bluuebunny/crossref_metadata_2025_split huggingface dataset:
Review: Treatment of primary biliary cirrhosis
Authors: HEATHCOTE JENNY 
Published: March 2008

ABSTRACTPrimary biliary cirrhosis (PBC) is a slowly progressive chronic cholestatic disease of the liver thought to be caused by immune destruction of the interlobular bile ducts. One‐third of patients are asymptomatic and one‐third of these develop symptoms within 5 years. Therapeutic regimens should be directed at the control of symptoms, prevention of complications and specific therapy aimed at controlling progression of the disease. Symptoms may be secondary to cholestasis or due to other associated diseases. The cause of pruritus secondary to cholestasis remains unknown; the anion exchange resin cholestyramine generally brings relief. In patients resistant or intolerant to this therapy, rifampin may be helpful, as well as ultraviolet light without sunblock. Liver transplantation may rarely be the only option for uncontrollable pruritus. Clinical manifestations of keratoconjunctivitis sicca and xerostomia need constant attention to prevent corneal ulcers and dental caries. Preventative therapy includes regular screening for thyroid dysfunction and replacement therapy when necessary and the administration of the fat soluble vitamins A, D and K once hyperbilirubinaemia is present. Osteoporosis is a complication of all cholestatic liver disease. There is no satisfactory preventative therapy. It may be appropriate to give hormone replacement therapy to all post‐menopausal women with PBC to reduce osteoporosis. Liver transplantation is the best option for those with fractures. Oesophageal varices may develop early in the course of PBC, non‐selective beta‐blocker therapy should be used as prophylaxis against variceal haemorrhage. The only specific therapy shown to cause both a biochemical and survival benefit in patients with PBC is ursodeoxycholic acid (UDCA). Treatment with UDCA delays progression, but does not result in a cure of this disease. Currently, liver transplantation is the only definitive treatment available for end‐stage disease.
Plasma interleukin‐8 levels in patients with post‐hepatitic cirrhosis: Relationship to severity of liver disease, portal hypertension and hyperdynamic circulation
Authors: LI CHUNG‐PIN , LEE FA‐YAUH , TSAI YANG‐TE , LIN HAN‐CHIEH , LU REI‐HWA , HOU MING‐CHIH , WANG TEH‐FANG , CHEN LING‐SHENG , WANG SUN‐SANG , LEE SHOU‐DONG 
Published: March 2008

ABSTRACTThe present study investigated plasma levels of interleukin‐8 (IL‐8) in patients with post‐hepatitic cirrhosis and correlated it with the severity of liver diseases and haemodynamic parameters. Plasma IL‐8 levels were significantly higher in 57 post‐hepatitic cirrhotic patients (7.5 ± 1.8 pg/mL; P< 0.005) than those in 41 healthy subjects (2.0 ± 0.2 pg/mL). Elevated (> 5 pg/mL) plasma IL‐8 levels were found in up to 30% of cirrhotic patients. In cirrhotic patients, plasma IL‐8 levels progressively increased in relation to the severity of liver dysfunction (4.5 ± 1.0, 4.9 ± 1.4 and 20.5 ± 8.3 pg/mL for Pugh's class A, B and C, respectively; P<0.005). A significant correlation was observed between plasma IL‐8 levels and serum bilirubin levels (r = 0.72; P<0.001). There were no differences in the hepatic venous pressure gradient (15.4 ± 1.1 vs 15.1 ± 0.9 mmHg; P>0.05) and systemic vascular resistance (1119 ± 118 vs 1199 ± 54 dyn.s/cm5; P>0.05) between cirrhotic patients with and without elevated plasma IL‐8 levels. In addition, plasma IL‐8 levels did not correlate with hepatic venous pressure gradient (r = 0.26; P>0.05) and systemic vascular resistance (r=‐0.24; P>0.05). These results demonstrate that plasma IL‐8 levels are increased in patients with post‐hepatitic cirrhosis. The severity of liver cirrhosis is an important factor for the occurrence of enhanced IL‐8 levels. IL‐8 does not play a role in the hyperdynamic circulation observed in patients with post‐hepatitic cirrhosis.
High acid secretion may protect the gastric mucosa from injury caused by ammonia produced by Helicobacter pylori in duodenal ulcer patients
Authors: SHIBATA TOMOYUKI , IMOTO ICHIRO , TAGUCHI YUKIKO , TAKAJI SATOSHI , IKEMURA NORIHISA , NAKAO KAZUYUKI , KOSHIYAMA MASUMI , SHIMA TERUO 
Published: March 2008

ABSTRACTThe aim of the present study was to investigate the mechanism by which gastric atrophy does not tend to occur in patients with duodenal ulcer despite frequent Helicobacter pylori infection. This investigation was performed in 60 patients with duodenal ulcer and 63 age‐matched gastritis patients. Endoscopic findings in the antrum and corpus were classified as normal, atrophic and superficial changes. Biopsy specimens were taken from the antrum and corpus. Ninety per cent of patients with duodenal ulcer and 63.5% of patients with gastritis had H. pylori infection (P<0.01). The incidence of normal findings in duodenal patients was 30% in antral regions and 50% in the corpus (P<0.05). Atrophic change was observed in 21.7% of patients in the antrum and 3.3% of patients in the corpus (P<0.01). The grade of inflammation in duodenal ulcer specimens was significantly higher in the antrum than in the corpus (P<0.01). >H. pylori density was significantly higher in the antrum than in the corpus in ulcer patients (P<0.01). No significant difference in endoscopic findings, >H. pylori density or the grade of inflammation was found between the antrum and corpus in patients with gastritis. The mean intragastric ammonia concentration was 10.3 mg/dL in duodenal ulcer patients and 6.2 mg/dL in gastritis patients (P<0.01). The mean pH was 3.5 and 4.6 in ulcer and gastritis specimens, respectively (P<0.01). Our data suggest that gastric mucosa injury is less frequently associated with duodenal ulcers than with gastritis due to the low >H. pylori density in the corpus and to the higher acid output that neutralizes the ammonia produced by H. pylori.
Epithelial cell proliferation during colonic chemical carcinogenesis in the rat
Authors: OKADA HIROYUKI , MIZUNO MOTOWO , IKEDA NOBUMASA , TOMODA JUN , TSUJI TAKAO 
Published: March 2008

ABSTRACTTo define the significance of alterations in epithelial cell proliferation as a marker of high risk mucosa for colorectal cancer, we examined cell proliferative events in the colonic mucosa during chemical carcinogenesis using in vitro bromodeoxyuridine labelling and by analysing serial colonoscopic biopsy specimens from dimethylhydrazine (DMH)‐treated rats. In both the rectum and flexure of the colon, an increased labelling index of colonic epithelial cells, an upward extension of the proliferating zone and an upward shift of the major area of DNA synthesis of epithelial cells were observed during DMH‐induced colonic carcinogenesis in rats. These changes preceded the development of the colonic tumour and were observed in endoscopically normal rectal mucosa where the tumour was absent. We confirmed the altered cell proliferative events preceding the development of the tumour by examining serial colonoscopic biopsies. The results suggest that these alterations are features that identify premalignant colonic mucosa in DMH‐treated rats.
Lymphocyte proliferative responses to recombinant hepatitis C virus antigens in patients with chronic hepatitis C
Authors: MORI HIROMITSU , YABU KOJI , YOSHIZAWA KANAME , TANAKA EIJI , KIYOSAWA KENDO 
Published: March 2008

ABSTRACTThe purpose of the present study was to analyse lymphocyte proliferative responses to recombinant hepatitis C virus (HCV) antigens in chronic hepatitis C. Four recombinant peptides derived from the NS3, core, E1 and E2/NS1 regions of the HCV genome were used as antigens in lymphocyte proliferative responses. Forty‐two patients, classified into various sub‐groups, and 17 healthy control subjects were tested and the specific response was expressed as a stimulation index. Responses were analysed with alanine aminotransferase (ALT) level and histological diagnosis. NS3‐ and core‐antigen specific responses in all patient groups were significantly higher than in the healthy control group. E1‐ and E2/NS1‐antigen‐specific responses in the patient group with ALT levels exceeding 100 IU/L were significantly higher than those in other patient groups. Histological diagnosis was not correlated to the intensity of the core‐ and NS3‐specific responses. E1‐ and E2/NS1‐antigens induced significantly elevated responses in patients with chronic active hepatitis and liver cirrhosis compared with results in the healthy control group and in patients with chronic persistent hepatitis. In conclusion, the significantly elevated responses to core‐ and NS3‐antigens may be related to HCV infection and such responses to E1‐ and E2/NS1‐antigens could be related to the severity and activity of the disease.
Case Report: Intrahepatic cholangiocarcinoma with rhabdoid transformation
Authors: HONDA MASANAO , ENJOJI MUNECHIKA , SAKAI HIRONORI , YAMAMOTO ICHIRO , TSUNEYOSHI† MASAZUMI , NAWATA HAJIME 
Published: March 2008

ABSTRACTSarcomatous transformation is found in approximately 5% of patients with intrahepatic cholangiocarcinoma. According to previous reports, sarcomatous cholangiocarcinomas are composed of spindle‐shaped cells and/or multinucleated giant cells. Usually, vimentin is expressed by these sarcomatoid cells. We report a case of intrahepatic cholangiocarcinoma with an element of rhabdoid cells that occurred in a 61‐year‐old woman admitted for back pain. Various imaging techniques demonstrated multiple liver masses. Histologically, these tumours formed in both sarcomatous and ordinary tubular adenocarcinomatous areas. The sarcomatoid areas were occupied mainly by loosely arranged, eosinophilic rhabdoid cells, which expressed both keratin and vimentin. These findings suggest that rhabdoid cells may occur in an undifferentiated stage of cholangiocarcinoma and possess a strong tendency to metastasize.
DNA flow‐cytometric analysis in colorectal cancer: A comparison of metastasizing and non‐metastasizing tumours
Authors: YANG JIA‐LIN , CROWE PHILIP J , OW KIM T , HAM JOHN M , CROUCH ROGER L , RUSSELL PAMELA J 
Published: March 2008

AbstractThe most common cause of death in patients with colorectal cancer is metastatic liver disease. In order to identify patients at a high risk of developing hepatic secondaries from colorectal cancers, DNA content was measured in metastasizing colorectal primaries (Group I, n= 32) as well as in their subsequently resected liver secondaries and in sections of non‐metastasizing colorectal cancers (Group II, n= 25). A modified interpretation system involving both a DNA index and percentage of cycling cells (those in S and G2 + M phases) was developed. DNA content was measured in paraffin‐embedded sections by flow cytometry using internal controls (human peripheral blood mononuclear cells) and non‐malignant tissue controls (19 patients with diverticular disease). In Group I there were significantly more tumours with both abnormal ploidy (aneuploid or abnormal tetraploid peak) and > 15% cycling cells compared with Group II (Chi‐squared; P= 0.034). The combination of abnormal ploidy and > 15% cycling cells was superior to Dukes’ classification for identifying metastasizing tumours (Logistic Regression; P= 0.047). However, it was not possible to discriminate between the two groups using either DNA ploidy or the percentage of cycling cells alone. The metastasizing colorectal cancers exhibited similar DNA ploidy characteristics and had a similar percentage of cycling cells compared with their liver metastases. These results suggest that tumour DNA ploidy plus the percentage of cycling cells may predict the development of liver metastases and thus survival in patients with colorectal cancer.
Regeneration of nerve fibres across a colonic anastomosis in the guinea‐pig
Authors: BROOKES SJH , LAM TCF , LUBOWSKI DZ , COSTA M. , KING† DW 
Published: March 2008

AbstractResection and re‐anastomosis of the bowel interrupts enteric neuronal pathways. The re‐establishment of neuronal connections across a colonic anastomosis was studied using immunohistochemical, retrograde tracing and physiological techniques. In control guinea‐pig proximal colon, retrograde labelling with 1,1′‐didodecyl‐3,3,3,3′‐tetramethylindocarbocyanine perchlorate (DiI) revealed that enteric neurons with anally‐directed projections are more numerous and have longer axons than orally‐projecting neurons. In resected bowel, up to 26 weeks after re‐anastomosis, descending neuronal pathways were substantially interrupted. Immunohistochemical labelling of nerve fibres revealed that some enteric nerve fibres did regenerate across narrow regions of the anastomosis, growing preferentially in the oral to anal direction. However, nerve fibres immunoreactive for neurofilament protein triplet were substantially depleted in myenteric ganglia anal to the anastomosis, even after the longest recovery periods, demonstrating that axonal regrowth was limited. This was confirmed in retrograde tracing studies, as no nerve cell bodies oral to an anastomosis were labelled when DiI was placed on myenteric ganglia just anal to the anastomosis. Physiological studies confirmed that regrowth of nerve fibres across the anastomosis occurred and that it was asymmetric, as electrical stimulation led to aboral conduction across the anastomosis more reliably than oral conduction, as measured by circular muscle contraction. After resection and re‐anastomosis of the colon, the disruption of neuronal pathways in the enteric nervous system was observed, with limited and preferential re‐establishment of aborally‐directed long connections.
Response to interferon in chronic hepatitis C due to mixed genotype infection
Authors: HORIIKE NORIO , MASUMOTO TOSHIKAZU , MICHITAKA KOJIRO , KUROSE KIYOTAKA , AKBAR SM FAZLE , ONJI MORIKAZU 
Published: March 2008

AbstractWe examined the response to interferon (IFN) in patients with chronic hepatitis C (CHC) due to two different genotypes of hepatitis C virus (HCV) infection. Among 64 CHC patients studied, one (2%) had HCV‐RNA genotype I, 36 (56%) had genotype II, 19 (30%) had genotype III, 2 (3%) had genotype IV and 6 (9%) had both genotypes II and III. There was no significant difference in age, sex, history of blood transfusion and liver histology among patients with genotypes II, III and II + III. The HCV‐RNA titre of genotype II patients was significantly higher than that of genotype III patients (P < 0.05). However, there was no significant difference in the HCV‐RNA titre between genotype II + III and the other groups. The complete response rate achieved with IFN therapy was significantly higher in genotype III patients (74%) than in genotype II patients (17%; P < 0.01). Of the six patients with genotype II + III, a complete response to IFN was only achieved by two patients (33%), both of whom had a low HCV‐RNA titre (≦ 104,5 copies/mL) and HCV serotype 2. The remaining four patients had HCV serotype 1 and three of the patients had a high HCV‐RNA titre (≧ 105 copies/mL). The HCV genotype III was lost in two patients after IFN therapy. These data suggest that HCV‐RNA titre and HCV serotype are important factors for predicting the efficacy of IFN therapy in patients with mixed genotype infection and show direct evidence of higher susceptibility towards CHC of patients with genotype III than genotype II.
Increase of sulfated ursodeoxycholic acid in the serum and urine of patients with chronic liver disease after ursodeoxycholic acid therapy
Authors: NAKAMURA KIMIHIDE , YONEDA MASASHI , KIMURA ATSUSHI , TAMORI KEISUKE , YOKOHAMA SHIRO , SATO YOICHI , KATO TAKAFUMI , HASEGAWA TAKENAO , SAITO HIDEAKI , AOSHIMA MASARU , FUJITA MASANORI , MAKINO ISAO 
Published: March 2008

AbstractThe present study was undertaken in order to investigate the influence of ursodeoxycholic acid (UDCA) on the composition of sulfate‐conjugated bile acids in the serum and urine of patients with chronic active hepatitis and compensated liver cirrhosis. After a 12 week UDCA treatment (600 mg/day), total serum bile acid concentration increased two‐fold in patients with compensated liver cirrhosis and increased slightly in patients with chronic active hepatitis. The percentage of sulfated bile acids significantly increased in patients with both compensated liver cirrhosis and chronic active hepatitis. UDCA made up 63% of the total serum bile acids in compensated liver cirrhosis and 61% in chronic active hepatitis after UDCA treatment. Of the serum bile acids after UDCA treatment, 35.2 and 53.9% of UDCA was sulfate conjugated in compensated liver cirrhosis and chronic active hepatitis, respectively. Urinary excretion of total bile acid and UDCA after UDCA treatment in compensated liver cirrhosis were higher than in chronic active hepatitis. UDCA made up 68% of the total urinary bile acids in compensated liver cirrhosis and 64% in chronic active hepatitis after UDCA treatment. Of the urinary bile acids after UDCA treatment, 51.8 and 54.8% of UDCA was sulfate conjugated in compensated liver cirrhosis and chronic active hepatitis, respectively. UDCA treatment for compensated liver cirrhosis was less effective than for chronic active hepatitis. We found that sulfate conjugation is one of the major metabolic pathways for UDCA after UDCA treatment in chronic liver diseases.
A distinctive aphthous ileitis linked to Ancylostoma caninum
Authors: CROESE JOHN , FAIRLEY STEPHEN , LOUKAS ALEX , HACK JOHN , STRONACH PAM 
Published: March 2008

AbstractIleal ulceration is diagnosed commonly at colonoscopy in northeastern Australia. This observation has occurred contemporaneously with the description of a painful enteritis caused through supposedly rare infections by Ancylostoma caninum, the cosmopolitan dog hookworm. In this study, we describe the morphology and prevalence of ileal ulcers and investigate their cause. There were 182 patients with a distinctive aphthous ileitis highlighted by haemorrhage into the tips of surrounding villi. The annual rate reached 4.7% of ileal examinations. Eosinophilic enteritis was the characteristic, but inconsistent, histological appearance. Ulceration was linked to infection by A. caninum through serological testing and, in three patients, by the retrieval of single hookworms. Affected patients were also more likely to own a dog (53%) than the total colonoscopic population (43%; P< 0.02). The monthly rates of diagnosis were related to climate with fewest recordings during winter. Pain was the chief indication for colonoscopy (49%), proportionally higher than in controls (28%; P< 0.0001). Patients with ulcers had increased blood eosinophil, immunoglobulin E and serological values. These results were higher still in the subset with pain compared with the rest. Most patients, however, had colonoscopy performed for unrelated reasons, such as bowel cancer surveillance, and were identified as having subclinical ulceration (rate 3.2%). The findings establish a distinctive aphthous ileitis characterized by tissue eosinophilia. The cause has been tentatively linked to canine hookworms. It is proposed that infection in this geographic region is common and only rarely does a painful enteritis develop as a consequence of hypersensitization.
Point mutation in precore region of hepatitis B virus: Sequential changes from ‘wild’ to ‘mutant'
Authors: EHATA TOSHIKI , YOKOSUKA OSAMU , IMAZEKI FUMIO , OMATA MASAO 
Published: March 2008

AbstractOne point mutation to make a stop codon in the precore (pre‐C) region of the hepatitis B virus DNA in anti‐HBe‐positive patients has been reported recently. This mutation disturbs the formation of the pre‐C protein that is processed to make HBeAg. The relationship between the point mutation and HBe antigen antibody status was investigated in B‐viral liver diseases. The pre‐C region was amplified by a polymerase chain reaction (PCR) method and the nucleotide sequences were determined by a direct sequencing method. In seven cases who were persistently HBeAg‐positive, the wild type (no mutation in pre‐C region) was detected in all. In 20 cases who were anti‐HBeAg‐positive at diagnosis, the mutant type (point mutation at nucleotide 1896 in pre‐C region, which makes a stop codon) was detected in 16 cases and the wild type in two cases. In HBe seroconversion (SC) cases, the types of virus were investigated in serial blood samples. No mutant type was detected in initial sera during the HBeAg‐positive period. In two ‘natural’ SC cases, the mutant type appeared before anti‐HBe formation. However, in three anti‐viral ‘drug‐induced’ SC cases, the mutant type appeared after the formation of anti‐HBe. In two ‘reversed’ seroconversion cases only the wild type was detected throughout the follow‐up period. These data suggest that the appearance of a pre‐C mutant may help to predict seroconversion from HBeAg to anti‐HBe and may help distinguish ‘natural’ and ‘drug‐induced’ seroconversion of HBeAg.
Clinical assessment of the bacterial load of Helicobacter pylori on gastric mucosa by a new multi‐scaled rapid urease test
Authors: CHOU CHANG‐HUA , SHEU BOR‐SHYANG , YANG HSIAO‐BAI , CHENG PIN‐NAN , SHIN JENG‐SHIANN , CHEN CHIUNG‐YU , LIN XI‐ZHANG 
Published: March 2008

ABSTRACTThe present study tests the efficacy of the multi‐scaled urease test (MUT) in detecting Helicobacter pylori infection and determines whether the MUT can predict the bacterial density on histology. A total of 111 sets of gastric specimens were obtained from patients with dyspepsia but without recent bleeding. Two biopsies were taken as closely as possible in each set. One sample was used for the MUT (Hp fast; GI Supply, Camp Hill, PA, USA), while the other was used to determine the histological density of H. pylori by modified Giemsa stain (grade 0–5). The results of MUT were interpreted as negative if the colour was yellow or bright green (reaction score 0) and positive if the colour was green, light blue, or blue (reaction score 1, 2 and 3, respectively). The reaction scores of MUT were recorded sequentially at 15 and 30 min and 1, 4 and 24 h. On the basis of histological confirmation, MUT had a sensitivity of 89.6%, a specificity of 88.2%, a positive predictive value of 94.5% and a negative predictive value of 78.9%. Focusing on specimens with the presence of bacteria under histology, 77 specimens were divided into five subgroups by grades of density of H. pylori (HPD1–5). The reaction scores had become sequentially elevated from 30 min through to 24 h in each subgroup. For subgroups HPD4 and 5, the positive rates of MUT were 70.6 and 66.6%, respectively, as early as 30 min and progressed to 100% within 4 h. In contrast, the positive rate for the HPD1 subgroup was 16.6% at 4 h and increased to only 62.5% at 24 h. In subgroups HPD 2 and 3, the positive rates were less than 30% at 30 min, but became more than 66.6% at 4 h and were 100% at 24 h. The early (i.e. mean value of reaction scores before 4 h) and late (24 h) mean reaction scores disclosed two elevated trends as the density of H. pylori increased (early: 0.2, 0.7, 0.8, 1.5, 1.2; late: 1.4, 2.3, 2.6, 3.0, 3.0; P < 0.05). In conclusion, MUT is a reliable method for the diagnosis of H. pylori infection. It can also indirectly predict the density of H. pylori on histology.
Can misoprostol and omeprazole reduce nicotine and ethanol induced gastric mucosal injury? A quantitative macroscopic and microscopic analysis in rats
Authors: HUI WM , HO J , CHEN BW , CHO C‐H , BRANICKI FJ , LAM SK 
Published: March 2008

ABSTRACTWe compared the effects of misoprostol, omeprazole and methylcellulose (control) on gastric mucosal injury induced by nicotine and/or ethanol. The results demonstrate that misoprostol and omeprazole each significantly reduce macroscopic injury and deep injury at a microscopic level (P < 0.05) induced by nicotine alone, ethanol alone or a combination of ethanol and nicotine. Misoprostol and omeprazole each reduced the leakage of fluorescein isothiocyanate‐albumin into the interstitium in the gastric mucosa. Misoprostol and omeprazole are each effective in preventing injury induced by nicotine and ethanol and vascular factors are involved.