bluuebunny/crossref_metadata_2025 huggingface dataset:
Does Helicobacter pylori infection affect gastric emptying in patients with functional dyspepsia?
Authors: GOH KL , PARAMSOTHY M , AZIAN M , PARASAKTHI N , PEH SC , BUX S , LO YL , ONG KK
Published: March 2008

The objectives of the study were first, to determine if gastric emptying was altered in patients with functional dyspepsia with and without Helicobacter pylori infection compared with normal healthy volunteers; and second, to determine if there were further alterations in gastric emptying when the infection was eradicated. Gastric emptying was measured using a 99mtechnetium radiolabelled solid meal and gastric emptying time was measured as t1/2, viz. time taken for half the radiolabelled meal to be emptied from the stomach. The mean gastric emptying time for H. pylori‐positive patients (n= 20) was 56.4±24.8 min; H. pylori‐negative patients (n= 19) 67.8±31.8 min; and normal controls (n= 20) 58.8 ± 18.8 min. No significant difference was obtained between the groups (ANOVA; P= 0.348). Thirteen of 18 H. pylori‐positive patients successfully eradicated the infection following treatment with omeprazole 40 mg o.m. and amoxycillin 500 mg t.d.s. for 2 weeks. The mean difference in the gastric emptying time before and H. pylori eradication was 23.9 + 13.2 min (P= 0.556). There was no significant difference in the frequency of specific dyspeptic symptoms as well as the overall mean symptom score between the H. pylori‐positive and ‐negative patients. Gastric emptying was not different between patients with functional dyspepsia and normal controls. Helicobacter pylori infection does not appear to affect gastric emptying in patients with functional dyspepsia.
Mesenteric and portal venous obstruction associated with primary antiphospholipid antibody syndrome
Authors: LEE HEON JU , PARK JONG WON , CHANG JAE CHUN
Published: March 2008

A 58‐year‐old Korean man who had a past history of appendicitis, superior mesenteric vein thrombosis and intestinal obstruction presented 7 years later suffering from colicky right upper quadrant pain, epigastric discomfort after fatty meals, nausea and vomiting. He was found to have thrombosis of the superior mesenteric and portal veins, portal hypertension with oesophageal varices, cholangitis, and a biliary stone. The serum anti‐cardiolipin antibody (aCL) titres were 103 immunoglobulin (Ig)G antiphospholipid units (GPL) and 50 IgM antiphospholipid units (MPL) and the aCL‐IgG titre was still high at 106 2 years after the initial diagnosis. No evidence of disease states known to be associated with antiphospholipid antibodies was found. We report a patient with mesenteric and portal venous obstruction associated with the primary antiphospholipid syndrome (APS).
REVIEW: Present and future directions in the treatment of chronic hepatitis B infection
Authors: NICOLL AMANDA , LOCARNINI STEPHEN
Published: March 2008

The last decade has witnessed substantial progress in the development of chemotherapeutic agents for chronic hepatitis B. However, the only currently licensed treatment in Australia, interferonalpha, has low initial response rates and the adverse effects are often unacceptable. Of the newer agents in the class of nucleoside analogues, famciclovir and lamivudine are in phase III clinical trials with encouraging preliminary results, while other agents, such as bis‐POM PMEA (Adefovir), are at phase I/II development. Future approaches to therapy will be governed by an understanding of the effects of nucleoside analogues on the natural history of the disease as well as on the hepatitis B virus‐hepatocyte interaction. Combination antiviral therapy should theoretically offer improved response rates, decrease the development of viral resistance, and provide the greatest reduction in viral load, but it has not yet been widely examined in the clinical setting. In this article, we review the currently available strategies, discuss potential problem areas, and speculate on promising approaches with combination chemotherapy and the features of agents soon to be trialed.
Endoscopic management of acute calculous cholangitis
Authors: SHARMA BC , AGARWAL DK , BAIJAL SS , SARASWAT VA , CHOUDHURI G , NAIK SR
Published: March 2008

Acute cholangitis is associated with significant morbidity and mortality. Endoscopic drainage procedures have been shown to be a safe and effective mode of treatment in acute cholangitis. As there is paucity of large series on endoscopic management of acute cholangitis, a study was performed to evaluate safety and efficiency of endoscopic biliary decompression in acute cholangitis. The study included 89 consecutive patients (mean age 55 ± 15 years; range 35–70 years; 50 males) with acute cholangitis requiring biliary drainage. Main presenting features were upper abdominal pain (84%), fever with chills (90%) and jaundice (74%). Altered sensorium, hypotension, features of peritonitis and acute renal failure were present in 15, 11, 18 and 5%, respectively. Endoscopic procedures performed were endoscopic sphincterotomy (ES) with stone extraction (n= 40); ES with endoscopic nasobiliary drainage (ENBD; n= 30); ENBD without ES (n= 8); and ES with stent placement (n= 11). Of the 89 patients, 85 (95%) responded within 48–72 h. Endoscopic common duct clearance could be achieved in 58 of 78 (74%) patients, whereas in 11 patients undergoing stent placement, stone extraction was not attempted. Complications included post‐sphincterotomy bleed (n= 2), retroduodenal perforation (n= 1) and acute pancreatitis (n= 1) with an overall complication rate of 4.4%. All the complications were seen in patients undergoing ES with stone extraction. Mortality was 3.3%. In conclusion, endoscopic biliary drainage is a safe and effective mode of treatment for acute cholangitis. Endoscopic nasobiliary drainage or stent placement is safer than ES in acute cholangitis as an initial step.
Risk factors and the effect of interferon therapy in the development of hepatocellular carcinoma: A multivariate analysis in 343 patients
Authors: KUWANA KENJI , ICHIDA TAKAFUMI , KAMIMURA TOMOTERU , OHKOSHI SHOWGO , OGATA NORIO , HARADA TAKESHI , ENDOH KAZUO , ASAKURA HITOSHI
Published: March 2008

The aims of the present study were to clarify the risk factors for the development of hepatocellular carcinoma (HCC) in chronic hepatitis C virus (HCV) infection and to investigate the effectiveness of interferon (IFN) therapy. We retrospectively studied 343 patients who had been admitted to our hospital; 161 with chronic hepatitis, 49 with liver cirrhosis, 42 with chronic hepatitis bearing HCC and 91 with liver cirrhosis bearing HCC. The mean (±SD) observation period was 41.6 ± 31.1 months. The mean age of HCC and non‐HCC patients was 63.5 ± 7.6 and 56.9 ±12.5 years, respectively (P< 0.001). The HCV genotype II (1b) was the most prevalent genotype (92.5%) in HCC patients and the mean age was highest among patients with this genotype (63.6 ± 7.7 years). Multivariate analysis identified age (P< 0.001), the male gender (P<0.01), HCV genotype II (1b) (P<0.05) and excessive alcohol intake (P<0.05) as independent factors associated with the development of HCC. There was no relationship between the development of HCC and serum HCV levels as quantified by branched DNA assay or competitive reverse transcription polymerase chain reaction. The incidence of HCC in patients who had not received IFN therapy was 10.4/100 person‐year, while that of patients who had received IFN therapy was 1.2/100 person‐year (P<0.01) by the person‐year method. The low incidence of HCC in patients treated with IFN suggests that IFN may prevent the development of HCC.
CASE REPORT: Haemothorax due to hepatocellular carcinoma rupture successfully controlled by transcatheter arterial embolization
Authors: MASUMOTO AKIHIDE , MOTOMURA KENTA , UCHIMURA KOUTARO , MOROTOMI IKUO , MORITA KAZUNORI
Published: March 2008

A 64‐year‐old man was admitted to our hospital with multiple hepatocellular carcinoma (HCC) lesions in the liver and lung. On the seventh hospital day, a chest radiograph showed a marked increase in right pleural effusion. A thoracentesis revealed a haemothorax. Despite repeated pleural taps and blood transfusions, the patient's clinical status worsened and he developed severe dyspnoea. An inferior phrenic arteriography on the 19th hospital day showed a tumour growing over the diaphragm into the right thoracic cavity, suggesting a tumour rupture. A transcatheter arterial embolization (TAE) of the inferior phrenic artery successfully controlled the bleeding and improved the haemothorax. There was no rebleeding; however, the patient died of advanced HCC 3 months later. To our knowledge, this is the first case of a haemothorax secondary to a ruptured HCC that was treated successfully with TAE.
Relationship between hepatic blood flow, liver tests, haemodynamic values and clinical characteristics in patients with chronic liver disease*
Authors: GADANO ADRIÁN , HADENGUE ANTOINE , VACHIERY FLORENCE , MOREAU RICHARD , SOGNI PHILIPPE , SOUPISON THIERRY , YANG SONG , CAILMAIL STÉPHANE , LEBREC DIDIER
Published: March 2008

Although hepatic blood flow (HBF) has been measured in patients with liver disease for many years, the results of these studies have not provided clear information concerning the usefulness of this measurement. Hepatic blood flow was measured in 392 patients with either cirrhosis (n= 356) or hepatic fibrosis (n= 36). The control group included 59 subjects with normal liver architecture. Hepatic clearance of indocyanine green (ICG) was markedly reduced in patients with cirrhosis and hepatic fibrosis compared with controls (182±5, 276±22 and 421±25 mL/min, respectively). In patients with cirrhosis, ICG clearance and extraction were significantly correlated, but were not correlated to HBF. Although HBF did not differ between patients with cirrhosis and controls (1.26±0.04 vs 1.35±0.07 L/min, respectively), patients with hepatic fibrosis had lower HBF (1.04±0.07 L/min; P< 0.05). In patients with cirrhosis, no correlation was observed between HBF and cardiac output, mean arterial pressure, azygos blood flow, the hepatic venous pressure gradient or Pugh's score. However, a significant difference in HBF was observed in patients with and without hepatic encephalopathy (1.00±0.09 vs 1.28±0.03 L/min, respectively; P<0.05). In conclusion, the present study shows that, in patients with cirrhosis, HBF is normal and is not related to other haemodynamic values or liver tests. These results discourage the measurement of HBF in the evaluation of patients with cirrhosis.
Immunohistochemical evidence of insulin‐like growth factor II in human small hepatocellular carcinoma with hepatitis C virus infection: Relationship to fatty change in carcinoma cells
Authors: SOHDA TETSURO , KAMIMURA SEIICHIRO , IWATA KAORU , SHIJO HIROSHI , OKUMURA MAKOTO
Published: March 2008

It has recently been reported that insulin‐like growth factor II (IGF‐II) may play a role in the pathogenesis of hepatocellular carcinoma (HCC). We studied the relationship between the expression of IGF‐II and fatty change in human small HCC using immunohistochemical staining techniques. Liver biopsy specimens were obtained from 35 patients with HCC (consisting of 15 patients with fatty change and 20 patients without fatty change). All patients had serum markers for the hepatitis C virus (HCV) and histological findings obtained from non‐tumourous lesions showed liver cirrhosis or chronic active hepatitis. Immunohistochemical staining was performed using a monoclonal antibody against rat IGF‐II. A positive immunoreaction was found in 69% (24/35) of HCC. Insulin‐like growth factor II was immunodetected in 80% (12/15) of HCC with fatty change but only in 60% (12/20) of those without fatty change. In most cases, IGF‐II was not found in hepatocytes from non‐tumourous lesions. We believe this to be the first time that IGF‐II has been detected immunohistochemically in small HCC derived from HCV infection. This growth factor was more frequently immunodetected in HCC with fatty change than without. As insulin is an essential factor for the metabolism of fatty acids, IGF‐II may play an important role in both fatty degeneration and in the proliferation of HCC cells. Furthermore, immunohistochemical IGF‐II staining may contribute to the diagnosis of HCC, particularly in early stages accompanied by fatty change.
Nitric oxide synthase in neurons of the human gall‐bladder and its colocalization with neuropeptides
Authors: UEMURA SADASHIGE , POMPOLO SUELI , FURNESS JOHN B , HARDY KENNETH J
Published: March 2008

The distributions of nerve cells and fibres that are immunoreactive for nitric oxide synthase (NOS) have been investigated in the human gall‐bladder. In addition, the colocalization of NOS immunoreactivity (IR) with neuropeptide Y (NPY), pituitary adenylyl cyclase activating peptide (PACAP), somatostatin (SOM), substance P (SP), tyrosine hydroxylase (TH) and vasoactive intestinal peptide (VIP)‐IR was determined. Nitric oxide synthase‐IR nerve cell bodies comprised 13 and 30% of nerve cells in ganglia of the fibromuscular and subepithelial layers, respectively. To determine these percentages, neuron‐specific enolase‐IR was used as a marker for all nerve cells. Although SOM‐ and VIP‐IR nerve cell bodies were found in both ganglia, they rarely contained NOS‐IR. In the fibromuscular layer, NOS‐IR nerve fibres were abundant and most PACAP‐, SOM‐ and VIP‐IR fibres and many NPY‐IR fibres were also NOS positive. No colocalization was observed between NOS‐ and SP‐ or TH‐IR. In the mucosal layer, moderate numbers of NOS‐IR fibres were found and the degree of colocalization of NOS‐IR with each of NPY‐, PACAP‐, SOM‐, SP‐ and VIP‐IR were as follows: PACAP and NPY > VIP > SOM and SP. Nitric oxide synthase and TH were not colocalized in mucosal fibres. These results suggest that nerve fibres in the fibromuscular layer in the human gall‐bladder with the chemical coding NOS/NPY/PACAP/SOM/VIP are axons of inhibitory motor neurons. Nitric oxide synthase‐IR fibres in the mucosal layer that contained NPY, PACAP, SOM, SP and VIP with various degrees of colocalization probably contribute to the control of epithelial secretion or absorption.
REVIEW: Nutritional support for patients with cirrhosis
Authors: FAN ST
Published: March 2008

Nutritional support is indicated when cirrhotic patients undergo surgery becasue they are malnourished, hypercatabolic and immunocompromised. However, the choice of nutrient may be problematic as the liver itself is the central organ of protein, fat and glucose metabolism. Branched chain amino acid‐enriched solution may be the choice of protein source, as it is anticatabolic and it stimulates liver regeneration. Excessive glucose is undesirable as it may suppress endogenous fat utilization, which may be the preferred pathway of metabolism after hepatectomy. Medium chain triglycerides are preferred to long chain triglycerides as they are readily utilized and are not deposited in the liver; however, the tendency of cirrhotic patients to accumulate free fatty acids and glycerol after infusion of triglycerides dictates their use intermittently. Clinical studies have shown that perioperative nutritional support is beneficial in cirrhotic patients undergoing major hepatectomy or liver transplantation. The judicious choice of nutrient, care of the catheter and a limitation of the fluid infused are all prerequisites for the efficient use of perioperative nutritional support, which is complementary to a technically perfect operation.
CASE REPORT: Cytomegalovirus infection as a cause of acute portal vein thrombosis
Authors: INACIO CRISTINA , HILLAIRE SOPHIE , VALLA DOMINIQUE , DENNINGER MARIE‐HÉLÈNE , CASADEVALL NICOLE , ERLINGER SERGE
Published: March 2008

We report on the case of a 31‐year‐old woman who developed acute portal vein thrombosis during the course of an acute cytomegalovirus (CMV) infection. We suggest a relationship between CMV infection, its endothelial cell‐damaging effects and portal vein thrombosis.
Cytoprotective effect of epidermal growth factor on acid‐ and pepsininduced damage to rat gastric epithelial cells: Roles of Na+/H+ exchangers
Authors: FURUKAWA O , OKABE S
Published: March 2008

We have previously established a cell damage model, with damage induced by either acid or pepsin treatment for 30 min, involving a rat gastric epithelial cell line (RGM1). In the present study, pretreatment of cells with epidermal growth factor (EGF; 0.1–10ng/mL) or sucralfate (0.1–3 mg/mL) for 4 h prevented such cell damage in a concentration‐dependent manner. Protection of cells by these drugs was not affected by pretreatment with indomethacin (10−5 mol/L) for 4 h. Removal of Na−, but not Ca2+, from the acidified medium totally abolished the inhibitory effect of EGF, but not that of sucralfate. Genistein (a tyrosine kinase inhibitor) apparently reduced the inhibitory effect of EGF. DNA synthesis by RGM1 cells did not increase when cells were incubated with EGF for 4 h. We conclude that both EGF and sucralfate protect RGM1 cells from acid‐ and pepsin‐induced damage and that the mechanism of protection by EGF against acid‐induced damage seems to be via activation of Na+/H+ exchangers.
Analysis of pathogenic elements involved in gastric lesions induced by non‐steroidal anti‐inflammatory drugs in rats
Authors: TAKEUCHI K , KATO S , NISHIWAKI H , HIRATA T
Published: March 2008

Pathogenesis of gastric damage induced by non‐steroidal anti‐inflammatory drugs (NSAID) involves multiple elements, such as deficiency of prostaglandins (PG), gastric hypermotility, neutrophil activation and luminal acid. The present study was performed to examine the effects of these elements, either alone or in combination, on the rat gastric mucosa and investigate which element is most closely associated with the gastric ulcerogenic response to NSAID. The following treatments were used to express various pathogenic elements: (i) a low dose of indomethacin (IM) to cause PG deficiency; (ii) 2‐deoxy‐D‐glucose (2DG) to induce gastric hypermotility and acid secretion; (iii) histamine to induce acid hypersecretion; and (iv) n‐formyl‐Met‐Leu‐Phe (fMLP) to elicit neutrophil activation. When rats fasted for 18 h were subjected to each treatment alone, only 2DG caused slight macroscopic damage in the gastric mucosa within 4 h. Indomethacin showed over 90% inhibition of mucosal PG generation and fMLP increased myeloperoxidase activity four‐fold greater than normal values, yet either of these treatments alone did not cause any damage in the stomach. However, the combination of IM with 2DG or His provoked severe lesions in the stomach or the duodenum, respectively, while fMLP did not modify or potentiate the mucosal ulcerogenic response to other treatments. We conclude that among various pathogenic elements only gastric hypermotility is sufficient, by itself, to induce mild damage in the mucosa, that PG deficiency may be critical in the increase of mucosal susceptibility to injury and that neutrophil activation alone is not ulcerogenic in the gastric mucosa nor does it potentiate the ulcerogenic effect of other elements. Luminal acid may be a prerequisite for later extension of damage to severe lesions.
Analysis of interleukin‐8 secretion induced by Helicobacter pylori from the gastric epithelial cell line MKN45: A mechanism independent of the intensity of cytotoxicity
Authors: TAKAGI ATSUSHI , KAMIYA SHIGERU , KOGA YASUHIRO , OHTA UKI , KOBAYASHI HIROHISA , SHIRAI TAKAYUKI , HARASAWA SHIGERU , MIWA TAKESHI
Published: March 2008

Interleukin (IL)‐8, a potent chemoattractant and activator of neutrophils, has been implicated to have a major role in the pathogenesis of gastric mucosal injury by Helicobacter pylori infection. We examined the relationship between cytotoxicity and IL‐8 secretion induced by H. pylori. Furthermore, whether the vacuolating cytotoxin of H. pylori mediates IL‐8 secretion from gastric epithelial cell lines was examined. Among the inflammatory cytokines, messages for IL‐6, IL‐8 and transforming growth factor‐β1 were produced by gastric cancer (MKN45) cells in response to exposure to the cytotoxic strain of H. pylori. MKN45 incubated with the viable cytotoxic strain of H. pylori. secreted IL‐8. In contrast, the supernatant of neither the cytotoxic nor the non‐cytotoxic strain induced IL‐8 secretion. There was no correlation between IL‐8 secretion and the intensity of cytotoxicity. In conclusion, these findings suggest that IL‐8 secretion from MKN45 induced by H. pylori is mediated by factors other than cytotoxicity.
Effect of ageing on pancreatic hyperplasia after 90% proximal small bowel resection
Authors: SASAKI MASAYA , SAKAMOTO KENICHIRO , FUJIYAMA YOSHIHIDE , BAMBA TADAO
Published: March 2008

The present study was performed to examine the effect of ageing on pancreatic hyperplasia observed after proximal small bowel resection (PSBR). Young and old Wistar rats were randomly assigned to two groups, which underwent either an approximate 90% PSBR or a jejunal and ileal transection (TRC). One week after the operation, the pancreatic wet weight and the protein, DNA and RNA content of the pancreas were all significantly higher in young PSBR rats than in young TRC rats. However, no differences were seen in the old rat groups. Plasma enteroglucagon levels were elevated in both young and old PSBR rats, but the ratio of increase between the PSBR and TRC groups was significantly higher in young rats. Plasma cholecystokinin and gastrin levels did not increase after PSBR in either the young or old rats. These findings suggest that pancreatic hyperplasia observed after PSBR is attenuated by ageing, probably due to an insufficient increase in plasma enteroglucagon levels.
CASE REPORT: Right‐sided periadrenal metastasis supplied by the hepatic artery. Clue to the genesis of pedunculated hepatocellular carcinoma
Authors: IWAMOTO SHOZO , OKUDA KUNIO , TAKEDA NARIAKI , SONODA KOSHI , SANEFUJI HAYATO
Published: March 2008

The adrenal is the second most common site of haematogenous metastasis of hepatocellular carcinoma (HCC). The right adrenal is much more frequently affected than the left, but no reason has been offered for this difference. An aetiological connection has never been suggested between adrenal metastasis and pedunculated HCC. Hepatocellular carcinoma was resected in two patients who subsequently developed right‐sided adrenal metastasis diagnosed by imaging. The adrenal mass was enhanced by hepatic arteriography and took up lipiodol injected into the hepatic artery. Reoperation was performed to remove the adrenal mass, which was abutting on the liver but was readily separable. Histopathologically, the adrenal gland was compressed by a metastatic HCC that developed in the immediate periadrenal tissue or adrenal capsule. By conventional imaging, the adrenal gland could not be recognized and the mass was thought to have arisen within the adrenal gland. In conclusion, periadrenal growth of HCC is a hitherto unrecognized type of metastasis and must have been mistaken either for an adrenal metastasis or a pedunculated HCC in the past. If left unresected, it would have fused with the liver and grown into a pedunculated HCC. Cancer cell invasion through an adreno‐hepatic fusion is the most likely mode of periadrenal metastasis; it explains the arterial communication between the mass and the liver.
Review: Barrett's Oesophagus in Taiwan
Authors: CHEN PAO‐HUEI
Published: March 2008

Barrett's oesophagus is the eponym applied to the columnar epithelium‐lined lower oesophagus which is acquired as a complication of chronic gastro‐oesophageal reflux (GER). Various complications seen in the Barrett's oesophagus, such as peptic ulcer, stricture, adenocarcinoma are named as Barrett's ulcer, Barrett's stricture and Barrett's carcinoma, respectively. It is now generally accepted that Barrett's oesophagus is an acquired condition resulting from chronic repetitive GER. The frequency of Barrett's oesophagus seems to be higher in Caucasian than in Oriental or Negro populations. There is a tendency towards increasing prevalence rates all over the world, including Taiwan, due to the Westernization of diet, rapid growth in the elderly population, obesity etc. Almost 6% of the patients who manifest heartburn in GI clinics in Taiwan now suffer from GER, which is almost similar to the 7% reported by Nabel, (USA) in 1976. During the last 30 years, the incidence of esophageal adenocarcinoma has increased rapidly. Patients with Barrett's oesophagus have an increased risk of developing oesophageal adenocarcinoma and should be kept under surveillance. Regular follow‐up, at least twice a year or preferably, every 2–3 months, for those patients with SCE using endoscopic surveillance and biopsy for those with severe dysphasia (oesophageal columnar intraepithelial neoplasia) in the surrounding area to detect Barrett's oesophagus cancer, is very important.
Peptic ulcer disease in the 1990s: An Asian perspective
Authors: FOCK KWONG MING
Published: March 2008

Peptic ulcer disease is still a common disease in many parts of Asia, although it is less common today than it was 2–3 decades ago. Contrary to this general trend, peptic ulcers are on the rise in the elderly, particularly elderly females. Two important factors that could explain the observed changes in the trends of peptic ulcer disease are: Helicobacter pylori and NSAID. The seroprevalence of H. pylori, determined in three previous studies, would appear to have decreased over the last few decades, while NSAID and aspirin are used increasingly for arthritis, cerebrovascular disease and coronary artery disease. The major complication of peptic ulcer disease is gastrointestinal haemorrhage and in the 1990s endoscopic haemostatic therapy has replaced surgery as the treatment of choice. Treatment of peptic ulcer disease caused by H. pylori is directed at eradication of H. pylori itself; four classes of drug regimens are currently available for this. Antibiotic resistance, particularly metronidazole resistance, is an important factor that determines the outcome of therapy. Metronidazole resistance is reported to be present in 50% of all strains of H. pylori in Hong Kong and Singapore, and is present in 80–90% of all strains in India. Eradication rates in Asia, may for this reason, differ from those in the West, if the regimen contains metronidazole. Treatment of NSAID‐associated ulcer consists of discontinuation of NSAID, if possible, and administration of anti‐secretory drugs such as H2 blockers, proton pump inhibitors or mucosal protective agents. Co‐prescription with misoprostol has been shown to reduce the risk of NSAID‐induced ulcer. New NSAID or NO NSAID are being developed with few gastrointestinal side effects.
Prevalence of and risk factors for Helicobacter pylori infection in a multi‐racial dyspeptic Malaysian population undergoing endoscopy
Authors: GOH KL
Published: March 2008

The aim of the present study was to determine the risk factors for Helicobacter pylori in a dyspeptic Malaysian population. A cross‐sectional survey of 1060 consecutive patients presenting with dyspepsia at the Endoscopic Unit, University Hospital, Kuala Lumpur, Malaysia from January 1994 to July 1995 was undertaken. All patients answered a detailed questionnaire and underwent endoscopy, with two antral biopsies taken for diagnosis of H. pylori using a rapid urease test. An overall H. pylori prevalence of 49.0% was recorded. Helicobacter pylori prevalence in relation to the major endoscopic diagnoses were as follows: non‐ulcer dyspepsia (NUD) 31.2%; duodenal ulcer (DU) 91.4%; and gastric ulcer (GU) 74.1%. The prevalence among the races were as follows: Malay 16.4%; Chinese 48.5%; and Indians 61.8%. Multiple logistic regression analysis identified the following as independent risk factors: > 45 years old 1.5 (1.1,2.0); male gender 1.6 (1.2,2.1); ethnic group: Chinese 2.5 (1.7,3.7); Indians 4.9 (3.2,7.5); level of education: low 2.3 (1.5,3.5); middle 1.7 (1.1,2.6); and smoking 1.6 (1.2,2.3). Analysis was also performed on DU, GU and non‐UD patients separately; in both DU and GU patients, H. pylori prevalence was high regardless of age, sex, race or level of education. However, in DU patients, Indian race had an independent risk factor (Odds ratio = 7.8 (1.2,48.4)). The findings in the NUD group reflected the findings in the ‘all patients’ group; > 45 years old, male gender, Indian and Chinese race, and low level of education were also significant, independent risk factors. The overall differences in H. pylori prevalence between the different subgroups were mainly due to differences in the NUD group. The increased risk of H. pylori infection in Chinese and Indians points to either an inherent ethnic genetic predisposition or to socio‐cultural practices peculiar to the particular race which may be responsible for transmission of the infection.
How to apply modern scientific and technological advances to the practice of clinical gastroenterology in Vietnam
Authors: VAN HA MAO
Published: March 2008

There are some differences between the spectrum of gastroenterological diseases in Vietnam compared with those of more developed countries. These may be due to different living standards, quality of nutrition, and different infection rates of intestinal parasites and hepatotropic viruses. Gastric carcinoma and hepatocellular carcinoma (HCC) are leading malignancies, while colorectal cancer is less frequent. Bile duct stones often have Ascaris eggs in the centre, and they prevail in incidence over gallbladder stones. The majority of digestive cancers are detected at a very late stage. The Vietnamese Association of Gastroenterology aims to contribute to the development of modern gastroenterology (GE) in Vietnam, to study and apply recent advances in imaging technology, such as fibre‐optic diagnostic and therapeutical endoscopy, ultrasonography, laparoscopic surgery etc. and to do further work in molecular biology. For this purpose, besides our self‐reliance, we need, and ask for, support and assistance from the Japanese Society of GE (JSGE), the Asian Pacific Association of GE (APAGE) and the Organisation Mondiale de GE (OMEGE). At the same time, we suggest a choice be made among the different technologies, bearing in mind their cost‐effectiveness, and to give preference to measures for the primary prevention and early detection of the diseases. Japanese experience in the early detection of gastric cancer and HCC, and in the Percutaneous Ethanol Injection Therapy (PEIT) for treatment of HCC, are highly appreciated. We recommend also a judicious and scientific combination of traditional medicine and modern technology in the research and the struggle against digestive diseases.
Review: Helicobacter pylori. Current issues and new directions
Authors: FORBES GEOFFREY M
Published: March 2008

The present review outlines current management issues and controversies related to Helicobacter pylori infection. Clearance of this infection markedly reduces the likelihood of duodenal and gastric ulcer recurrence and may result in the regression of low grade primary gastric lymphoma. Recent therapeutic advances have seen the development of simpler drug regimens to treat H. pylori that have fewer side effects and are shorter in duration. Clearance of the infection can be achieved in 80–95% of patients treated, depending on the drug regimen used, compliance with medications and antibiotic sensitivity. In developed nations reinfection is uncommon after successful treatment. Data do not currently support treatment of this infection for non‐ulcer dyspepsia or for the prevention of gastric cancer, although whether certain individuals or populations may benefit from such treatment remains to be clarified.
REVIEW: The controversy over the pathophysiology of ascites formation in cirrhosis
Authors: WONG FLORENCE , GIRGRAH NIGEL , BLENDIS LAURENCE
Published: March 2008

The pathogenesis of renal sodium retention and ascites formation in cirrhosis is a subject of much controversy. The generally accepted ‘peripheral arterial vasodilatation hypothesis’ seems to best explain the mechanism of sodium retention and other clinical findings, such as the hyperdynamic circulation of cirrhosis. However, recent data in pre‐ascites and in early ascites do not seem to conform to the peripheral arterial vasodilatation hypothesis. Sodium handling abnormalities can be demonstrated in pre‐ascitic cirrhosis when patients are challenged with a sodium load, in the absence of systemic vasodilatation or arterial underfilling. Therefore, an alternative hypothesis with a direct hepatorenal interaction, acting via sinusoidal portal hypertension and/or hepatic dysfunction as the affector mechanism, is proposed to be the initiating event in renal sodium retention in cirrhosis. The second and later process is the development of systemic arterial vasodilatation, possibly due to the presence of excess systemic vasodilators and/or decreased responsiveness of the vasculature to endogenous vasoconstrictors. This, in turn, will lead to a relatively underfilled circulation with consequent activation of neurohumoral systems, promoting further renal sodium retention as described by the peripheral arterial vasodilatation hypothesis and ultimately leading to ascites. When compensatory natriuretic mechanisms fail, refractory ascites develops and hepatorenal syndrome sets in. Thus, renal sodium retention in cirrhosis is the result of interplay of many factors, with direct hepatorenal interaction predominating in earlier stages of the cirrhotic process, while systemic vasodilatation becomes a more important pathogenetic factor as the disease progresses.
Quantitative analysis of interferon α/β receptor mRNA in the liver of patients with chronic hepatitis C: Correlation with serum hepatitis C virus‐RNA levels and response to treatment with interferon
Authors: YATSUHASHI HIROSHI , YAMASAKI KAZUMI , ARITOMI TOMOYUKI , DEL CARMEN PARQUET MARIA , INOUE OSAMI , KOGA MICHIAKI , YANO MICHITAMI
Published: March 2008

We analysed the expression of interferon (IFN) α/β receptor mRNA in the liver of patients with chronic hepatitis C and examined the relationship between the expression of this receptor gene and the level of hepatitis C virus (HCV)‐RNA as well as the response to 16 weeks of 6 × 106 units IFN. The mean level of IFNα/β receptor mRNA in patients with chronic HCV infection (expressed as δ cycle; 10.8±1.9 (mean±SD); n = 39) was significantly higher than that of control subjects (9.4±0.5; n=6; P<0.01). There was a significant negative correlation between the level of IFNα/β receptor mRNA and serum HCV‐RNA in 39 patients with chronic hepatitis C (R=‐0.546; P<0.01). The mean level of IFNα/β receptor mRNA in six patients who showed a complete response to IFN therapy (12.3±1.6) was higher than that of 15 patients who failed to respond to therapy (10.1±1.5; P< 0.01). Our results are consistent with the suggestion that the anti‐viral activity of IFN depends on the level of the IFNα/β receptor on hepatocytes in patients with chronic hepatitis C.
Sucralfate attenuates gastric mucosal lesions and increased vascular permeability induced by ischaemia and reperfusion in rats
Authors: AL‐SWAYEH OA , AL‐HUMAYYD MS , MUSTAFA AA , AL‐TUWAIJRI AS , AL‐RASHED RS , ALI ATMM
Published: March 2008

Recent evidence suggests that oxygen‐derived free radicals are involved in mediating gastric microvascular and parenchymal cell injuries induced by ischaemia and reperfusion. Therefore, the effect of the locally acting anti‐ulcer drug, sucralfate, was studied on ischaemia and reperfusion (e.g. induced gastric lesions, intraluminal bleeding, changes in vascular permeability and non‐protein sulfhydryl levels in the rat stomach). Allopurinol was used as a known standard antioxidant drug. Rats were subjected to 30 min of gastric ischaemia in the presence of 100 mmol/L hydrochloric acid and reperfusion periods of 15, 30 or 60 min duration. The gastric lesions were assessed microscopically under an inverted microscope. The vascular permeability was quantified by measuring the extravasated Evans blue in the stomach. There were significantly greater numbers of gastric lesions, intraluminal bleeding and leakage of Evans blue during all reperfusion periods as compared with those of ischaemia, with maximum effects occurring at 60 min following reperfusion. Pretreatment with sucralfate (31.25–250 mg/kg, p.o.) or allopurinol (12.5–50 mg/kg, i.p.) 30 min before the procedure, dose‐dependently reduced the gastric lesions, intraluminal bleeding, and decreased the vascular permeability induced by ischaemia and reperfusion. Furthermore, sucralfate dose‐dependently reverses the ischaemia and reperfusion‐induced depletion of mucosal non‐protein sulfhydryl levels and inhibited the superoxide radical production in both cell‐free xanthine‐xanthine oxidase and in the stimulated polymorphonuclear cellular systems. These results suggest that the protection produced by sucralfate against gastric injury may be due to its antioxidant effects.
CASE REPORT: Haemorrhagic colitis associated with royal jelly intake
Authors: YONEI YOSHIKAZU , SHIBAGAKI KEIGO , TSUKADA NOBUHIRO , NAGASU NAOKO , INAGAKI YASUTAKA , MIYAMOTO KEI , SUZUKI OSAMU , KIRYU YASUYOSHI
Published: March 2008

The case report of a 53‐year‐old woman with abdominal pain and bloody diarrhoea is described. Prior to the onset of symptoms the patient had taken royal jelly for 25 days. Colonoscopy revealed that the mucosa was haemorrhagic and oedematous throughout the 20 cm long sigmoid colon. Histopathologically, mucosal haemorrhage, oedema, and infiltration of inflammatory cells were observed. Transmission electron microscopic examination revealed platelet aggregation in 30% of capillaries in the mucosal lesions. The drug‐induced lymphocyte stimulation test was slightly positive for royal jelly (847 c.p.m., SI= 147%) compared with the control (576 c.p.m.). The patient's signs and symptoms disappeared within a few days after the initiation of conservative therapy, and the colonic lesions disappeared after 2 weeks of this therapy. This is the first reported case of haemorrhagic colitis associated with royal jelly intake.
Quantitative measurement of HCV RNA in the serum: A comparison of three assays based on different principles
Authors: ICHIJO TETSUYA , MATSUMOTO AKIHIRO , KOBAYASHI MASAKAZU , FURIHATA KENICHI , TANAKA EIJI
Published: March 2008

Quantitative measurement of hepatitis C virus (HCV) RNA is useful in patients with chronic hepatitis C, especially with interferon treatment. We examined the clinical usefulness of the AMPLICOR monitor assay, a newly developed assay for quantitative measurement, by comparing it with two other assays with different principles. A total of 48 patients with chronic hepatitis C who were treated with interferon‐α (IFN‐α) were studied: 19 were complete responders and 29 were non‐responders. Hepatitis C virus RNA was measured quantitatively by AMPLICOR, branched DNA (bDNA) probe, and competitive polymerase chain reaction (C‐PCR) assays. An internal quantification standard was used in the AMPLICOR assay. A cDNA competitor with a deletion of 15 base pairs in the middle portion was used in the C‐PCR method. The concentration of HCV RNA was significantly correlated between the three assays adopted in this study. Sensitivity of assays was 100% by C‐PCR, 90% by AMPLICOR and 69% by bDNA assays. The active quantitative range was best with the C‐PCR assay and worst with the bDNA assay. The bDNA assay had a tendency to exhibit lower values for patients with serotype 2 than did the other two assays. The predictive rate of the long‐term response to IFN‐α therapy, before its initiation, was over 75% in all three assays. The predictive rate just after completing IFN‐α therapy was as high as 80% by C‐PCR and the AMPLICOR assays, but was low (58%) with the bDNA assay. The handling of the bDNA and AMPLICOR assays was much easier than the C‐PCR assay, which required time and skill. These results indicate that the AMPLICOR assay is a simple and reliable method for measuring the serum concentrations of HCV RNA, and thus is suitable for clinical application.
Effect of taurolithocholate‐3‐sulphate on biliary excretion of sulphobromophthalein and dibromosulphophthalein in the Eisai hyperbilirubinaemic rat
Authors: TAKIKAWA HAJIME , SANO NAOYO , SATO AKIHIRO , YAMANAKA MASAMI
Published: March 2008

We previously reported that biliary lithocholate‐3‐sulphate excretion was inhibited by dibromosulphophthalein, not by sulphobromophthalein in Eisai hyperbilirubinaemic rats (EHBR); instead its excretion was inhibited by both organic anions in control rats. In the present study, the effect of taurolithocholate‐3‐sulphate on the excretion of sulphobromophthalein and dibromosulphophthalein was studied in EHBR and control Sprague‐Dawley rats. Taurolithocholate‐3‐sulphate infusion inhibited biliary excretion of sulphobromophthalein and dibromosulphophthalein in both EHBR and control rats. These findings indicate that in control rats biliary excretion of taurolithocholate‐3‐sulphate is mediated by a carrier common for both organic anions, and that in EHBR, in which the canalicular multispecific organic anion transporter is impaired, the excretory pathway for taurolithocholate‐3‐sulphate is also partly identical to that for both organic anions.
Transcytotic vesicle fusion with canalicular membranes is modulated by phospholipid species: Implications for biliary lipid secretion
Authors: HIRANO NAOMICHI , TAZUMA SUSUMU , KAJIYAMA GORO
Published: March 2008

Phospholipid species modulate bile metastability and the subselection of such species for biliary secretion occurs at the canalicular membrane. In this study, the role of phospholipid head groups and hydrophobic indices in transcytotic vesicle fusion with the canalicular membrane inner leaflet was investigated using rat canalicular membrane vesicles (CMV) and liposomes. The CMV were purified from Sprague‐Dawley rat liver, and small unilamellar vesicles (SUV) of phosphatidylserine (PS), phosphatidylcholine (PC) and mixtures of PS/PC (1:1, 2:1 and 4:1) were labelled with 8 mol% of octadecyl rhodamine B chloride (R18). The PC species used in this study were egg yolk PC (EYPC), soybean PC (SBPC), dipalmitoyl PC (DPPC) and dilinoleoyl PC (DLPC). Fusion of SUV with CMV was initiated by the addition of a millimolar concentration of Ca2+ and the degree of fusion was estimated by the increase of R18 fluorescence. Ca2+‐dependent fusion of SUV consisting of PS, and PS/PC (4:1) with CMV was observed (PS > PS/PC; 4:1), whereas no detectable fusion was evident between CMV and SUV of PC alone or PS/PC (1:1 or 2:1). The rank order of fusibility between CMV and SUV of PS/PC (4:1) containing various PC species was PS/DLPC > PS/SBPC > PS/EYPC > PS/DPPC. The hydrophobic index of PC as determined by high performance liquid chromatography (HPLC) was related closely to liposome fusibility (r=‐0.88). These results suggest that transcytotic vesicie fusion with the canalicular membrane inner leaflet is regulated by the phospholipid hydrophobicity of the vesicles.
Molecular biology of hepatitis B virus e antigen
Authors: OU JING‐HSIUNG
Published: March 2008

Hepatitis B virus (HBV) e antigen (HBeAg) was discovered in 1972 as one of the serological markers of HBV infection. Although 25 years have passed since its initial discovery, the function of this antigen in the life cycle of HBV has remained elusive. Mutations in the HBV genome that prevent the expression of HBeAg do not abolish the replication of HBV, indicating that this antigen is not essential for HBV replication. In contrast, the conservation of the HBeAg gene in the genomes of related animal viruses, including the distantly related duck HBV, argues for an important function of this antigen. The purpose of the present article is to review the molecular biology of HBeAg and to examine its possible functions in the life cycle of HBV.
Histopathology and pathobiology of hepatotropic virus‐induced liver injury
Authors: HUANG SN , CHEN TC , TSAI SL , LIAW YF
Published: March 2008

The present report concerns current knowledge regarding immunopathogenesis that can be applied in the interpretation of histopathological changes in acute and chronic viral hepatitis. The histopathological features of viral hepatitis have not been changed and light microscopic examination remains essential for making a diagnosis and classification of chronic hepatitis and for the provision of objective parameters on grading and staging. However, new understanding and knowledge of viral pathogenesis, host immune responses, the biological behaviour of the causative viral agents and, in particular, viral interference in multiple hepatotropic viral infections must be taken into consideration in the interpretation of histopathological and immunopathological findings of liver tissues. This report also presents some histopathological analyses on multiple hepatotropic viral infections. It can be concluded that the diagnostic histological criteria for acute hepatitis remain applicable in such settings. However, the cause of acute flare up in chronic hepatitis could not be determined without clinical, virological and serological information. Routine histopathology cannot distinguish a new infection from an acute exacerbation due to a high level of viral replication or mutant virus. A repertoire of immunocyto‐chemical stainings for viral antigens is helpful, but caution must be exercised in suggesting a specific viral aetiology due to the fact that suppression of pre‐existing viral antigens can be pronounced when the new or concurrent infection is hepatitis C virus related.
Evoked potentials in liver diseases
Authors: CHU NAI‐SHIN , YANG SIEN‐SING , LIAW YUN‐FAN
Published: March 2008

Evoked potentials are objective and quantitative methods capable of evaluating functions of both peripheral and central nervous systems (PNS and CNS). During the past 8 years, we have been using somatosensory, brainstem auditory, and pattern‐reversal visual evoked potentials (SEP, BAEP, VEP) to study hepatic encephalopathy (HE) as well as functional status of the PNS and CNS in various liver diseases including viral hepatitis B, alcoholic liver disease and Wilson's disease (WD). In HE irrespective of its etiologies, there is a sequential prolongation and eventual disappearance of cortical components of the median nerve evoked SEP while there is no change in BAEP, suggesting that HE is primarily due to a disturbance in cerebral cortical function and that median SEP may be used for early detection of HE and for monitoring its clinical course. In addition, absence of the N20‐P25 component, or presence of only the N20 component of the wave complex in fulminant hepatic failure is associated with high mortality, whereas presence of late cortical components in HE is usually associated with reversibility of clinical course. Central conduction time (CCT) of the BAEP is prolonged in patients with WD, alcoholic liver disease and liver cirrhosis due to hepatitis B. Furthermore, BAEP abnormality is most severe in WD, followed by alcoholic liver disease, and finally hepatitis B. Peripheral nerve conduction as determined by the N9 latency of SEP is slowed in alcoholic liver disease and liver cirrhosis of chronic hepatitis B, but normal in WD. Our studies, therefore, suggest that evoked potentials may be useful in the evaluation of both CNS and PNS functions in various liver diseases and also in the diagnosis and monitoring of HE.