bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ethnicity, socioeconomic status, transfusions and risk of hepatitis B and hepatitis C infection
Authors: AKBAR NURUL , BASUKI BASTAMAN , GARABRANT DAVID H , SULAIMAN ALI , NOER HM SJAIFOELLAH , MULYANTO  
Published: March 2008

ABSTRACTThis study identifies the risk factors for hepatitis B virus (HBV) and hepatitis C virus (HCV) and measures the prevalence of hepatitis B surface antigen (HBsAg) and antibody to hepatitis C (anti‐HCV) in the general population of Jakarta. A population‐based sample of 985 people aged 15 and above was surveyed. Risk factors were identified through questionnaires and home visits. Serum was analysed for HBsAg, antibody to hepatitis B surface antigen (anti‐HBs), anti‐HCV, aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The seroprevalence was: 4.0% (39/985) for HBsAg, 17.2% (170/985) for anti‐HBs, and 3.9% (38/985) for anti‐HCV. The risk factors for hepatitis B and hepatitis C infection had little in common. Low socioeconomic status was a strong risk factor for HBsAg (adjusted odds ratio (OR) 18.09; 95% confidence interval (CI) 2.35–139.50). In addition, the Chinese group has 2.97 higher risk of having HBV infection compared with the Malayan ethnic group (adjusted OR 2.97; 95% CI 1.22–7.83). There was moderate positive trend between family size and risk of HBsAg positivity (P= 0.130). Age over 50 (adjusted OR 14.72; 95% CI 4.35–49.89) and history of transfusion were significant risk factors for hepatitis C (adjusted OR 3.03; 95% CI 1.25–7.33). Hepatitis B and hepatitis C infections have different risk factors in Jakarta, a high risk in population for both diseases. Hepatitis B transmission is associated with low socioeconomic status, Chinese ethnic group and large family size, while hepatitis C is associated with an older age and a history of transfusions.
Functional and phenotypical activation of leucocytes in inflamed human colonic mucosa
Authors: OSHITANI NOBUHIDE , SAWA YOSHINORI , HARA JUNICHI , ADACHI KENJI , NAKAMURA SHIRO , MATSUMOTO TAKAYUKI , ARAKAWA TETSUO , KUROKI TETSUO 
Published: March 2008

ABSTRACTInfiltrating leucocytes are activated to generate reactive oxygen species or to produce several molecules in inflamed colonic mucosa. To clarify the phenotypical and functional properties of activating cells in colitic mucosa, 23 patients with ulcerative colitis and 13 controls were studied using a combined method for determining in situ nitroblue tetrazolium reducing activity and immunohisto‐chemical characterization. Antibodies 25F9 (anti‐macrophage), EG2 (anti‐eosinophil cationic protein), MAC387 (anti‐calprotectin, expressed by activated myeloid‐histiocytes lineage), and MAC‐1 (anti‐CD11b) were used. The proportion of EG2, calprotectin, and CD11b‐positive cells were significantly increased in inflamed mucosa. The proportion of EG2, calprotectin, and CD11b‐positive cells significantly correlated with the histological degree of inflammation. Proportion of EG2‐positive cells but not calprotectin nor CD11b‐positive cells was significantly correlated with nitroblue tetrazolium reducing activity. Aggregated cells reducing nitroblue tetrazolium seen in severely inflamed mucosa were found to be EG2 positive. Most of the calprotectin‐positive cells were 25F9 negative. In addition to activation of neutrophils and macrophages, eosinophil activation has been shown to be involved in inflamed colonic mucosa.
CASE REPORT: Clinical and virological analyses of a patient positive for hepatitis C virus‐RNA by branched DNA assay but negative for anti‐hepatitis C virus antibodies
Authors: SUZUKI FUMITAKA , CHAYAMA KAZUAKI , NAKAJIMA TAKEYUKI , KAWASAKI TSUNEHISA , KUMADA HIROMITSU , YOSHIMI TERUYA 
Published: March 2008

ABSTRACTInfection with hepatitis C virus (HCV) is usually diagnosed by the presence of antibodies against fusion proteins or peptides derived from different regions of the HCV genome. However, a subgroup of patients with HCV viraemia are seronegative for antibody against hepatitis C virus (anti‐HCV) by conventional antibody assays. We analysed serum samples from a patient with liver cirrhosis who tested negative for anti‐HCV by a second‐generation assay, but positive for HCV‐RNA by reverse transcription‐polymerase chain reaction (RT‐PCR) and branched DNA signal amplification. To identify possible mutations that could explain the failure of detection of anti‐HCV by second‐generation assay, PCR‐amplified DNA fragments of the core region derived from the serum were cloned and sequenced. Nucleotide (nt) and amino acid (aa) sequence analyses (nt 1–486, aa 1–162) showed no mutations revealing stop codons, frame‐shifts, deletions or insertions, but the presence of two amino acid substitutions (aa 75 and 91) when compared with HCV‐J, a prototype strain of genotype 1b isolated from a Japanese patient. One of these two mutations (aa 75) was situated in the second hydrophilic domain of the core peptide, but analysis of the hydropathy profile showed only a little change. The two mutations were identical to those identified in other Japanese HCV isolates. The serum immunoglobulin level and T and B cell counts were normal in our patient. Our data suggest that the absence of anti‐HCV in this patient was not due to mutations of major epitopes of HCV. Low‐dose prednisolone administration just after transfusion may have induced immunological tolerance against HCV in this patient.
All‐trans retinoic acid suppresses liver injury induced by Propionibacterium acnes and lipopolysaccharide in rats
Authors: MOTOMURA KENTA , SAKAI HIRONORI , ISOBE HIDEHIKO , NAWATA HAJIME 
Published: March 2008

ABSTRACTAll‐trans retinoic acid (ATRA) has been reported to exert major effects on the immune system, including monocytes/macrophages. The present study was designed to determine whether ATRA would modulate macrophage‐associated liver injury induced by Propionibacterium acnes and lipopolysaccharide (LPS) in rats. All‐trans retinoic acid administration alleviated the liver injury and reduced the incidence of death following hepatic failure. Serum alanine aminotransferase (ALT) levels 5 h after, and survival rates within 12 h after the administration of LPS were significantly lower in the ATRA‐treated group (134 ± 119 IU/L and 72.7%) compared with the control group (713 ± 411 IU/L and 18.2%; P < 0.05). Histological findings supported these results. These effects may be due to suppression of tumour necrosis factor‐α (TNF‐α) and superoxide anions produced by activated macrophages. Serum levels of TNF‐α 1 h after LPS administration were significantly lower in the ATRA‐treated group (60.5 ± 7.0 ng/mL) as compared with the control group (105.2 ± 39.3 ng/mL; P < 0.05). Formazan deposition that was generated by the perfusion of the liver with nitroblue tetrazolium, also suggested suppression of the release of superoxide anions from hepatic macrophages. These results suggest that ATRA acts as an immunomodulator in liver injury by suppressing the activation of liver macrophages.
Lansoprazole and amoxycillin: Observations on the treatment of Helicobacter pylori infection
Authors: HAZELL STUART L , DASKALOPOULOUS GEORGE , MITCHELL HAZEL M , MASSEY DAN 
Published: March 2008

ABSTRACTSymptomatic patients (n=101) with Helicobacter pylori infection were enrolled into a double‐blind, double‐dummy study to assess the efficacy of lansoprazole plus amoxycillin in the treatment of H. pylori infection. Patients were randomized to either lansoprazole 30 mg once daily (days 0‐28) together with placebo (matched to amoxycillin) three times a day (days 0‐14) followed by either placebo or amoxycillin 500 mg three times daily (days 15‐28). Biopsy specimens for culture and histology were collected on days 0 and 56 or upon symptomatic relapse. Blood for serology was collected at days 0, 56 and 168. A [14C]‐urea breath test was performed on day 168. Eighty‐one (80.2%) patients completed the 56 day assessment. Of patients treated with lansoprazole plus amoxycillin, 35.1% (13/37) were cured of infection as assessed at day 56 (26.5% on an intention‐to‐treat basis), compared with 4.8% (2/42) of the placebo group (4% on an intention‐to‐treat basis). Recrudescence/re‐infection occurred in one patient upon re‐evaluation at day 168. Analysis of prognostic factors indicated that smoking and alcohol intake had little impact on the treatment outcome. Inflammation (both acute and chronic) improved in patients treated with lansoprazole plus amoxycillin. The relatively low efficacy of the treatment may relate to a single daily dose of lansoprazole (30 mg) being prescribed, treatment with amoxycillin being commenced 2 weeks after the initiation of lansoprazole or accurate assessment of treatment efficacy (both antral and body biopsy specimens taken).
Quality of ulcer healing influences the relapse of gastric ulcers in humans
Authors: NEBIKI HIROKO , ARAKAWA TETSUO , HIGUCHI KAZUHIDE , KOBAYASHI KENZO 
Published: March 2008

ABSTRACTThe usefulness of dye‐contrast endoscopy for the evaluation of the quality of gastric ulcer healing and the prediction of relapse was investigated. Sixty consenting patients whose ulcers healed during 3 months of treatment underwent endoscopy for the identification of the pattern of mucosal regeneration. Patients were monitored for relapses for up to 18 months after antiulcer therapy had ended. The pattern of regeneration was flat in 24 patients, nodular in 25 and intermediate in 11. Internal hypoechoic areas seen by endoscopic ultrasonography were less common and histological maturity was better in the patient group with the flat pattern compared with the patient group with the nodular pattern of mucosal regeneration. Prostaglandin E, synthesis was highest in the group with the flat pattern of mucosal regeneration and the relapse rate was lowest in this group. We conclude that the evaluation of the quality of ulcer healing is possible and that findings in individuals may aid the prediction of relapse for particular patients.
Gall‐bladder wall thickening in patients with liver cirrhosis
Authors: WANG TEH‐FANG , HWANG SHINN‐JANG , LEE FA‐YAUH , TSAI YANG‐TE , LIN HAN‐CHIEH , LI CHUNG‐PIN , CHENG HUEI‐MIN , LIU HAW‐JANG , WANG SUN‐SANG , LEE SHOU‐DONG 
Published: March 2008

ABSTRACTGall‐bladder wall thickening is commonly seen in patients with cirrhosis, but its exact causes have not been well established. We evaluated clinical, biochemical and haemodynamic data of patients with cirrhosis with respect to the presence of thickening of the gall‐bladder wall. After excluding patients who presented with gallstones, acute or chronic cholecystitis, heart failure, a serum creatinine level greater than 2 mg/dL and/or a serum alanine aminotransferase level greater than 400 U/L, 77 patients with cirrhosis (75 male, two female; mean age 58±8 years) were enrolled in the study. Clinical, biochemical, ultrasound and haemodynamic data were obtained in every patient. Fortyone (53%) of 77 patients with cirrhosis had gall‐bladder wall thickening (>4mm). Compared with patients with a normal gall‐bladder wall, patients with gall‐bladder wall thickening had significantly lower serum albumin levels (3.6±0.6 vs 2.9±0.7 gm/dL, respectively; P< 0.05), a longer prothrombin time (13±6 vs 16±6s, respectively; P<0.05), more patients with Child‐Pugh class C (6 vs 37%, respectively; P<0.05) and more patients with ascites (8 vs 50%, respectively; P<0.05). In addition, compared with patients with a normal gall‐bladder wall, those patients with gall‐bladder wall thickening had a higher hepatic venous pressure gradient (13.9±4.5 vs 17.1±4.1 mmHg, respectively; P<0.01) and a lower systemic vascular resistance (SVR; 1144±332 vs 1010±318 dyn.s/cm5, respectively; P< 0.05). Using a multivariate analysis, the presence of ascites and SVR lower than 900 dyn.s/cm5, were independently correlated with the presence of gall‐bladder wall thickening, while a hepatic vein pressure gradient greater than 10 mmHg had only a marginally significant association. The presence of ascites, decreased SVR and portal hypertension are related to the occurrence of gall‐bladder wall thickening in patients with cirrhosis, indicating that the development of gall‐bladder wall thickening may be multifactorial.
Clinical study of cryoglobulinaemia in Chinese patients with chronic hepatitis C
Authors: HWANG SHINN‐JANG , LEE SHOU‐DONG , LI CHUNG‐PIN , LU REI‐HWA , CHAN CHO‐YU , WU JAW‐CHING 
Published: March 2008

ABSTRACTCryoglobulinaemia is the most common immunological disorders seen in patients with chronic hepatitis C virus (HCV) infection. We evaluated the incidence and clinical significance of cryoglobulinaemia in 122 Chinese patients with chronic hepatitis C. The pathogenic roles of HCV genotypes and viraemia in this phenomenon were also evaluated. Fifty‐four (44%) of the 122 patients with chronic hepatitis C had cryoglobulinaemia. Eleven (20%) of the patients with cryoglobulinaemia had symptoms and signs of cutaneous vasculitis, arthralgia, neuropathy and renal involvement. The patients with cryoglobulinaemia were predominantly female and had a significantly higher mean serum level of rheumatoid factor and a lower mean serum C4 level compared with patients without cryoglobulinaemia (50 vs 29%, 23 vs 15 IU/mL, 25 vs 31 mg/dL, respectively, P < 0.05). The mean serum HCV RNA level, HCV genotype, the presence of serum auto‐antibodies, and the rate of cirrhosis were not significantly different between the two groups. Univariate logistic regression analysis showed female serum levels of alanine aminotransferase (> 90 U/L), rheumatoid factor (> 15 IU/mL), C3c (< 100 mg/dL) and C4 (< 20 mg/dL) to be significant predictors of cryoglobulinaemia in chronic hepatitis C patients. However, multivariate analysis showed only serum C4 levels (< 20 mg/dL) as a significantly independent predictor. We concluded that 44% of Chinese patients with chronic hepatitis C had cryoglobulinaemia. Serum C4 levels were significantly lower in chronic hepatitis C patients with cryoglobulinaemia and the serum C4 level was the only clinical independent predictor associated with this phenomenon. Hepatitis C virus genotype and serum viral load were not clinical independent predictors.
Natural history of chronic hepatitis B virus infection: An immunopathological study
Authors: CHU CHIA‐MING , LIAW YUN‐FAN 
Published: March 2008

ABSTRACTThree clinicopathological phases of chronic hepatitis B virus (HBV) infection are identified. First, is immune tolerance of HBV. High levels of viraemia are associated with normal alanine aminotransferase (ALT) levels and minimal histological lesions. More than 30–40% of hepatocytes have the hepatitis B core antigen (HBcAg), predominantly in their nuclei. Maternally derived hepatitis B e antigen (HBeAg) crossing the placenta may result in the elimination of T helper cells responsive to HBeAg/HBcAg. This phase can last for periods ranging from a few weeks to 10 or more years until the immune tolerance is lost. Second, is the immune clearance of HBV. Intermediate levels of viraemia are associated with fluctuating ALT levels and active and ongoing hepatitis. Approximately 20–30% of hepatocytes have HBcAg, predominantly in their cytoplasm. Expression of pre‐core defective HBV mutants during chronic HBV infection may lead to a reduction in the secretion of HBeAg and may trigger the beginning of the immuno‐elimination phase. The mechanism of intrahepatic shift of HBcAg from the nucleus to the cytoplasm and the decreased levels of viraemia in this phase may be, at least in part, secondary to liver damage and regeneration. Third, is latent infection with residual integrated HBV. Undetectable viraemia is associated with normal ALT levels and no virus‐induced liver damage. With regard to hepatocyte expression of HBsAg in chronic HBV infection, membrane staining of HBsAg on hepatocytes has been shown to correlate well with the presence of viraemia. The degree of cytoplasmic hepatitis B surface antigen (HBsAg) expression inversely correlates with the level of viraemia. Therefore, HBsAg carriers with high levels of viraemia have low levels of cytoplasmic hepatitis B surface antigen (HBsAg) expression, while those with low levels of viraemia have high levels of cytoplasmic HBsAg expression. However, several exceptions have been identified. High levels of viraemia associated with high levels of cytoplasmic HBsAg expression were recognized in patients with fibrosing cholestatic hepatitis. In contrast, low levels of viraemia associated with low levels of cytoplasmic HBsAg expression were recognized in patients with hepatitis C virus but not hepatitis D virus superinfection.
Hepatitis in patients with end‐stage renal disease
Authors: HUANG CHIU‐CHING 
Published: March 2008

ABSTRACTABSTRACTHepatitis B and hepatitis C are two common pathogens causing chronic hepatitis in patients with end‐stage renal disease (ESRD). With the acceptance of hepatitis B s antigen (HBsAg) screening, infected patients have been identified and isolated over the past 20 years. Consequently, hepatitis B is now being seen less frequently in dialysis units. Even though hepatitis B has become less of a problem, non‐A, non‐B hepatitis has been recognized as a sigmlicant problem since 1979. With the availability of serological testing for hepatitis C virus (HCV), more specific information is now available in regard to HCV infection in dialysis patients. The prevalence of anti‐HCV in haemodialysis (HD) patients is quite variable, ranging from 5 to over 50%. Anti‐HCV positivity is associated with previous blood transfusions, mode of therapy and duration of haemodialysis. In Spain and Italy, the annual seroconversion rates of HCV antibodies in dialysis patients are 2–9%; this rate was much higher in Taiwan (15%). Whether patients with HCV infection should be identified and isolated during HD treatment is an issue of controversy. Transplantation is associated with increases in hepatitis B virus (HBV) replicative markers. The survival disadvantage in HBsAg‐positive recipients usually did not become apparent until 8 years after transplantation. Hepatitis C virus‐infected renal transplant recipients are presumably in a similar situation to patients with hepatitis B, although confirmatory data are currently lacking. Coinfection of HBV and HCV may lead to aggressive liver disease and cirrhosis. A hepatitis B vaccine is recommended for all susceptible dialysis patients. Dialysis patients have lower response rates to hepatius B vaccines than do other people. Currently, no vaccine is available for hepatitis C. To date, there are no effective treatments available for hepatitis B and hepatitis C. Combination therapy with interferodlamivudine for hepatitis B and interferodribavirin for hepatitis C may offer a promise of effective control of viral replication in the future.
Drug‐induced hepatic injury
Authors: FARRELL GEOFFREY C 
Published: March 2008

ABSTRACTDrugs and other chemical toxins account for less than 5% of cases of jaundice or acute hepatitis and fewer cases of chronic liver disease, but they are an important cause of more severe types of hepatic injury. Drug reactions produce an array of hepatic lesions that mimic all known hepatobiliary diseases; this poses a diagnostic challenge for physicians and pathologists. Diagnosis of drug‐induced hepatic injury is circumstantial, with positive rechallenge being the only factor that unequivocally implicates a particular agent. Nonetheless, other aspects of the temporal relationship between drug ingestion and adverse reaction, exclusion of other diseases, the presence of extrahepatic features of drug hypersensitivity and some findings on liver biopsy can lend support to the diagnosis. Some of these issues will be explored in this review by considering contemporary paradigms of drug‐induced hepatic injury. Factors that predispose to dose‐dependent hepatic injury will be considered in relation to acetaminophen, an example of acute hepatotoxicity, and methotrexate, an agent that can produce hepatic fibrosis. Flucloxacillin will be discussed as an example of drug‐induced cholestatic hepatitis often associated with prolonged cholestasis and the vanishing bile duct syndrome. Minocycline and diclofenac will be mentioned as two drugs for which drug hepatitis is an exceedingly rare complication. Finally, the evidence that Chinese herbal medicines can be hepatotoxic will be reviewed.
Review: Molecular approaches to inherited liver disease. Focus on Wilson disease
Authors: COX DIANE W 
Published: March 2008

ABSTRACTAlthough infectious agents account for a large proportion of liver disease, inherited forms of liver disease, often treatable, must not be overlooked. New approaches to the cloning of disease genes are allowing an increased understanding of the basic defect of human diseases. Identification of disease genes can have practical applications for diagnosis, can provide information on prognosis and can lead to new therapies. This review focuses on selected inherited liver diseases and the knowledge to be gained from molecular studies. Three genetic diseases affecting the liver, Wilson disease, haemochromatosis and α1‐antitrypsin deficiency, are selected as examples of current approaches to the study of genetic liver disease.
Pathogenesis of alcoholic liver disease with particular emphasis on oxidative stress
Authors: ISHII HIROMASA , KUROSE IWAO , KATO SHINZO 
Published: March 2008

ABSTRACTOxidative stress is well recognized to be a key step in the pathogenesis of ethanol‐associated liver injury. Ethanol administration induces an increase in lipid peroxidation either by enhancing the production of oxygen reactive species and/or by decreasing the level of endogenous antioxidants. Numerous experimental studies have emphasized the role of the ethanol‐inducible cytochrome P450 in the microsomes and the molybdo‐flavoenzyme xanthine oxidase in the cytosol. This review shows the putative role of ethanol‐induced disturbances in iron metabolism in relation to iron as a pro‐oxidant factor. Ethanol administration also affects the mitochondrial free radical generation. Many previous studies suggest a role for active oxygens in ethanol‐induced mitochondrial dysfunction in hepatocytes. Recent studies in our laboratory in the Department of Internal Medicine, Keio University, using a confocal laser scanning microscopic system strongly suggest that active oxidants generated during ethanol metabolism produce mitochondrial membrane permeability transition in isolated and cultured hepatocytes. In addition, acetaldehyde, ethanol consumption‐associated endotoxaemia and subsequent release of inflammatory mediators may cause hepatocyte injury via both oxyradical‐dependent and ‐independent mechanisms. These cytotoxic processes may lead to lethal hepatocyte injury. Investigations further implicate the endogenous glutathione—glutathione peroxidase system and catalase as important antioxidants and cytoprotective machinery in the hepatocytes exposed to ethanol.