concordance was total between OCT and histology for villi morphology in both patients and normal subjects. OCT appears to be a promising method for correctly identifying villous atrophy; it may help in selecting patients for intestinal biopsies, considering the limited usefulness of endoscopic criteria, and may also help the endoscopist to perform target biopsies in mucosal areas where the villi are damaged or absent, considering that CD often causes patchy mucosal lesions.
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2256-60.
• Article: Evaluation of solitary and scattered esophageal varices according to infrared endoscopy and endoscopic ultrasonography.

  Koji Tsujigami, Seisuke Okamura, Tamotsu Fukuda, Soichi Ichikawa, Masahiko Nakasono, Yoshio Okita, Naoki Muguruma, Susumu Ito
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  ABSTRACT: The aim of this study was to clarify the etiology and clinical significance of solitary and scattered esophageal varices by evaluating their hemodynamics and other characteristics using infrared endoscopy and endoscopic ultrasonography. The study group comprised 44 lesions of these two related types detected in 28 patients by visible-light endoscopy. Infrared endoscopy was used to characterize blue-black coloration before and after rapid intravenous injection of indocyanine green (2 mg/kg). During endoscopic ultrasonography, depth within the esophagus and echo patterns of these varices were characterized. Diameters of these varices were significantly smaller in lesions more strongly staining by infrared endoscopy. Lesion diameter was significantly smaller in varices showing homogeneous low echogenicity than in those showing mixed echogenicity. Lesions showing homogeneous high echogenicity stained most weakly followed in turn by lesions with mixed echogenicity and finally those showing homogeneous low echogenicity. Indocyanine green injection was useful for infrared observation of the hemodynamics of solitary and scattered esophageal varices, as was endoscopic ultrasonography in defining the location and morphology of these lesions. Varices with larger diameters stained more persistently when hemodynamics were evaluated by infrared endoscopy, and often showed a mixture of low and high echogenicity by endoscopic ultrasonography. These observations suggest that blood flow in the varices is slowed, and that the risk of hemorrhage increases with increased diameter especially with uniform enhancement and uniform echogenicity.
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2064-8.
• Article: Highly endemic hepatitis B infection in rural Vietnam.

  Van Thi-Thuy Nguyen, Mary-Louise McLaws, Gregory J Dore
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  ABSTRACT: Hepatitis B is a major public health problem in Vietnam; however, estimates of the prevalence of hepatitis B virus (HBV) and hepatitis delta virus (HDV), and risk factors in rural Vietnam are limited. The aim of this study was to determine HBV and HDV prevalence, and identify risk factors for HBV infection. A cross-sectional seroprevalence study was undertaken in two rural districts in Thai Binh province. The study population was randomly selected using multistage sampling. Demographic and behavioral risk information and serological samples were obtained from 837 participants. Mean age was 42.3 years +/- 15.8 (range, 16-82 years), and 50.8% were female. Prevalence of anti-HBV core antibody (anti-HBc) and hepatitis B virus surface antigen (HBsAg) was 68.2% and 19.0%, respectively, and hepatitis B e antigen HBeAg was detected in 16.4% of the HBsAg-positive group. Prevalence of HDV was 1.3% in the HBsAg-positive group. Factors associated with HBV infection (anti-HBc or HBsAg positive) were age 60 years or older (OR, 3.82; 95% CI, 1.35-10.80; P = 0.01), residence in Vu Thu district (OR, 3.00; 95% CI, 2.16-4.17; P < 0.0001), hospital admission (OR, 2.34; 95% CI, 1.33-4.13; P = 0.003) and history of acupuncture (OR, 2.01; 95% CI, 1.29-3.13; P = 0.002). Household contact with a person with liver disease (OR, 2.13; 95% CI, 1.29-3.52; P = 0.003), reuse of syringes (OR, 1.81; 95% CI, 1.25-2.62; P = 0.002) and sharing of razors (OR, 1.69; 95% CI, 1.03-2.79; P = 0.04) were independent predictors of HBsAg positivity. Alanine aminotransferase (ALT) level was elevated (>40 IU/L) in 43% of the HBsAg-positive group; proportion elevated was higher in HBeAg-positive (65%) compared with HBeAg-negative (39%) individuals in this group (P = 0.02). Hepatitis B virus infection is highly endemic in rural Vietnam. Poor infection control activities in health-care settings contribute to high HBV prevalence in this region. Universal HBV infant vaccination and improved infection control procedures are required for improved HBV control in Vietnam.
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2093-100.
• Article: Clinical application prospects of gastric pacing for treating postoperative gastric motility disorders.

  Fu-Yu Li, Li-Sheng Jiang, Jing-Qiu Cheng, Hui Mao, Ning Li, Nan-Sheng Cheng
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  ABSTRACT: Similar to the heartbeat, gastric peristalsis is regulated by an electrical rhythm generated by a pacemaker. Thus, electrical dysrhythmia of gastric slow waves will inevitably affect gastric peristalsis and emptying. The recurrence of postoperative gastroparesis is thereby closely related to the abnormalities of electrical dysrhythmia and ectopic pacemakers, resulting in postoperatively persistent gastric motility disorders in some severe cases, despite the use of prokinetic and antiemetic drugs. Recent studies have demonstrated that gastric pacing, analogous to pacing the human heart, is an attractive and promising therapy that is both feasible and safe. Gastric pacing has been shown to be strikingly effective in normalizing gastric dysrhythmia, increasing the activity of the gastric slow wave and thereby prompting gastric dynamia and emptying. Furthermore, the long-term utilization of gastric pacing can (i) relieve patients from clinical symptoms, such as nausea and vomiting; (ii) release patients with severe postoperative gastroparesis from relying on prokinetic drugs and the jejunal feeding tube; (iii) return patients to normal oral nutritional intake and provide a more satisfactory nutritional status and most importantly; and (iv) give patients a better quality of life. Overall, research focused on gastric pacing has demonstrated excellent prospects for clinical application in the treatment of postoperative gastroparesis disorders, especially for those unresponsive to prokinetic drugs.
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2055-9.
• Article: Prospective evaluation of indeterminate ERCP findings by intraductal ultrasound.

  Shyam Varadarajulu, Mohamad A Eloubeidi, C Mel Wilcox
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  ABSTRACT: Although the role of intraductal ultrasound (IDUS) in the evaluation of specific disease entities is well known, its utility in evaluating indeterminate findings in a heterogeneous group of patients undergoing endoscopic retrograde cholangiopancreatography (ERCP) is unknown. This study evaluates the diagnostic accuracy of IDUS in patients with indeterminate findings at ERCP. This was a prospective study of all patients who underwent IDUS for evaluation of an indeterminate biliary stricture or main pancreatic duct (MPD) dilation noted at ERCP over an 8-month period. The accuracy of IDUS was established based on long-term follow-up, surgery, or further investigations. Twenty-nine (5%) of 600 patients who underwent ERCP had an indeterminate finding that warranted further evaluation by IDUS: this was biliary stricture in 19 patients and MPD dilation in 10. Technical success was 100%. Mean duration of follow-up was 435 days (range 192-614 days). In patients with biliary stricture, IDUS diagnosed 11 as benign and eight as malignant. In patients with MPD dilation, IDUS diagnosed intraductal papillary mucinous tumor in six patients and chronic pancreatitis in four. Findings on IDUS supported the correct diagnosis in 27 of 29 patients (93%). In two patients with dominant hilar stricture in the setting of primary sclerosing cholangitis, IDUS was false positive in one and false negative in the other. One patient died of multiorgan failure due to post-ERCP pancreatitis. A technically easy procedure, IDUS offers unique advantages in the evaluation of patients with indeterminate findings at ERCP.
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2086-92.
• Article: Influence of Helicobacter pylori genotype on triple eradication therapy.

  Jian Jun Zhao, Jiang Bin Wang, Lei Yang, Yan Li
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  ABSTRACT: The efficiency of Helicobacter pylori eradication varies geographically, as do many parameters that might affect therapeutic efficiency. The aims of this study were to investigate the relationship between different genotypes of H. pylori and bacterium-related histopathological lesions in patients with duodenal ulcer and to determine the effect of genotype on triple eradication therapy. Helicobacter pylori infections were analyzed in 78 duodenal ulcer patients. The cytotoxin-associated gene (cagA) and vacuolating cytotoxin gene (vacA) subtype status of cultured strains were studied by PCR. Histopathological findings were graded using a described grading system. The patients were treated with triple-therapy regimens consisting of a proton pump inhibitor and two antibiotics twice daily for 7 days. Endoscopy was repeated at 4 weeks post-therapy to monitor ulcer healing and H. pylori eradication. The bacteria were genotyped from 66 patients, 57 of whom had H. pylori eradicated. The absence of cagA was associated with unsuccessful treatment. No difference was found with regard to vacA subtype between the successful and unsuccessful eradication groups. On histopathological examination, high H. pylori colonization density and intestinal metaplasia were associated with low eradication rate, while a high grade of neutrophil infiltration was associated with a significantly higher eradication rate. The data confirm the importance of cagA positivity as a predictor of successful eradication. When high H. pylori colonization density and intestinal metaplasia are present, therapy appears to be less effective. Therefore, these histopathological features may be involved in an unsuccessful therapeutic outcome.
  Journal of Gastroenterology and Hepatology 01/2008; 22(12):2251-55.