bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasma human hepatocyte growth factor concentrations in patients with biliary obstruction
Authors: Kimura Fumio , Miyazaki Masaru , Suwa Toshikazu , Sugiura Toshiyuki , Shinoda Tokuzou , Itoh Hiroshi , Ambiru Satoshi , Shimizu Hiroaki , Nakagawa Kouji 
Published: March 2003

AbstractBackground: It has been suggested that human hepatocyte growth factor (hHGF) maintains the growth and viability of hepatocytes and biliary epithelial cells. The purpose of this study was to determine plasma hHGF concentrations in patients with obstructive jaundice and to correlate these findings with clinical outcome.Methods: The study included 22 patients who had biliary obstruction and underwent percutaneous transhepatic biliary drainage. The plasma concentrations of hHGF, standard liver function tests, daily bile flow and the half‐life of serum total bilirubin were measured following the drainage.Results: Plasma hHGF concentrations were significantly higher in patients with biliary obstruction compared with a control group (P< 0.01). The plasma hHGF concentrations correlated with white cell count, prothrombin time and bilirubin half‐life (P< 0.05), but not with the values from other liver function tests. Seven patients who died within 3 months after biliary drainage had significantly higher concentrations of plasma hHGF than the 15 patients who survived for at least 3 months (P< 0.05). The patients who experienced a poor outcome also had lower bile flows and prolonged bilirubin half‐lives compared with the survivors (P< 0.05). The plasma hHGF concentrations decreased significantly after biliary drainage in the survivors (P< 0.01), but not in the patients with a poor outcome.Conclusions: These results suggest that systemic inflammation and the hepatic dysfunction caused by obstructive jaundice cause an increase in the plasma concentrations of hHGF. In addition, the plasma concentrations of hHGF may be a predictor of poor outcome in jaundiced patients.
Public health measures to control hepatitis B virus infection in the developing countries of the Asia–Pacific region
Authors: Chen Ding‐Shinn 
Published: March 2003

AbstractHepatitis B virus (HBV) infection is prevalent in the Asia–Pacific region and the disease burden caused by chronic HBV infection has been enormous. Although vaccination programmes have been implemented in the past decade, and there are extremely successful countries in the region, many countries still cannot afford a control program. These countries are often populous and highly endemic for HBV infection. To overcome this, aid from developed countries or private foundations should be actively sought. In the developing countries of this region, HBV infection in early childhood is the main cause of chronic HBV status, and thus universal vaccination of all infants is the best way to control HBV infection. Because of the expense and extra costs of screening pregnant women, the use of hepatitis B immune globulin may not be essential. To achieve the goal of universal infant vaccination, public education should be done in parallel with education of health professionals and control measures. The Asia–Pacific region has more people with chronic hepatitis B than any other part of the world, and control of HBV infection in this region will no doubt be the most important and challenging task to be taken in the beginning of the new millennium.
A 15‐minute [13C]‐urea breath test for the diagnosis of Helicobacter pylori infection in patients with non‐ulcer dyspepsia
Authors: Peng Nan‐Jing , Hsu Ping‐I , Lee Shui‐Cheng , Tseng Huei‐Hwa , Huang Wen‐Keui , Tsay Daw‐Guey , Ger Lu‐Ping , Lo Gin‐Ho , Lin Chiun‐Ku , Tsai Chi‐Chang , Lai Kwok‐Hung 
Published: March 2003

Abstract
Background
: Non‐ulcer dyspepsia (NUD) accounts for the majority of dyspeptic patients and studies on the epidemiology of Helicobacter pylori infection in NUD depend on a non‐invasive and rapid diagnostic test. This study was performed to determine the sensitivity and specificity of a 15‐min simplified protocol of the [13C]‐urea breath test ([13C]‐UBT) for the diagnosis of H. pylori infection in patients with NUD.
Methods
: One hundred and thirty‐six patients with a clinical and endoscopic diagnosis of NUD were included. The [13C]‐UBT was modified from the European standard protocol. The baseline breath sample was collected 5 min after the patient took a test meal and the 13CO2 was collected 15 min after the patient drank 100 mg [13C]‐urea. The gold standard used for comparison was either a positive culture or positive histology + positive rapid urease test sampled on upper gastrointestinal endoscopy.
Results
: The prevalence of H. pylori infection in NUD by the gold standard was 59.6%, whereas that calculated by the [13C]‐UBT was 60.3%. The sensitivity and specificity of [13C]‐UBT was 93.8 and 89.1% compared with the gold standard. The shortened collection time and simplification of the procedure may have led to a decline in specificity.
Conclusion
: The 15‐min [13C]‐UBT is a rapid but less specific protocol for detecting the presence of H. pylori infection in patients with NUD.© 2000 Blackwell Science Asia Pty Ltd
Interaction between hyaluronan and CD44 in the development of dimethylnitrosamine‐induced liver cirrhosis
Authors: Satoh Tomomi , Ichida Takafumi , Matsuda Yasunobu , Sugiyama Motoya , Yonekura Kenji , Ishikawa Tohru , Asakura Hitoshi 
Published: March 2003

Abstract
Background
: A significant increase in serum hyaluronan (HA) levels has been reported in patients with liver cirrhosis. This mechanism is not yet clear, and receptors for HA have not been characterized. In this study, we examined the expression of both HA and its receptors, CD44 and intercellular adhesion molecule‐1 (ICAM‐1), in dimethylnitrosamine‐induced liver cirrhosis.
Methods and Results
: Using biotinylated HA binding protein, HA was detected in the area of periportal fibrosis and around the sinusoidal wall where hepatic fibrosis was developing. Electron microscopy revealed that HA was localized on Ito cells and sinusoidal endothelial cells (SEC). Conversely, CD44, which was only expressed weakly in normal liver, was present in large amounts in cirrhotic liver. The distribution pattern of CD44 was similar to that of HA, however, CD44 was mainly localized on the infiltrating lymphocytes and Kupffer cells. Moreover, CD44 was detected on part of factor VIII‐positive SEC. intercellular adhesion molecule‐1, another receptor for HA, was detected on the surface of hepatocytes and around the sinusoidal wall in cirrhotic liver, but its distribution was not accompanied by expression of HA. With respect to CD44 isoforms, the standard form m‐RNA predominated in both normal and cirrhotic liver. Variant pMeta‐1 mRNA was detected at low levels.
Conclusions
: An interaction between HA and CD44 may play a role in the recruitment of numerous infiltrating cells and HA accumulation in hepatic sinusoids. Together with phenotypic changes in the SEC, these results may lead to a disturbance in the elimination of HA during the progression of liver cirrhosis.
Temporary use of an accuflex stent for unextractable common bile duct stones
Authors: Mizukami Yusuke , Saito Hiroya , Obara Takeshi , Arisato Satoshi , Nakano Yasuhiro , Sakurai Yasuo , Izawa Tsutomu , Kohgo Yutaka 
Published: March 2003

AbstractEndoscopic management has become the main therapeutic approach for the extraction of common bile duct (CBD) stones, and successful removal can be achieved in 80–90% patients using conventional balloon and basket techniques. However, if it is difficult to completely fragment a stone, or to clear the CBD, which may occur for a variety of reasons, the therapeutic problem will remain. When bile duct stones can not be removed, a viable management option is to place a biliary stent to ensure drainage. However, recent studies of long‐term biliary stenting, with a plastic stent, showed a relatively high rate of morbidity and mortality. We report an alternative, unique treatment for unextractable common bile duct stones, using the temporal placement of an expandable metallic stent (EMS) to facilitate passage of fragments through the papilla.
Iron excretion in iron‐overloaded rats following the change from an iron‐loaded to an iron‐deficient diet
Authors: Oates Phillip S , Jeffrey Gary P , Basclain Kerrie A , Thomas Carla , Morgan Evan H 
Published: March 2003

Abstract
Background
: Iron stores in the body are thought to be regulated by a mechanism associated with the rate of iron absorption from the diet, with no significant role played by iron excretion. We report the existence of an iron excretory process that results in the loss of significant amounts of liver iron.
Methods and Results
: Rats were fed 3% carbonyl iron for 9 weeks, which resulted in a 20‐fold increase in liver non‐haem iron. When the rats on this iron‐loaded diet were switched to a low iron diet for 2 and 7 days, liver non‐haem iron levels fell 30% and 45%, respectively. A similar fall in transferrin‐bound plasma iron was also seen. As the liver iron had not redistributed to other body compartments, it was concluded that the iron had been excreted and that the excreted iron represented a loss of 22% and 28% in total body non‐haem iron over 2 and 7 days, respectively. Ligation of the common bile duct in iron loaded rats that had been switched to the iron‐deficient diet was accompanied by a similar loss of liver iron and also hepatocellular damage. In addition, measurement of enterocyte iron levels showed that only approximately 5% of the total iron excreted was found in these cells.
Conclusion
: Neither bile nor enterocytes play a significant role in iron excretion. The similarity in the degree of fall in transferrin‐bound iron levels with a change in diet suggests that iron excretion involves the uptake and excretion of transferrin bound‐iron, possibly by goblet cells. The observed hypertrophy of the intestinal mucosa associated with carbonyl iron feeding may facilitate hypersecretion of mucous and the excretion of this iron.
Cardiac tamponade caused by spontaneous rupture of mediastinal lymph node metastasis of hepatocellular carcinoma
Authors: Seki Shuichi , Kitada Takuya , Sakaguchi Hiroki , Nakatani Kazuki , Kamino Toshio , Nakamura Kenji , Yamada Ryusaku 
Published: March 2003

AbstractRupture of a hepatocellular carcinoma (HCC) is a well‐known cause of death in patients with HCC. This report describes a rare case of HCC presenting as cardiac tamponade caused by a spontaneous rupture of mediastinal lymph node metastasis into the pericardial space. A transcatheter arterial embolization (TAE) of internal thoracic artery successfully controlled the bleeding, and the patient was rescued from cardiac tamponade. Although there was no rebleeding, the patient died from liver failure 2 months later. An autopsy revealed a poorly differentiated HCC in the liver, lung and mediastinal lymph nodes.
Coagulation profile and platelet function in patients with extrahepatic portal vein obstruction and non‐cirrhotic portal fibrosis
Authors: Bajaj Jasmohan S , Bhattacharjee J , Sarin Shiv‐Kumar 
Published: March 2003

AbstractBackground and Aims:Coagulation disorders commonly develop in patients with cirrhosis of the liver. They have also been reported in patients with non‐cirrhotic portal fibrosis (NCPF) and extra‐hepatic portal venous obstruction (EHPVO); the two conditions with portal hypertension and near‐normal liver functions. The spectrum and prevalence of coagulation abnormalities and their association with the pathogenesis of these diseases and with hypersplenism was prospectively studied.Methods:Eighteen EHPVO patients that included an equal number of NCPF patients and 20 healthy controls were prospectively studied. The coagulation parameters assessed included: international normalized ratio, partial thromboplastin time, and fibrinogen and fibrinogen degradation products. Platelet aggregation and malondialdehyde levels were measured.Results:Both EHPVO (83%) and NCPF (78%) patients had a significantly prolonged international normalized ratio and a decrease in fibrinogen and platelet aggregation. The EHPVO patients had a significant prolongation in partial thromboplastin time (67% patients), with increased levels of fibrinogen degradation product levels occurring in all patients; these were normal in NCPF patients. Platelet malondialdehyde levels were normal in both groups. Hypersplenism was present in four EHPVO and seven NCPF patients. It did not significantly influence the coagulation profile in either NCPF or EHPVO patients.Conclusions:Coagulation anomalies are common and significant in both NCPF and EHPVO patients, suggestive of a mild disseminated intravascular coagulation disorder. These imbalances could be caused by chronic subclinical endotoxemia and cytokine activation after the initial portal thromboembolic event. The persistence of these abnormalities in adolescent patients indicates an ongoing coagulation derangement.
Hepatic steatosis in chronic hepatitis C virus infection: Prevalence and clinical correlation
Authors: Hwang Shinn‐Jang , Luo Jiing‐Chyuan , Chu Chen‐Wei , Lai Chiung‐Ru , Lu Ching‐Liang , Tsay Shyh‐Haw , Wu Jaw‐Ching , Chang Full‐Young , Lee Shou‐Dong 
Published: March 2003

AbstractBackground and Aims: Hepatic steatosis is a histological characteristic in patients with chronic hepatitis C virus (HCV) infection. The aim of this study was to evaluate the prevalence of hepatic steatosis in Chinese patients with chronic hepatitis C, and to look for possible correlation with various histopathological changes and to look for possible correlation with various clinical and pathologic variables.Methods: One hundred and six patients were enrolled, and patients with alcoholism or diabetes mellitus were excluded. Clinical, biochemical and virologic data, including HCV genotype and serum HCV‐RNA titer and histological findings, were compared between patients with and without hepatic steatosis.Results: Fifty‐five (52%) of the 106 patients with chronic hepatitis C had hepatic steatosis. Patients with hepatic steatosis had significantly higher mean serum levels of triglyceride and γ‐glutamyl transpeptidase, higher body mass index, and a higher incidence of obesity compared with patients without hepatic steatosis. No significant differences in serum HCV‐RNA titer and HCV genotype or the response to interferon therapy were noted between the two groups. Histological analysis showed patients with hepatic steatosis had a significantly higher mean fibrotic score than patients without hepatic steatosis (1.9 ± 1.2 vs 1.3 ± 1.0; P = 0.016). There were no significant differences in the severity of necroinflammation, the presence of lymphoid aggregation/follicle or bile duct damage between the two groups. Multivariate logistic regression analysis showed that independent predictors associated with hepatic steatosis were obesity or a histology fibrotic score of ≥ 2.Conclusion: It was found that 52% of Chinese patients with chronic hepatitis C had hepatic steatosis. Patients with hepatic steatosis were more frequently obese and had more severe hepatic fibrosis.
Comparison of clinical, virologic and pathologic features in patients with acute hepatitis B and C
Authors: Chu Chen‐Wei , Hwang Shinn‐Jang , Luo Jiing‐Chyuan , Wang Yuan‐Jen , Lu Rei‐Hwa , Lai Chiung‐Ru , Tsay Shyh‐Haw , Wu Jaw‐Ching , Chang Full‐Young , Lee Shou‐Dong 
Published: March 2003

AbstractBackground and Aims:The clinical outcomes of adult‐acquired acute infection of hepatitis C virus (HCV) and hepatitis B virus (HBV) are quite different. In order to compare the clinical, biochemical, virologic and pathologic pictures in these two groups of patients, we enrolled 22 adult patients with acute hepatitis C and 16 adult patients with acute hepatitis B, on whom liver biopsies were performed within 3 months of acute onset of the illness.Results:The results showed that a significantly younger age, a higher ratio of the clinical symptoms of jaundice, nausea, vomiting, and poor appetite, a higher mean serum level of alanine transaminase, aspartate transaminase, and total bilirubin were present in patients with acute hepatitis B patients than in those with acute hepatitis C (P< 0.05). There was a significantly higher degree of periportal inflammation and total necro‐inflammatory activity in the acute hepatitis B patients (P= 0.002 and 0.049, respectively). Fifteen (68.2%) of the 22 patients with acute hepatitis C had detectable serum HCV‐RNA, but only two (14.3%) of the 14 tested patients with acute hepatitis B had detectable serum HBV‐DNA, detected by using the branched DNA signal amplification assay. Eighteen (82%) of the 22 acute hepatitis C patients and none of the 16 acute hepatitis B patients progressed into a chronic hepatitis stage (P< 0.001).Conclusion:The manifestations of mild clinical symptoms, lower mean serum transaminases and bilirubin levels, a lesser degree of histological periportal necroinflammation, and more patients with a high circulatory viral load among the acute hepatitis C patients, may lead to more of that group developing chronicity than patients with acute hepatitis B.
Reduced colonization of gastric mucosa by Helicobacter pylori in mice deficient in interleukin‐101
Authors: Chen Wangxue , Shu Dairu , Chadwick Vinton S 
Published: March 2003

AbstractBackground and Aims: Interleukin‐10 (IL‐10) is a potent anti‐inflammatory and immunoregulatory cytokine. Mice deficient in IL‐10 production (IL‐10−/−mice) develop a spontaneous chronic enterocolitis, suggesting that IL‐10 is an important regulator of the mucosal immune response in vivo. The objective of this study was to determine the role of endogenous IL‐10 in the host defense against gastric colonization by Helicobacter pylori by using IL‐10‐deficient mice.Methods: The IL‐10−/−mice were inoculated intragastrically with a mouse‐adapted H. pylori isolate (Sydney Strain 1). Gastric colonization by H. pylori (biopsy urease test and bacterial colony counts), serum levels of H. pylori‐specific immunoglobulin (Ig) M, A, G, isotypes of IgG, and the gastric mucosal inflammatory scores were determined 6 weeks after inoculation. Results were compared with those obtained from H. pylori‐infected control mice (IL‐10 +/−mice).Results: The colonization of gastric mucosa by H. pylori was reduced approximately 100‐fold (P≤ 0.0001) in IL‐10−/−mice (log10 4.87 ± 0.26 CFU/g tissue) as compared to IL‐10+/−mice (log10 6.64 ± 0.22 CFU/g tissue). Furthermore, IL‐10−/−mice infected with H. pylori had significantly higher H. pylori‐specific IgA and IgG antibodies in serum (P≤ 0.01), and developed much more severe chronic active gastritis than infected IL‐10+/−mice. The median scores of the infiltration of gastric mucosa by mononuclear cells and neutrophils were up to threefold higher in IL‐10−/−mice than they were in IL‐10+/−mice.Conclusion: Our studies suggest that endogenous IL‐10 is an inhibitor of the protective immune response to H. pylori infection. Interleukin‐10 participates in the downregulation of H. pylori‐induced gastric inflammatory responses, which apparently confers a survival advantage to the organism promoting more effective colonization of gastric mucosa.
Endoscopic duodenitis, gastric metaplasia and Helicobacter pylori
Authors: Urakami Yoshihito , Sano Toshiaki 
Published: March 2003

AbstractBackground and Aims: The purpose of this study was to investigate the relationship between gastric metaplasia and Helicobacter pylori in patients with endoscopic duodenitis.Methods: The subjects were 57 patients with endoscopic duodentitis with or without H. pylori‐associated gastritis. Biopsy specimens were obtained from the stomach and duodenal bulb to assess the histological findings and H. pylori infection. Gastric metaplasia was divided into three types: complete, intermediate and incomplete, according to the amount of mucus in the metaplastic cells. In 10 H. pylori‐positive patients, endoscopic and histological findings of duodenitis were compared before and after eradication of the bacteria.Results: There was no significant difference in the extent of gastric metaplasia or the appearance and severity of endoscopic duodenitis between H. pylori‐positive and ‐negative groups. The complete type of gastric metaplasia was frequently detected in the H. pylori‐negative group, whereas the incomplete type was frequently observed in the H. pylori‐positive group. After eradication of H. pylori, the incomplete type changed to the complete type with a decrease of histological inflammation.Conclusions: The complete type of gastric metaplasia occurred frequently without H. pylori infection, whereas the incomplete type was frequently associated with H. pylori infection.
Long‐term histological prognosis and serum fibrosis markers in chronic hepatitis C patients treated with interferon
Authors: Kojima Hiroshi , Hongo Yasushi , Harada Hideharu , Inoue Toshihiro , Miyaji Katsuhiko , Kashiwagi Motomi , Momose Tetsuya , Arisaka Yoshifumi , Fukui Hideo , Murai Seiyo , Tokita Hajime , Kamitsukasa Hiroshi , Yagura Michiyasu , Katsu Kenichi 
Published: March 2003

AbstractBackground:Interferon (IFN) therapy is effective in 20–40% of patients with chronic hepatitis C, but the relationship between histological changes and the response to interferon is still unclear. We investigated the long‐term histological prognosis and the changes of serum fibrosis markers after interferon therapy relation to the response.Methods and Results:One hundred and eighteen patients with chronic hepatitis C who received interferon therapy were divided into four groups based on the detection of viremia and the serum alanine aminotransferase (ALT) level after treatment. A histological examination was performed by using the histological activity index and the criteria of the METAVIR score. Serum fibrosis markers were used to measure the levels of hyaluronic acid and type IV collagen 7s. Responders, whose serum ALT levels became normal after treatment, demonstrated histological improvement. Histological improvement was more rapid in sustained virological responders with hepatitis C virus (HCV) RNA seronegativity than in biochemical responders with HCV‐RNA seropositivity. Only sustained virological responders exhibited histological cure. In partial responders, whose serum ALT levels decreased to less than twice the upper of normal, and non‐responders whose serum ALT levels were not reduced, liver fibrosis was unchanged or showed progression. Serum fibrosis markers increased with progression of the histological stage and varied depending on the response to interferon.Conclusion:Normalization of serum ALT levels after interferon therapy led to a histological improvement, and that with viral clearance achieved histological cure. Serum fibrosis markers were useful indicators for long‐term according to the response of IFN therapy.