bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long‐term follow‐up of gastric histology after Helicobacter pylori eradication
Authors: FORBES GEOFFREY M , WARREN J ROBIN , GLASER MARK E , CULLEN DIGBY JE , MARSHALL BARRY J , COLLINS BRENDAN J 
Published: March 2008

ABSTRACT Helicobacter pylori causes chronic active gastritis and is thought to be associated with the development of gastric atrophy, intestinal metaplasia and carcinoma. As the effect of H. pylori eradication on this process is poorly understood, we sought to determine the long‐term effects of H. pylori eradication on gastric histology. Fifty‐four patients with duodenal ulceration associated with H. pylori infection received H. pylori eradication therapy in 1985/86 and either remained infected (n= 22) or had the infection eradicated (n= 32); patients were followed up by endoscopy with gastric antral biopsy for 7.1 years (mean). Histopathological analysis of gastric antral mucosa from patients rendered H. pylori‐negative revealed a marked decrease in both inflammatory cells within the lamina propria and intraepithelial neutrophils and an increase in epithelial mucinogenesis. Gland atrophy remained unchanged in both H. pylori‐positive and ‐negative patients. When examined for the presence and severity of intestinal metaplasia, there was neither a difference between the two patient groups nor a change with time. These data demonstrate that significant long‐term improvements in gastric histology accompany H. pylori eradication when compared with histology in patients with persistent infection. Whether this confers a protective effect by reducing the risk of gastric carcinoma remains unknown.
Measurement of faecal α1‐antitrypsin: Methodologies and clinical application
Authors: CHOUDHARY SITARAM , GIBSON PETER R , DEACON MELISSA C , YOUNG GRAEME P 
Published: March 2008

AbstractPresence of the serum protein, α1‐antitrypsin, in the faeces is a potentially useful marker for gastrointestinal disease and/or blood loss. In an effort to simplify faecal sampling procedures, we evaluated the performance of measuring α1‐antitrypsin in eluants of thin smears of faeces made on filter paper, relative to conventional measurement in aqueous extracts of stool. Faecal specimens and smears were collected from healthy subjects (n= 22) and from patients with gastrointestinal bleeding (n= 12) or inflammation (n= 22), colorectal neoplasia (n= 15), or miscellaneous diseases with a low risk of excessive faecal protein loss (n= 30). α1‐Antitrypsin was measured by ELISA and haem porphyrins (as a measure of blood loss) by HemoQuanttm. Results from smears were highly correlated (r = 0.81; P < 0.001) with faecal α1‐antitrypsin. The smear method detected an elevated faecal α1‐antitrypsin with 93% specificity and 75% sensitivity. Sensitivity was high (> 88%) where levels were markedly elevated in inflammatory and bleeding groups and low (< 62%) where abnormal levels were mildly elevated (neoplasia and miscellaneous groups). Elevated α1‐antitrypsin detection by either method positively predicted > 90% of patients with gastrointestinal inflammatory disease when levels were elevated 6‐fold and 1.5‐fold or more, respectively. In 15 patients with colorectal neoplasia, faecal α1‐antitrypsin was elevated in 10 patients, haem porphyrins in nine patients and either in 12; however, smear eluant levels were elevated in only six patients. Blood loss was probably a major contributor to elevated faecal α1‐antitrypsin in some patients but not in the inflammatory group as a whole. The sampling and aesthetic advantages of the smear eluant method are offset by reduced sensitivity, precluding its use as a screening test for colorectal neoplasia. However, its performance in predicting inflammatory disease is equivalent to that of conventional measurement and warrants a prospective evaluation as an early investigative test. Concurrent evaluation of blood loss may improve its interpretation.
Current concepts of hepatic uptake, intracellular transport and biliary secretion of bile acids: Physiological basis and pathophysiological changes in cholestatic liver dysfunction*
Authors: AZER SAMY A , STACEY NEILL H 
Published: March 2008

AbstractHepatic sinusoidal uptake of bile acids is mediated by defined carrier proteins against unfavourable concentration and electrical gradients. Putative carrier proteins have been identified using bile acid photoaffinity labels and more recently using immunological probes, such as monoclonal antibodies. At the sinusoidal domain, proteins with molecular weights of 49 and 54 kDa have been shown to be carriers for bile acid transport. The 49 kDa protein has been associated with the Na+‐dependent uptake of conjugated bile acids, while the 54 kDa carrier has been involved in the Na+‐independent bile acid uptake process. Within the hepatocyte, cytosolic proteins, such as the glutathione S‐transferase (also designated the Y protein), the Y’ binders and the fatty acid binding proteins, are able to bind bile acids and possibly facilitate their movement to the canalicular domain. At the canalicular domain a 100 kDa carrier protein has been isolated and it has been shown by several laboratories that this particular protein is concerned with canalicular bile acid transport. The system is ATP‐dependent and follows Michaelis‐Menten kinetics. Interference with bile acid transport has been demonstrated by several chemicals. The mechanisms by which these chemicals inhibit bile acid transport may explain the apparent cholestatic properties observed in patients and experimental animals treated with these agents. Several studies have shown that Na+/K+‐ATPase activity is markedly decreased in cholestasis induced by ethinyloestradiol, taurolithocholate and chlorpromazine. However, other types of interference have been described and the cholestatic effects may be the result of several mechanisms. Cholestasis is associated with several adaptive changes that may be responsible for the accumulation of bile acids and other cholephilic compounds in the blood of these patients. It may be speculated that the nature of these changes is to protect liver parenchymal cells from an accumulation of bile acids to toxic levels. However, more detailed quantitative experiments are necessary to answer questions with regard to the significance of these changes and the effect of various hepatobiliary disorders in modifying these mechanisms. It is expected that the mechanisms by which bile acid transport is regulated and efforts to understand the molecular basis for these processes will be among the areas of future research.
Interferon‐α therapy for individuals with normal serum alanine aminotransferase levels before treatment
Authors: ORITO ETSURO , MIZOKAMI MASASHI , SUZUKI KAORU , OHBA KEN‐ICHI , OHNO TOMOYOSHI , MIZUNO MAKOTO , IIJIMA YOSHIHIKO , SAITOH HIROSHI , NEMOTO AKIRA , NUKUTA NOBUO 
Published: March 2008

ABSTRACTWhile interferon (IFN) therapy is approved for patients with chronic hepatitis C infection, the effectiveness of IFN therapy for anti‐hepatitis C virus (HCV)‐positive individuals with normal ALT levels remains poorly understood. Twenty‐five individuals (M:F = 9:16; age = 51.8±15.1 years) who showed a normal alanine aminotransferase (ALT) level (< 30 IU/L) at least 6 months before treatment and were positive for both anti‐HCV and serum HCV‐RNA by reverse transcription polymerase chain reaction (RT‐PCR) were studied. Of these, 16 received IFN therapy for 24 weeks (780 million units total IFN‐α2b) and nine were followed for 12 months as controls. The serum HCV‐RNA level was determined by bDNA assay and HCV genotype was detected by enzyme immunoassay. All were shown to have chronic hepatitis by liver biopsy. Six (37.5%) of 16 individuals lost serum HCV‐RNA by RT‐PCR 6 months after cessation of therapy (complete response; CR), while the remaining individuals were defined as non‐responders (NR). Of the six individuals in the CR group, five had HCV type 2 infection, compared with none of 10 individuals in the NR group (P < 0.01). There was a trend towards a lower pretreatment viraemia level in the CR group than in the NR group. These data suggest that IFN therapy for individuals with HCV type 2 infection and normal ALT levels was effective
Natural anticoagulants and the liver
Authors: CASTELINO DANIEL J , SALEM HATEM H 
Published: March 2008

ABSTRACTThe regulation of blood coagulation is dependent on a complex interplay between procoagulant, anticoagulant and fibrinolytic proteins. Most of these proteins are synthesised in the liver and their levels are altered in patients with liver disease. The liver also plays an important role in the regulation of haemostasis throughout the clearance of activated clotting factors. It is therefore not surprising that the critically balanced coagulation system is dysregulated in patients with liver disease. In moderate liver failure bleeding disorders predominate, whereas in more advanced liver disease intravascular coagulation is commonly observed and contributes to the overall dysregulation of blood coagulation. In some patients, liver disease can be primarily caused by an abnormality of the coagulation system. These patients usually have a hypercoagulable state caused by a deficiency of a component of the natural anticoagulant system. These include protein C, protein S and antithrombin III. More recently, activated protein C resistance caused by a point mutation in the Factor V gene has been identified as an important risk factor for thrombosis. In these patients the abnormal Factor V is resistant to cleavage by activated protein C resulting in ongoing uncontrolled procoagulant drive. Both hepatic and portal vein thrombosis have been reported in these patients. Appropriate management of these patients should include a thorough assessment of their natural anticoagulant proteins and exclusion of activated protein C resistance as the cause of their thrombotic disorder.
Effect of tauro‐α‐muricholate and tauro‐β‐muricholate on oestradiol‐17β‐glucuronide‐induced cholestasis in rats
Authors: TAKIKAWA HAJIME , SANO NAOYO , AISO MITSUHIKO , TAKAMORI YORIYUKI , YAMANAKA MASAMI 
Published: March 2008

ABSTRACTThe effect of tauro‐β‐muricholate (βMC‐tau) and tauro‐α‐muricholate (αMC‐tau) on oestradiol‐17β‐glucuronide (E217G)‐induced cholestasis was compared with that of taurourso‐deoxycholate (UDC‐tau) in rats. Like UDC‐tau, αMC‐tau and βMC‐tau infused at the rate of 0.2 μmol/min per 100 g bodyweight (BW) completely inhibited the cholestasis induced by E217G infused at the rate of 0.06 μmol/min per 100 g BW for 20 min. These findings indicate that βMC‐tau and αMC‐tau are useful in protecting against various types of experimental cholestasis, as well as against bile acid‐induced cholestasis.
A prospective clinical study of isoniazid‐rifampicin‐pyrazinamide‐induced liver injury in an area endemic for hepatitis B
Authors: HWANG SHINN‐JANG , WU JAW‐CHING , LEE CHUN‐NIN , YEN FU‐SHUN , LU CHING‐LIANG , LIN TAO‐PING , LEE SHOU‐DONG 
Published: March 2008

ABSTRACTIn order to evaluate the incidence, predisposing factors and clinical course of antituberculous drug‐induced liver injury in hepatitis B surface antigen (HBsAg)‐positive carriers and non‐carriers, in an area endemic for hepatitis B, we prospectively followed 240 patients (154 male, 86 female; mean age 40 years) who had received daily isoniazid, rifampicin, ethambutol and pyrazinamide for the treatment of pulmonary tuberculosis. Patients with heavy alcohol consumption, with pretreatment serum alanine aminotransferase (ALT) elevation and who had less than 3 months post‐treatment follow‐up were excluded from the study. Thirty‐one (13%) patients were positive for serum HBsAg before treatment. Sixty‐three (26%; 95% CI: 21–32%) patients developed antituberculous drug‐induced liver injury. The incidence of drug‐induced liver injury was significantly more frequent in patients > 35 years of age than in patients > 35 years of age (33 vs 17%; P < 0.05), but was not different between HBsAg carriers and non‐carriers (29 vs 26%; P > 0.05). Using step‐wise logistic regression analysis, patient age > 35 years was the only independent variable for predicting antituberculous drug‐induced liver injury, while sex, acetylator phenotype, HBsAg carrier status and severity of tuberculosis were not. The peak serum ALT levels in antituberculous drug‐induced liver injury were not significantly different between HBsAg carriers and non‐carriers. Only one 61‐year‐old HBsAg carrier developed severe jaundice after 6 months antituberculous therapy; he subsequently died of hepatic failure. In conclusion, the incidence of antitubercuious drug‐induced liver injury was significantly higher in patients > 35 years of age than in patients > 35 years of age, but was not different between HBsAg carriers and non‐carriers. Mortality occurred in an aged HBsAg carrier superimposed with antituberculous drug‐induced liver injury.
Hepatitis C virus (HCV) genotypes and chronic liver disease in Pakistan
Authors: SHAH HASNAIN A , JAFRI WASIM , MALIK IMTIAZ , PRESCOTT LINDA , SIMMONDS PETER 
Published: March 2008

ABSTRACTHepatitis C virus (HCV) is classified into different types depending on nucleotide sequence variability. Detailed information on the distribution of various HCV genotypes in some geographical areas is available but little is known about Pakistan. In this study, a 5’ non‐coding region (NCR)‐based restriction fragment length polymorphism (RFLP) genotyping assay was used to investigate the genotype distribution in a large series of HCV‐infected patients in Karachi, Pakistan. Serum samples from 74 hepatitis B surface antigen (HBsAg)‐negative patients with a clinical diagnosis of chronic liver disease (60 patients) and hepatocellular carcinoma (HCC) (14 patients) were assayed for anti‐HCV antibody by second generation enzyme immunoassay and 48 were confirmed anti‐HCV‐positive (33 males, 15 females). Other causes of chronic liver disease (e.g. haemochromatosis, Wilson's disease and immunemediated injury) were ruled out. Liver biopsy was done in 27/48 anti‐HCV‐positive patients and in all HCC patients. Genotypes were determined for 45/48 anti‐HCV‐positive study patients; 39/45 (87%) were type 3; four (9%) were type 1; one was type 2; and one was type 5. Past blood transfusion was the main identifiable risk factor found in 10 patients, all type 3. Seven of the 14 HCC patients were anti‐HCV positive, (six were type 3). Most patients with hepatitis C presented with established cirrhosis and complications of portal hypertension and liver failure. In conclusion: (i) genotype 3 is the most common isolate in HCV‐associated chronic liver disease in Pakistan; (ii) a significant proportion of HBsAg‐negative cirrhotics are non‐B, non‐C in aetiology; and (iii) half of the patients with HCC have serological evidence of HCV infection.
Diagnosis and treatment of superficial oesophageal carcinoma
Authors: CHEN YI‐JEN , LEE MENG‐DAR , CHEN PAO‐HUEI 
Published: March 2008

ABSTRACTOesophageal carcinoma is a major cause of cancer death in certain parts of the world. Early detection provides the only chance of cure. In this study, one female and nine male patients with superficial oesophageal carcinoma were investigated to determine the pertinent clinical and pathological features. All male patients were smokers and six patients drank various amounts of alcohol on a daily basis. Histologically, five cases were confined within the mucosal layer and five within the submucosal layer. All five mucosal cancer cases and two of the live submucosal cancer cases were asymptomatic. Endoscopically, all five mucosal cancer patients had flat lesions, whereas the five submucosal cancer tumours appeared either protruding or depressed. Barium oesophagography failed to demonstrate the lesions in four of five mucosal cancer and one of five submucosal cancer cases. Endoscopic ultrasonography correctly detected the depth of cancer invasion in six out of eight superficial oesophageal carcinoma cases. All patients received a one‐stage operation that included oesophagectomy and lymph node dissection. All five mucosal cancer patients had no lymph node involvement and have experienced no tumour recurrence. Among them, one who had concomitant hepatocellular carcinoma died early. Of the five submucosal cancer cases, four died 1–5 years after the operation. It is concluded that oesophageal carcinoma is curable in its early stage. Physicians should be alert while performing endoscopic examination. We believe that the dyeing technique is a useful adjunct to endoscopic examination.
Gastro‐oesophageal reflux disease: Medical or surgical treatment? Report of an interactive workshop
Authors: SCHWAB GP , BLUM AL , BODNER E , DALLEMAGNE B , GLASER K , KOOP H , PACE F , RÖSCH W , SIEWERT JR , WETSCHER G 
Published: March 2008

ABSTRACTGastroesophageal reflux disease (GERD) is the most common disease of the upper gastrointestinal tract. With the introduction of proton pump inhibitors medical treatment of GERD has been significantly improved. However, the development of laparoscopic antireflux surgery resulted in an increasing interest of surgeons in this disease. An interactive meeting was organized in order to develop an agreement between gastoenterologists and surgeons regarding therapeutic decisions and this is the main topic of this paper.
Absorption of unconjugated bile acids and tauroursodeoxycholate in the rat intestine
Authors: TAKIKAWA HAJIME , YOKOTE MICHIKO , SANO NAOYO , KUYAMA YASUSHI , YAMANAKA MASAMI 
Published: March 2008

ABSTRACTThe absorption of ursodeoxycholate and its tauro‐conjugate by the jejunum and the terminal ileum of rat intestine was compared with that of other unconjugated bile acids and taurocholate. In the ligated jejunum, the efficacy of absorption of unconjugated bile acids was in the following order: ursodeoxycholate = deoxycholate > chenodeoxycholate = cholate > lithocholate. This order cannot be explained by the theory that the passive diffusion of bile acids is faster the less hydroxyl bonds in the molecule. These findings on the unconjugated bile acids in the ligated jejunum were further confirmed by perfusion experiments. In the ligated terminal ileum, ursodeoxycholate, cholate and deoxycholate were absorbed as fast as taurocholate or tauroursodeoxycholate, whereas absorption of chenodeoxycholate was significantly slower. The Na+‐dependency of the absorption of ursodeoxycholate and cholate in the terminal ileum was confirmed by perfusion studies. In conclusion, intestinal absorption of ursodeoxycholate was efficient in both the jejunum and ileum and these results may contribute to the high availability of ursodeoxycholate in various hepatobiliary diseases.
Dose‐related effects of dietary iron supplementation in producing hepatic iron overload in rats
Authors: PLUMMER JOHN L , MACKINNON MALCOLM , CMIELEWSKI PATRICIA L , WILLIAMS PHIL , AHERN MICHAEL J , ILSLEY ANTHONY H , HALL PAULINE DE LA M 
Published: March 2008

ABSTRACTThe influence of varying the level of supplemental dietary iron on the development of hepatic iron overload was examined in rats. Two days after giving birth, Porton rats were fed a diet supplemented with 0, 0.5, 1 or 2% carbonyl iron, to institute dietary iron supplementation to the young via breast milk. After weaning, the offspring continued to receive the assigned diet until 32 weeks of age. Liver biopsies were taken from some rats at 8, 16 and 24 weeks of age and from all rats at 32 weeks of age, for assessment of iron overload. For both male and female rats, hepatic iron content was increased in a dose‐related manner by feeding supplemented diet. Hepatic iron content of male rats tended to reach a plateau after 8–16 weeks of supplementation, while that of female rats continued to rise throughout the experimental period, such that the hepatic iron content of female rats was 2.8‐fold that of similarly treated males at 32 weeks of age. Iron supplementation was associated with only moderate retardation of growth. By choosing an appropriate level of iron supplementation, good (grade III‐IV) hepatic iron loading can be achieved with minimal adverse effects on the animals’ overall health.
HCV and HBV coexist in HBsAg‐negative patients with HCV viraemia: Possibility of coinfection in these patients must be considered in HBV‐high endemic area
Authors: LEE DONG‐SOON , HUH KWANG , LEE ENU‐HEE , LEE DONG‐HO , HONG KI‐SOOK , SUNG YOUNG‐CHUL 
Published: March 2008

ABSTRACTHepatocellular carcinoma (HCC) is one of the most common cancers and is highly associated with hepatitis B virus (HBV) infection in Korea. The role of HBV and hepatitis C virus (HCV) in HCC patients who are negative for hepatitis B surface antigens (HBsAg) remains poorly defined. It has been suggested that HCV core protein may impair the polymerase activity of HBV in vitro, potentially lowering HBV titre in coinfected patients. Therefore, routine enzyme immunoassay may not detect HBV, in spite of the presence of HBV viraemia in low titres. The aim of this study was to confirm the coexistence of HBV viraemia in hepatitis C‐infected patients with HCC who have apparent HBsAg seronegativity and to establish the need for clinical reinterpretation of enzyme immunoassay (EIA) serological tests of HBsAg in patients with HCV viraemia and HCC. The serological profiles of HBV and HCV in 616 patients with HCC were analysed and the coinfection rate of HCV and HBV investigated. Sera were obtained from 16 patients who were both anti‐HCV and HCV‐RNA positive but HBsAg negative, and tested for HBV by polymerase chain reaction (PCR). Eleven non‐A and non‐B chronic hepatitis patients without HCC who had the same profiles of anti‐HCV, HCV‐RNA, and HBsAg were tested for HBV by PCR. As a control group, sera were obtained from 15 patients with HCC and 30 non‐A and non‐B chronic hepatitis patients without HCC; both were anti‐HCV, HCV‐RNA, and HBsAg negative and tested for HBV PCR. Of the 616 patients with HCC, 450 (73.1%) had current HBV infection, 48 (7.8%) had anti‐HCV antibodies, and nine (1.5%) had viral markers of both HCV and HBV by serological profiles. Of the 27 patients with HCV viraemia and HBsAg seronegativity (16 with HCC; 11 with non‐A non‐B chronic hepatitis), 14 (51.9%) showed HBV viraemia by PCR. In contrast, of the 75 patients in the control group (45 with HCC; 30 with non‐A and non‐B chronic hepatitis) who were both HCV PCR negative and HBsAg negative, five (11.1%) showed HBV viraemia by PCR. The PCR for HBV revealed coexistent HBV viraemia in HCV viraemia patients, despite HBsAg negativity by EIA. In HBV‐endemic areas, the possibility of coinfection of HBV in HBsAg‐negative patients with HCV viraemia should be considered and molecular analysis for HBV‐DNA performed.
Relationship between interleukin‐8 levels and myeloperoxidase activity in human gastric mucosa
Authors: SASAYAMA YOSHIAKI , KAWANO SUNAO , TSUJI SHINGO , FUSAMOTO HIDEYUKI , KAMADA TAKENOBU , FUKUI HIROYUKI , YONEDA SHOTARO , OKISHIO TATSUO 
Published: March 2008

ABSTRACTAlthough interleukin (IL)‐8 is well known as a chemotactic agent for neutrophil migration in vitro, the relationship between IL‐8 activity and the degree of neutrophil infiltration in gastric mucosa is still unclear. In the present study, we investigated IL‐8 and myeloperoxidase activity, a marker of neutrophil infiltration, in gastric antral mucosa using biopsy samples in 23 patients with no gastric lesions. The results indicate that there is a good correlation between IL‐8 and myeloperoxidase activity (y = 0.173x + 13.9; r = 0.49, P<0.01). Furthermore, IL‐8 and myeloperoxidase activity are significantly higher in Helicobacter pylori‐positive patients than in H. pylori‐negative patients. In conclusion, an increase of IL‐8 activity in the gastric mucosa causes increased neutrophil infiltration in human gastric mucosa and H. pylori infection acclerates these reactions in the mucosa.