bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gastrin release and gastric acid secretion in the rat infected with either Helicobacter felis or Helicobacter heilmannii
Authors: DANON STEPHEN J , MOSS NATHAN D , LARSSON HÅKAN , ARVIDSSON SUZANNE , OTTOSSON SOULTANA , DIXON MIKE F , LEE ADRIAN 
Published: March 2008

ABSTRACT Helicobacter pylori infection in humans has been shown to be associated with changes in gastric physiology, including exaggerated basal and meal‐stimulated gastrin levels. This has been suggested to be due to the direct effects of the bacterium through inflammation and its urease enzyme. The gastric bacteria Helicobacter felis and Helicobacter heilmannii colonize the antrum of rats in large numbers and induce no significant inflammatory response. Thus, the direct effect of Helicobacter infection on gastric physiology, independent of gastritis, could be studied. Basal, freely fed and stimulated acid and gastrin levels were recorded from animals infected with H. felis, H. heilmannii or uninfected controls over a 30 week period. No significant difference was found between freely fed gastrin over 7 weeks or fasting gastrin over 24 weeks or basal and stimulated acid over 30 weeks between all three groups. Triple therapy did not alter gastrin or acid output. The antrum of all Helicobacter‐infected rats was well colonized; triple therapy cleared H. felis but not H. heilmannii. Very little inflammation was seen in control or Helicobacter‐infected animals. In conclusion, Helicobacter‐induced effects on gastric physiology are unlikely to be due to direct bacterial effects, but are best explained by other factors (i.e. inflammatory damage).
Spontaneous bacterial peritonitis in fulminant hepatic failure
Authors: PODDAR U , CHAWLA Y , DHIMAN RK , VAIPHEI K , VASISHTA RK , DILAWARI JB 
Published: March 2008

ABSTRACTAscites may be associated with fulminant hepatic failure (FHF), but spontaneous bacterial peritonitis (SBP) is an extremely rare complication. We report on two patients with FHF who developed SBP. One patient died and the other recovered.
Progress in the endoscopic management of benign biliary strictures
Authors: GIBBONS JOHN C , WILLIAMS STEPHEN J 
Published: March 2008

ABSTRACTBenign biliary strictures can now be effectively treated with endoscopic therapy in a variety of clinical situations. Despite recent developments in imaging techniques (endoscopic ultrasound and magnetic resonance imaging), it is often difficult to differentiate benign from malignant biliary strictures. The sensitivity of tissue diagnosis (cytology and needle biopsy) at endoscopic retrograde cholangiopancreatography (ERCP) remains poor (40–50%), and further diagnostic methods are required. Endoscopic therapy offers a definitive treatment in 70–90% of patients following post‐operative biliary stricture, including anastomotic strictures following liver transplant. Endoscopic therapy successfully achieves symptomatic, biochemical, and cholangiographic response, and may improve survival in patients with primary sclerosing cholangitis. Strictures secondary to chronic pancreatitis are resistant to standard endoscopic therapy and metallic endoprotheses have been trialed with varying success. Endoscopic therapy is technically difficult and should be performed in specialized centres using a multidisciplinary approach.
Detection of hepatitis C and E virus genomes in sera of patients with acute viral hepatitis and fulminant hepatitis by their simultaneous amplification in PCR
Authors: MADAN K , GOPALKRISHNA V , KAR P , SHARMA JK , DAS UP , DAS BC 
Published: March 2008

ABSTRACTA study was undertaken to investigate the role of hepatitis C virus (HCV) and hepatitis E virus (HEV), either alone or together, in the causation of sporadic acute viral hepatitis (AVH) and fulminant hepatitis (FH) by simultaneous detection of their genomes in serum samples using the reverse transcription and nested polymerase chain reaction (RT‐PCR). A total of 50 patients were enrolled in the study of which 34 had AVH and 16 had sporadic FH. The serum samples were first tested for hepatitis B surface antigen (HBsAg) and immunoglobulin (Ig)M antibodies against hepatitis A virus (HAV), hepatitis B core antigen (HBcAg) and HEV and also antibodies against HCV using commercially available enzyme‐linked immunosorbent assay (ELISA) kits. All samples were then subjected to RT‐PCR using primers for both HCV and HEV simultaneously in the same reaction mixture. Hepatitis C or hepatitis E was diagnosed when either the antibodies or PCR or both were positive for the respective viruses. Evidence of hepatitis C was present in six of the 34 (17.6%) cases of AVH and two out of 16 (12.5%) cases of FH. Four patients in the AVH group and one of the fulminant hepatic failure (FHF) group were found to be positive by PCR and the rest by serology. But as a sole aetiological agent, HCV infection was found in only one (2.9%) case of AVH and in none of the FHF cases. Evidence of HEV infection was found in 22/34 (64.7%) and 8/16 (50%) cases of AVH and FHF, respectively. Excluding co‐infection with other viruses, HEV was found to be the sole aetiological agent in 15/34 (44.1%) of AVH and 7/16 (43.7%) cases of FHF. In five (10%) (four AVH and one FHF) of the 50 cases, evidence of infection with both HCV and HEV was present. But only in two of these five cases, genomes of both HCV and HEV were co‐amplified. In seven (four AVH and three FHF) out of 50 (14%) cases, no known viral agent could be detected. Our results suggest that HEV is the most common aetiological agent for both acute viral hepatitis and fulminant hepatic failure and that HCV is a rare cause of acute liver diseases although along with other viruses, evidence of either present or past HCV infection may be present in a substantial number of cases. Furthermore, advanced‐stage pregnancy appears to be a potential risk factor for HEV infection and high rate of mortality in women. The study suggests that the method of simultaneous amplification of both HCV and HEV genomes could reduce the time, labour and cost involved in diagnostic work up of acute liver disease patients.
Progression of the proportion of hepatitis B virus precore stop mutant following acute superinfection of hepatitis C
Authors: YEH CHAU‐TING , CHU CHIA‐MING , LIAW YUN‐FAN 
Published: March 2008

ABSTRACTTo examine the progression of the proportion of hepatitis B virus (HBV) precore stop mutant (codon 28 of precore sequence; TGG to TAG) in the viral population of patients with dual hepatitis virus (B and C) infection, a series of serum samples obtained from six cases with chronic hepatitis B with acute hepatitis C superinfection were analysed by the method of amplification‐created restriction site. At the time of superinfection, all patients included in the study were negative for hepatitis B e antigen and positive for its antibody. During the follow up of 30–90 months, in five of the six patients, three different patterns were observed: (i) the proportion of precore stop mutant increased in the first 20 months after acute hepatitis C virus superinfection and then decreased progressively thereafter (two cases); (ii) the proportion of precore stop mutant decreased progressively after superinfaction (two cases); and (iii) no precore stop mutant was found during the course (one case). The remaining patient showed a progressive increase in the proportion of precore stop mutant over a period of 9 months after superinfection. Rather than the progressive increase in the proportion of precore stop mutants during the natural course of chronic HBV infection alone, the results of the present study showed a reverse course of progression following acute hepatitis C virus superinfection. This observation raised the possibility of a preferential or accumulative suppression on precore stop mutant by hepatitis C virus in the later stage of dual infection.
Mortality and rebleeding following Transjugular Intrahepatic Portosystemic Stnt Shunt for variceal haemorrhage
Authors: WILLIAMS DAVID , WAUGH RICHARD , GALLAGHER NEIL , PERKINS KENNETH , DILWORTH PAMELA , DUGGAN ANNE , SELBY WARWICK 
Published: March 2008

ABSTRACTThe present study investigates clinical factors associated with decreased survival following Transjugular Intrahepatic Portosystemic Stent Shunt (TIPSS). Sixty‐seven patients underwent TIPSS for bleeding related to portal hypertension, 42 (63%) on an urgent basis. TIPSS was successfully placed in 65 (97%) patients with no fatal procedural complications. Thirty day mortality was 21%, there being several predictive factors: transfer from another institution, urgency of procedure, sepsis, encephalopathy, higher mean serum bilirubin and low serum albumin. However, using regression analysis, 30 day mortality was predicted independently only by severe liver disease (Child‐Pugh C, P= 0.003) and older age (P= 0.003). When stratified by Child‐Pugh class, cumulative survival rates at 1 year for class A, B and C were 100, 90 and 34%, respectively. Only three of 25 patient deaths were due to variceal rebleeding. Thirty (46%) patients had a total of 41 rebleeding episodes, with mean time to first rebleed of 4.8 months (range, 3 days‐38 months). Cumulative rebleeding rate at 1 year was 25%. Log‐rank analysis did not reveal a significant difference in overall survival between rebleeders and non‐rebleeders (P= 0.125). When investigated, shunt abnormalities (stenosis, occlusion) were identified in all cases of rebleeding. Our findings confirm TIPSS can be safe and effective in the control of refractory variceal haemorrhage. However, prognosis remains poor for patients with advanced liver disease, particularly if older and in the emergency setting. Vigilant surveillance and high rate of intervention is necessary to maintain shunt patency. Consideration could be given to elective shunt surgery instead of TIPSS for patients with recurrent bleeding and good prognosis liver disease.
Characteristics of hepatocellular carcinoma presenting with variceal bleeding
Authors: CHEN CHIEN‐HUNG , SHEU JIN‐CHUAN , HUANG GUANG‐TARN , LEE HSUAN‐SHU , YANG PEI‐MING , WONG JAU‐MIN , CHEN DING‐SHINN 
Published: March 2008

ABSTRACTPatients with hepatocellular carcinoma may present with variceal bleeding as the initial symptoms. The aims of this study is to investigate the characteristics of such patients. A total of 1046 hepatocellular carcinoma cases were retrospectively retrieved from our computer records between 1980 and 1993. The medical records and image studies were reviewed. The status of each patient was assessed at the time of presentation. A total of 14 (about 1%) patients with hepatocellular carcinoma presented with variceal bleeding. Five (36%) did not have past history of liver disease. The tumour size ranged from 2.5 to 11.3 cm. Compared with hepatocellular carcinoma patients not presenting with variceal bleeding, these patients had a higher percentage of portal vein thrombosis (57.1 vs 19.4%). In two patients, the hepatic tumours were missed in the initial abdominal sonography. The average survival time was 71 days. Seven patients died within 2 months mainly due to variceal bleeding (41.6%). Variceal bleeding might be a clue to the presence of hepatocellular carcinoma with portal vein thrombosis even in patients without a previous history of liver disease. The tumours in such patients might be the infiltrative type, and thus the portal vein should be carefully worked‐up. Overall, these patients have an extremely poor prognosis. In the management of patients with variceal bleeding, the possibility of hepatocellular carcinoma with portal vein thrombosis should not be overlooked, especially in areas where this cancer is prevalent.
Effect of PGE1 on TNF‐α status and hepatic D‐galactosamine‐induced apoptosis in rats
Authors: MUNTANÉ JORDI , MONTERO JOSE LUIS , MARCHAL TRINIDAD , PEREZ‐SEOANE CARLOS , LOZANO JOSE MANUEL , FRAGA ENRIQUE , PINTADO CARMELO OSCAR , MATA MANUEL DE LA , MIÑO GONZALO 
Published: March 2008

ABSTRACTProstaglandin E1 has hepatoprotective properties in several clinical and experimental models of liver dysfunction. Hepatotoxicity induced by D‐galactosamine (D‐GalN) is a suitable animal model of human acute hepatic failure. The aim of the study was to investigate if prostaglandin E1 (PGE1) protection against hepatic D‐GalN‐induced apoptosis was related to tumour necrosis factor‐α (TNF‐α) content in serum. This cytokine is associated with in vitro apoptosis and general inflammatory disorders. In this study, PGE1 was administered 30 min before D‐GalN to rats. In other experiments, several doses of TNF‐α were administered 15 min after PGE1 to D‐GalN‐treated rats. Several parameters related to apoptosis and necrosis were measured by flow cytometry, gel electrophoresis, biochemical analysis, and optical and electron microscopy. Tumour necrosis factor‐α was quantified by competitive enzyme‐linked immunosorbent assay (ELISA). PGE1 by itself did not modify the cell cycle of hepato‐cytes and liver toxicity, but increased TNF‐α in serum in comparison with the control group. D‐Galactosamine increased the percentage of hepatocytes in apoptosis and in the S phase of the cell cycle, and decreased those in G0/G1. Such an increase of hepatocytes in apoptosis was correlated with a higher number of apoptotic bodies and DNA fragmentation in liver than control samples. Also, D‐GalN increased alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase and TNF‐α in serum compared with the control group. Pre‐administration of PGE1 to D‐GalN‐treated rats reduced all the parameters of apoptosis and necrosis in liver, and increased additionally TNF‐α content in serum. In those experiments where low doses of TNF‐α were administered to PGE1 and D‐GalN‐treated rats an inverse relationship appeared between TNF‐α and ALT content in serum. In conclusion, the protective effects of PGE1 on D‐GalN‐induced apoptosis may be linked to its capacity to modulate cell division and/or its immunomodulatory activity. In this sense, our experimental results suggest that TNF‐α could be involved in protection or exacerbation of liver damage in relation to the pathophysiological status of the liver.
p53 expression in gastric mucosa with Helicobacter pylori infection
Authors: KODAMA MASAAKI , FUJIOKA TOSHIO , KODAMA REIJI , TAKAHASHI KENJI , KUBOTA TOSHIHIRO , MURAKAMI KAZUNARI , NASU MASARU 
Published: March 2008

ABSTRACTExpression of p53 was examined immunohistochemically in the Japanese monkey model with Helicobacter pylori infection of the gastric mucosa to investigate the association between H. pylori infection and gastric carcinogenesis for a period of 4 years. In the course of these observations, from 3 years after H. pylori inoculation, nuclear staining for p53 was seen in the glandular cells of the mucosa infected with H. pylori, especially in the neck region of the glands. There was a gradual increase in the number of immunopositive cases among the infected animals. Three years after inoculation, three out of six cases, and 4 years after inoculation, four out of six cases exhibited positive staining for p53. Before inoculation, and up to 2 years after inoculation, the infected group showed no immunoreaction for p53. The non‐infected group likewise displayed no immunostaining for p53 through 4 years of observation. These results suggest that p53 alterations occur in the H. pylori‐infected gastric mucosa and that H. pylori infection may play an important role in gastric carcinogenesis.
Effect of sucralfate granules in suspension on endoscopic variceal sclerotherapy induced ulcer: Analysis of the factors determining ulcer healing
Authors: YANG WEN‐GUH , HOU MING‐CHIH , LIN HAN‐CHIEH , KUO BENJAMIN ING‐TIEU , LEE FA‐YAUH , CHANG FULL‐YOUNG , LEE SHOU‐DONG 
Published: March 2008

ABSTRACTOesophageal ulcers commonly occur after endoscopic variceal sclerotherapy and usually cause complications and a delay in further sclerotherapy. The aims of this study are to investigate the effect of sucralfate granules in suspension on the treatment of endoscopic variceal sclerotherapy induced ulcer and analyse the factors determining the ulcer healing. Fifty‐two patients with oesophageal variceal bleeding received elective endoscopic variceal sclerotherapy. After endoscopically proved oesophageal ulcers, they were randomized to receive either sucralfate granules in suspension (n= 22) or antacid (n= 23). Follow‐up endoscopy was performed weekly. Ulcer healing rates were compared between the groups using the log‐rank test. Forty‐one ulcers receiving sucralfate and 48 ulcers receiving antacid treatment were evaluated. The clinical characteristics of the ulcers were similar in both groups. The ulcers in patients receiving sucralfate healed faster than those receiving antacid (P < 0.02). On analysis of factors affecting ulcer healing, ulcers smaller than 1 cm2 (n= 59) appeared to heal faster than those larger than 1 cm2 (n= 30; P= 0.059) and shallow ulcers (n= 46) healed faster than deep ulcers (n= 43; P < 0.001). On multifactorial analysis, ulcer depth was the only factor determining ulcer healing. The ulcer healing effects of sucralfate became more prominent when the ulcer was larger than 1.0cm2 (1.7±0.6 weeks vs 2.3±0.6 weeks, P= 0.011) and deep (1.7±0.7 weeks vs 2.5±1.0 weeks, P= 0.013) when compared with those receiving antacid. Sucralfate granules in suspension speed the healing of endoscopic variceal sclerotherapy induced ulcer, especially deep and large ulcers.
Plasma transforming growth factor‐β1 concentrations in patients with chronic viral hepatitis
Authors: MURAWAKI YOSHIKAZU , NISHIMURA YUUKO , IKUTA YUJIRO , IDOBE YOUKO , KITAMURA YUKISATO , KAWASAKI HIRONAKA 
Published: March 2008

ABSTRACTTransforming growth factor (TGF)‐β1 is an important cytokine involved in the pathobiology of tissue fibrosis through its stimulation of the production of, and inhibition of the degradation of, extracellular matrix proteins. We examined the clinical usefulness of plasma TGF‐β1 concentration as a marker of fibrogenesis in patients with chronic viral hepatitis. Thirty‐five patients, 11 with minimal chronic hepatitis, 14 with mild chronic hepatitis and 10 with moderate chronic hepatitis and 20 healthy subjects were studied. Transforming growth factor‐β1 concentrations in platelet‐poor plasma were measured with a TGF‐β1 enzyme‐linked immunosorbent assay system kit after acid‐ethanol extraction. Plasma TGF‐β1 levels were significantly elevated in patients with mild and moderate chronic hepatitis, but not in those with minimal chronic hepatitis, compared with the levels in the controls. Plasma TGF‐β1 levels were increased in parallel with the histological degree of necroinflammation and of liver fibrosis. Plasma TGF‐β1 levels were positively correlated with blood levels of procollagen type III N‐peptide, and 7S fragment and central triple‐helix of type IV collagen. These results suggest that plasma TGF‐β1 level is a useful marker in assessing the situation of liver active fibrogenesis in patients with chronic viral hepatitis.
Intraductal ultrasonography for the diagnosis of proximal invasion in extrahepatic bile duct cancer
Authors: KUROIWA MASANORI , GOTO HIDEMI , HIROOKA YOSHIKI , FURUKAWA TUYOSHI , HAYAKAWA TETSUO , NAITOH YASUO 
Published: March 2008

ABSTRACTIntraductal ultrasonograpy (IDUS) was performed on 22 patients with extrahepatic bile duct cancer, using the percutaneous transhepatic approach. Intraductal ultrasonograpy images of the proximal invasion of the bile duct cancer were defined. In addition, three patients were examined through the peroral approach, to try to diagnose whether or not the cancer invaded to the bifurcation of the hepatic duct. Intraductal ultrasonograpy images obtained through the percutaneous approach could be classified into three patterns, types 1, 2 and 3, according to the features of the interior surface of the bile duct and the thickness of the bile duct wall. Type 1 images, which did not show protrusions into the bile duct lumen and had a bile duct wall of even thickness, were not likely to show bile duct cancer. Type 2 images showed protrusions of the tumour into the bile duct lumen and the surfaces of the protrusions were irregular. Type 3 images showed single or multiple low echoic papillary masses in the bile duct. Using the peroral technique, we considered all three cases to be type 1 and could diagnose that cancer had not invaded to the bifurcation of the hepatic ducts. From the results of this study, we suggest that proximal invasion of extrahepatic bile duct cancer can be diagnosed using IDUS.
Factors influencing Helicobacter pylori eradication with 2 week combination therapy of lansoprazole and amoxycillin: Intragastric distribution of colonization and gastric mucosal atrophy
Authors: SAITA HIROSHI , MURAKAMI MOTONOBU , TAKAHASHI YOUJI , SOU YASUNARI , KAITANI KAZUAKI , NISHIO KIYOSHI , KITA TORU 
Published: March 2008

ABSTRACTIn Japan, gastric ulcers are often accompanied by marked gastric mucosal atrophy. We evaluated the dual therapy of double‐dose lansoprazole and amoxycillin for Helicobacter pylori eradication in Japanese ulcer patients and investigated the effects of intragastric distribution of H. pylori colonization and gastric mucosal atrophy on eradication with this combination therapy. Seventy‐six H. pylori‐positive ulcer patients received lansoprazole (30 mg) plus amoxycillin (500 mg) twice daily for 2 weeks (LA‐60 group), lansoprazole (30 mg once daily) plus amoxycillin (500 mg twice daily) for 2 weeks (LA‐30 group) or lansoprazole (30 mg once daily) for 6 or 8 weeks (LPZ group). Infection was evaluated by light microscopy, culture and biopsy urease tests. Helicobacter pylori colonization was classified as localized to the corpus (localized type) or involving the antrum and corpus (whole type). Fundic mucosal atrophy was graded according to endoscopic and histological features. Eradication was achieved in 67.6% in the LA‐60 group, 31.6% in the LA‐30 group, and 0% in the LPZ group, and moderate or severe histological gastritis was improved in the LA‐60 group. Eradication was better in localized‐type colonization (92%) than whole‐type (56%), and better with fundic mucosal atrophy (84%) than without, but poor in both whole‐type colonization and scanty mucosal atrophy (47%). The LA‐60 therapy achieves better eradication in Japanese ulcer patients with localized H. pylori colonization and/or gastric mucosal atrophy, which are likely to be important predictors for the successful eradication with dual therapy.