bluuebunny/crossref_metadata_2025_split huggingface dataset:
Non‐surgical treatment of hepatocellular carcinoma
Authors: LIN DENG‐YN , LIN SHI‐MING , LIAW YUN‐FAN 
Published: March 2008

ABSTRACTA decade ago, surgery was the only satisfactory treatment modality for hepatocellular carcinoma (HCC), but it was limited only to selected cases. For the majority of cases of HCC, systemic chemotherapy was one of the few treatment alternatives, but provided only marginal benefit. In the past 20 years, diagnostic methods have improved to an extent that small HCC less than 1 cm can be detected. Moreover, non‐surgical treatment is available, of which regional therapy has been shown to prolong patients’ survival, and may even replace surgical resection in some cases. Regional therapy is indicated for the treatment of HCC when there is no extrahepatic metastasis and the patient has adequate liver function reserve, thus permitting repeated therapy. Transcatheter hepatic arterial embolization (TAE) using various embolizers has been well documented to include controlled studies. However, it is not indicated for patients with thrombosed main portal veins. Its therapeutic effect is also doubtful when the tumour is infiltrative in nature or is hypovascular, too large or too small. Additional chemotherapeutic agents mixed into the embolizer with lipiodol and degraded starch microspheres or styrene‐maleic acid‐neocarzinostatin in which chemotherapeutic agents are embedded, are used with a better response, but the survival rate has not shown significant improvement. Ultrasound‐guided local injection therapy is another new method of treatment of HCC. Of these techniques, percutaneous ethanol injection therapy (PEIT) is widely used with excellent results for small, encapsulated tumours in livers with less than three HCC. Percutaneous ethanol injection therapy can also be used in cases with portal vein thrombosis, but it is not suitable for patients having coagulopathy or ascites. Using acetic acid, OK‐432, interferon or anti‐cancer drugs in the injection therapy shows no further benefit over ethanol alone. Transcatheter echoguided thermotherapy or cryotherapy has been reported in small series of patients, as has target therapy with immune or radiotherapy and conformal radiotherapy. Preliminary studies show encouraging results. Systemic therapy with either single drug or multidrugs is ineffective, with a response rate of less than 20%. Immunotherapy, such as with interferon or other cytokines, is not beneficial. Hormone therapy has not been promising, except for treatment with tamoxifen, which has been reported to show some beneficial effect. Gene therapy is still in its infancy. In summary, recent progress in non‐surgical treatment of HCC has resulted in a breakthrough of regional therapy looking quite promising. Moreover, a combination of different types of regional therapies may yield better outcomes in selected individuals.
Distribution of hepatitis C virus genotypes among blood donors in Taiwan
Authors: WU CHII H , LEE MEY F , KUO HSIEN S 
Published: March 2008

ABSTRACTThe aim of this study was to investigate the prevalence and distribution of hepatitis C virus (HCV) genotypes of blood donors in Taiwan. RNA was extracted from the serum of anti‐hepatitis C virus‐positive carriers and this was followed by reverse transcriptase—polymerase chain reaction (RT‐PCR) using type‐specific primers for the presence of HCV genotypes, 1a, 1b, 2a, 2b, 3a and 6a. Of the 604 anti‐HCV‐positive specimens, the PCR demonstrated that 93.0% (562/604) were positive for at least one HCV genotype. The remaining 42 specimens (7%) were HCV negative. Among the 562 HCV‐positive specimens, 505 (89.8%) contained HCV 1a, 1b, 2a, 2b and 3a as the only genotype, with a prevalence of 0.4% (2/562), 60.1% (338/562), 15.5% (87/562), 11.9% (67/562), and 2.0% (11/562), respectively. No HCV genotype 6a was found. Thirty‐seven specimens (6.6%) exhibited mixed infections with multiple HCV genotypes that included types 1b, 2a and 2b, while 20 (3.5%) HCV RNA‐positive sera remained unclassified. These results confirm that the predominant HCV genotype in Taiwan is 1b. In addition, genotypes 1a and 3a can also be found in Taiwan at low frequency.
Diagnostic value of anti‐hepatitis D virus (HDV) antibodies revisited: A study of total and IgM anti‐HDV compared with detection of HDV‐RNA by polymerase chain reaction
Authors: HUANG YI‐HSIANG , WU JAW‐CHING , SHENG WEN‐YUNG , HUO TEH‐IA , CHANG FULL‐YOUNG , LEE SHOU‐DONG 
Published: March 2008

ABSTRACTA high serum titre (≥ 1000 or ≥ 5000) of total antibody to hepatitis D virus (anti‐HDV) and positive for immunoglobulin (Ig) M anti‐HDV have been used to represent HDV replication, while reverse transcription‐polymerase chain reaction (RT‐PCR) is currently the most sensitive assay for detecting HDV viraemia. The aim of the present study was to re‐evaluate the correlation of total anti‐HDV and IgM anti‐HDV with HDV viraemia based on RT‐PCR and to assess the clinical significance of these markers in acute and chronic HDV superinfection. Chronic HDV infection was defined as positive HDV‐RNA by RT‐PCR for more than 6 months, while total anti‐HDV titre was defined by serial dilution. Of 178 hepatitis B virus (HBV) carrier patients studied, 119 cases had been anti‐HDV positive for more than 6 months. Two‐thirds (79/119) were positive for HDV viraemia by RT‐PCR. Only half the chronic HDV viraemic patients had a high titre (≥ 1000) of total anti‐HDV, and there was only moderate agreement (K = 0.41) between total anti‐HDV titre/IgM anti‐HDV and HDV‐RNA and chronic HDV viraemia. Based on cross‐sectional and longitudinal follow‐up analyses, serum total anti‐HDV titres ≥ 100 appeared to be an excellent cut‐off titre (K = 0.91) in differentiating chronic from acute HDV infection among viraemic patients. In summary, IgM and a high titre total of anti‐HDV are not good markers of HDV viraemia, but an anti‐HDV titre of ≥ 100 appears to be an excellent marker for the differentiation of acute from chronic HDV superinfection.
Acute hepatitis C among renal failure patients on chronic haemodialysis
Authors: OKUDA KUNIO , HAYASHI HARUYUKI , YOKOZEKI KAZUO , KOBAYASHI SUSUMU , KASHIMA TAKASHI , IRIE YASUBUMI 
Published: March 2008

ABSTRACTHepatitis C virus (HCV) infection is common in haemodialysis units, yet little information is available about the clinical feature of acute hepatitis C among renal failure patients. The present study is based on 49 cases of acute hepatitis C seen at a haemodialysis centre where sporadic nosocomial infection was occurring up to June 1993. Liver function tests were done at 4 weekly intervals on all dialysis patients, anti‐HCV antibodies were tested by the C‐100 and second generation tests and serum HCV‐RNA was determined by the branched DNA and Amplicore tests. Diagnosis of acute hepatitis C was made on the basis of an acute rise in alanine aminotransferase (ALT) and seroconversion to positive anti‐HCV antibodies. Clinical presentation of acute hepatitis was generally mild with rare overt jaundice and the diagnosis was possible only from increased ALT, which was generally low. Spontaneous resolution of acute hepatitis within 8 months with clearance of viral RNA occurred in only four cases, 91.8% of patients developing chronic hepatitis. Biopsy in 12 cases with high ALT levels showed mild to moderate inflammatory activities. In conclusion, the clinical presentation of acute hepatitis C is generally mild in chronic haemodialysis patients, but spontaneous resolution is infrequent. A longer follow‐up period is required for defining the long‐term prognosis.
Computer morphometry for quantitative measurement of liver fibrosis: Comparison with Knodell's score, colorimetry and conventional description reports*
Authors: LIN XI‐ZHANG , HORNG MING‐HWUI , SUN YUNG‐NIEN , SHIESH SHU‐CHU , CHOW NAN‐HAW , GUO XIOU‐ZHEN 
Published: March 2008

ABSTRACTLiver fibrosis is currently described quite subjectively or, at best, semiquantitatively by scoring systems. In order to measure the severity of liver fibrosis quantitatively and to compare this with established methods, such as Knodell's scoring system, the colorimetric method and conventional description reports, we undertook the present study. A personal computer with an image grabber card and a microscope equipped with a computer‐controlled slide‐driver was used for computer morphometry. The principle behind morphometry is based on the different colours of hepatocytes and fibres following staining with Masson's trichrome stain. There were 31 patients (25 male, six female) recruited into the present study with a mean ±SD age of 41.6 ± 15 years (range 24–66 years). Of these patients, 16 had chronic hepatitis B, 12 had chronic hepatitis C and three were alcoholics. Colorimetric methods and Knodell's fibrosis score were performed according to established protocols. Conventional description reports were obtained from reviews of patient charts. The results from computer morphometry were highly correlated with results from the colorimetric method, with a correlation coefficiency γ= 0.85 (P < 0.0001). The results from computer morphometry also correlated with both Knodell's scoring system (γ= 0.69; P < 0.001) and conventional description reports (γ= 0.46; P < 0.01). Results from Knodell's scoring system were significantly correlated with computer morphometry, as follows: score 0, 2.7 ± 1.4; score 1, 5.7 ± 1.2; score 2, 7.7 ± 2.3; score 3, 10.7 ± 3.2; score 4, 21.8 ± 14.1. The trend was statistically significant by the Wilcoxon rank sum test. In conclusion, our computerized morphometry system is a reliable tool for the evaluation of the severity of liver fibrosis and can be used as a tool for the objective quantification of liver fibrosis.
Regulation of uridine diphosphate glucuronosyltransferase during the acute‐phase response
Authors: STRASSER SIMONE I , MASHFORD MAURICE L , DESMOND PAUL V 
Published: March 2008

ABSTRACTThe acute‐phase response is associated with profound effects on oxidative drug metabolism. However, the effects on glucuronidation are poorly characterized. The aim of the present study was to determine the role of mediators of the acute‐phase response in the regulation of hepatic uridine diphosphate glucuronosyltransferase (UGT) expression. Family 1 and family 2 UGT isoforms were studied in turpentine‐injected rats and in primary hepatocyte cultures exposed to cytokines and/or dexamethasone. In the in vivo model, glucuronidation of p‐nitrophenol was unaffected, while testosterone glucuronidation was reduced to 65% of control (P < 0.01). In contrast, the mRNA level of UGT1*1 (which metabolizes bilirubin, not phenols) was depressed to 16% of control (P < 0.002), while the mRNA level of UGT2B3 (which metabolizes testosterone) was reduced to 53% (P < 0.05). In primary hepatocyte culture, dexamethasone treatment resulted in a 3.4‐fold induction of UGT1*1 mRNA levels (P < 0.001) but only a 1.5‐fold induction of UGT2B3 (P=0.1). Interleukin‐6 in the presence of dexamethasone resulted in a marked dose‐dependent suppression of both UGT1*1 and UGT2B3, although to different degrees. Interleukin‐1 had no effect on UGT mRNA levels. Thus, inflammatory mediators, such as cytokines and glucocorticoids, may be important determinants of both oxidative and conjugative drug metabolism by the liver.
Antibody dependent cell‐mediated cytotoxicity using hepatocellular carcinoma reactive monoclonal antibody
Authors: KUWATA TOMO , HARUTA IKUKO , HASEGAWA KIYOSHI , YAMAUCHI KATSUMI , HAYASHI NAOAKI 
Published: March 2008

ABSTRACTWe have established monoclonal antibodies from mice immunized with the human hepatocellular carcinoma cell line, hu‐H2. One of the antibodies, designated 523(KY‐3), was reactive with this hepatocellular carcinoma cell line as well as with the human pancreatic cancer cell line, MIA. Another monoclonal antibody, 512(KY‐2), only reacted with the hepato‐cellular carcinoma cell lines. Neither antibody reacted with the colon cancer cell line CW3. Pretreatment of peripheral blood mononuclear cells with 523 resulted in enhancement of their natural cytotoxicity to hu‐H2 (9.0 vs 18.4% in subject 1, 3.5 vs 14.7% in subject 2, and 14.2 vs 31.0% in subject 3). In contrast, such antibody mediated enhanced natural cytotoxicity was not found by pretreatment of the same peripheral blood mononuclear cell with 512. With the similarity in reactivity of 523, this antibody dependent enhancement was found in natural cytotoxicity to hu‐H2 and MIA but not to CW3. Based on the facts that 523 did not have a direct cytopathic effect on these tumours and that this 523‐mediated enhanced natural cytotoxicity was inhibited by anti‐FcγRIII antibody, we concluded that the 523‐mediated enhanced cytotoxicity reflects its activity to induce antibody dependent cytotoxic cells. Thus, these results demonstrate that several distinct tumour‐specific antigens exist in hepatocellular carcinoma (HCC) and that one of them represents a potentially useful target for immunotherapy of human hepatocellular carcinoma.
Expression of insulin‐like growth factor II mRNA in hepatocellular carcinoma
Authors: NG IRENE OL , LEE JOYCE MF , SRIVASTAVA GOPESH , NG MATTHEW 
Published: March 2008

ABSTRACTInsulin‐like growth factor II (IGF‐II) is a mitogenic polypeptide closely related to insulin. Its gene has complex regulation of transcription, resulting in multiple mRNA initiated by different promoters. To study its role in hepatocarcinogenesis, we examined the expression of IGF‐II mRNA in hepatocellular carcinomas (HCC) and correlated it with the pathological features of the tumours. Using northern blot analysis, transcription of the normal adult promoter was repressed in all but two of the 30 HCC. Instead, there was re‐expression of two foetal transcripts (6 and 5 kb) in 12 tumours. In contrast, most (93.3%) of the non‐tumorous livers showed expression of adult transcript only, and there were three livers demonstrating expression of foetal transcripts in addition to the adult one. There was a significant association of IGF‐II expression with direct tumour invasion into the adjacent liver parenchyma but foetal expression did not influence other parameters directly related to tumour invasiveness, including venous permeation, formation of tumour microsatellites and positive resection margin. Besides, IGF‐II expression was significantly more frequently seen in tumours from older patients. To conclude, repression of normal adult promoter and re‐expression of foetal promoters of IGF‐II are common events in HCC. The observation that foetal IGF‐II expression was significantly more frequent in older patients suggests that spontaneous foetal expression of IGF‐II late in life may promote the growth of tumours which have already arisen through other mechanisms, but foetal reexpression itself is not enough to contribute to tumour progression.
Association between anomalous pancreaticobiliary ductal union and adenomyomatosis of the gall‐bladder
Authors: TANNO SATOSHI , OBARA TAKESHI , MAGUCHI HIROYUKI , FUJII TSUNESHI , MIZUKAMI YUSUKE , SHUDO RYUSHI , TAKAHASHI KUNIYUKI , NISHINO NORIYUKI , ARISATO SATOSHI , URA HITOSHI , KOHGO YUTAKA 
Published: March 2008

ABSTRACTA frequent association of biliary tract carcinoma and anomalous pancreaticobiliary ductal union (APBD) is well recognized, especially gall‐bladder carcinoma in undilated type APBD. However, little is known about the presence and incidence of adenomyomatosis (AMT) of the gall‐bladder, a presumed premalignant lesion, in patients with APBD. This retrospective study was conducted to elucidate the clinical features and incidence of AMT in APBD patients with relation to undilated type and dilated type APBD. We reviewed the clinicopathological records of 30 patients with APBD (28 women and two men) encountered during the past 10 years. Among them, 22 patients underwent cholecystectomy and the resected specimens were subjected to histopathological examinations. Eleven cases of APBD patients were undilated type and 11 cases were dilated type. Adenomyomatosis was found in six (55%) of 11 undilated type and one (9%) of 11 dilated type, and fundal type was predominantly observed in six (86%) of seven AMT. An overall incidence of AMT in APBD patients was 32%. An undilated type of APBD is frequently associated with AMT and we believe, therefore, that clinicians should be aware of a possible coexistence of APBD and AMT.
Colour Doppler‐guided spectral analysis of gall‐bladder wall flow
Authors: HAYAKAWA SHINYA , GOTO HIDEMI , HIROOKA YOSHIKI , ITOH AKIHIRO , TAKI TOMOYUKI , WATANABE YOSHIHIRO , HAYAKAWA TETSUO , NAITOH YASUO 
Published: March 2008

ABSTRACTFor the purpose of the present study to diagnose gall‐bladder cancers, which cannot be detected or are only partly visible by conventional ultrasonography (US), we attempted differential diagnoses of 69 patients with gall‐bladder diseases (12 with gall‐bladder cancer, five with acute cholecystitis, 11 with chronic cholecystitis, 27 with cholesterol polyp and 14 with adenomyomatosis) using the evaluation of gall‐bladder wall blood flow (GWBF). GWBF was evaluated by colour Doppler‐guided spectral analysis (CDSA). Thirty‐three healthy volunteers were selected as controls at random. Two parameters of GWBF, namely flow velocity and resistive index (RI), were compared between patients with gall‐bladder diseases and healthy volunteers. GWBF could be ultrasonically evaluated in 92 (90%) of 102 subjects. All 12 patients with gall‐bladder cancer had a significantly rapid blood flow value compared with other patients and healthy volunteers. There was no significant difference in RI among patients and healthy volunteers. When cut‐off level of the flow velocity was set at 30 cm/s, gall‐bladder cancer could be diagnosed by flow velocity with 100% sensitivity (12/12) and 96% specificity (50/52). Using the same cut‐off level of the flow velocity, 17 patients were analysed prospectively. In four asymptomatic gall‐bladder cancers and two acute cholecystitis cases with some symptoms, the flow velocity was over 30 cm/s. In two of four patients with gall‐bladder cancer, only a part of the tumour was visualized on conventional abdominal US. In conclusion, CDSA was more useful for diagnosing gall‐bladder lesions than the conventional abdominal US due to estimation of arterial flow velocity in the gall‐bladder wall.
Expression of progastrin‐derived peptides and gastrin receptors in a panel of gastrointestinal carcinoma cell lines
Authors: KELLY APRIL , HOLLANDE FRÉDÉRIC , SHULKES ARTHUR , BALDWIN GRAHAM S 
Published: March 2008

ABSTRACTTo assess the potential of gastrin receptor antagonists in the treatment of gastrointestinal cancer, the presence of an autocrine loop involving progastrin‐derived peptides has been investigated in two colorectal and one gastric carcinoma cell lines. Progastrin, glycine‐extended gastrin and amidated gastrin were detected in cell extracts or conditioned media by radio‐immunoassay. Low‐affinity binding sites for glycine‐extended gastrin and amidated gastrin were present, but high‐affinity binding sites were not detected with the appropriate iodinated ligands. In addition, neither glycine‐extended gastrin nor amidated gastrin in the concentration range 10 pmol/L‐10 nmol/L stimulated cell proliferation. We conclude that it is unlikely that the carcinoma cell lines LIM 1215, LIM 1839 and LIM 1899 use either amidated or glycine‐extended gastrins as extracellular autocrine growth factors.
CASE REPORT: Rupture of a gastric varix in liver cirrhosis associated with glycogen storage disease type III
Authors: HASHIMOTO MASAJI , WATANABE GORO , YOKOYAMA TSUYOSHI , TSUTSUMI KENJI , DOHI TAKEHIKO , MATSUDA MASAMICHI , OKUBO MINORU , NAKAMURA NORIMASA , TSURUMARU MASAHIKO 
Published: March 2008

ABSTRACTGlycogen storage disease type III, or Cori's disease, is caused by a deficiency of amylo‐1,6‐glucosidase (debranching enzyme), which leads to the storage of an abnormal glycogen in the liver and in skeletal and heart muscle. Glycogen storage disease type III is usually characterized by hepatic symptoms, growth failure and myopathy. Even though liver cirrhosis is reported, portal hypertension is a rare complication of this disease. We describe the case of a glycogen storage disease type III patient who was diagnosed at 3 years of age and developed complications (liver cirrhosis and rupture of a gastric varix) at 31 years of age. We discuss the histological progression to cirrhosis of the liver and describe the liver enzyme profile at 3 and 31 years of age.
Altered intrahepatic pathway of para‐umbilical vein in portal hypertension
Authors: OHHIRA MOTOYUKI , OHTA HITOYOSHI , OHHIRA MASUMI , MATSUMOTO AKINORI , OHTAKE TAKAAKI , FUJIMOTO YOSHINORI , MURAZUMI KAZUHIKO , ONO MINORU , KOHGO YUTAKA 
Published: March 2008

ABSTRACTThe object of this study was to determine the frequency and characteristics of altered paraumbilical vein in the hepatic parenchyma, developed from portal hypertension, using computed tomography (CT). Two hundred and ninety‐two patients who presented with portal hypertension from 1986 to 1996 were studied retrospectively. The pathway of the dilated para‐umbilical vein was demonstrated by contrast‐enhanced CT. Thirty‐one (11%) patients had a dilated para‐umbilical vein arising from the left portal vein into the falciform ligament. In 24 (77%) of these patients, the para‐umbilical vein followed the expected route, passing through the fissure of ligamentum teres hepatis. The remaining seven patients (23%) displayed the unusual pathway, with the vein arising from the left branch of the portal vein and passing into the hepatic parenchyma. In these seven patients, four had one collateral vein, and three patients had two collateral veins in the liver parenchyma. The dilated para‐umbilical vein frequently passes through the hepatic parenchyma in patients with portal hypertension.
Altered biliary bilirubin profile in patients with persistent hyperbilirubinaemia after hepatic resection: Analysis of bile bilirubin subfractions by high‐performance liquid chromatography
Authors: ISHIYAMA SHUICHI , FUSE AKIRA , KUZU HIROSHI , IGARASHI YUKIO , URAYAMA MASAHIRO , TSUKAMOTO MASARU 
Published: March 2008

ABSTRACTSubfractions of bilirubin in bile, obtained via biliary drainage tubes from 23 patients who had undergone radical surgery for bile duct cancer, were analysed by high‐performance liquid chromatography for 14 days after surgery. Five principal conjugated bilirubins were resolved: bilirubin diglucuronide (BDG); bilirubin monoglucuronide monoglucoside (BGG); bilirubin monoglucuronide monoxyloside (BGX); and two isomers of bilirubin monoglucuronide. After surgery, depression in concentration of BDG and elevation of BGG and BGX were found. These alterations were of higher magnitude in patients who had undergone hepatectomy, and especially prolonged in patients with hyperbilirubinaemia. These results suggest that the alteration in proportions of bilirubin conjugates might be a cause of hyperbilirubinaemia after hepatectomy.
Case Report: Secondary biliary cirrhosis possibly related to congenital hepatic fibrosis. Evidence for decreased number of portal branch veins and hypertrophic peribiliary vascular plexus
Authors: DE LÉDINGHEN VICTOR , LE BAIL BRIGITTE , TRILLAUD HERVÉ , BERNARD PIERRE‐HENRI , SARIC JEAN , BALABAUD CHARLES , BIOULAC‐SAGE PAULETTE 
Published: March 2008

ABSTRACTA 30‐year‐old man with presinusoidal portal hypertension was transplanted for cryptogenic cirrhosis. On the explanted liver, few intrahepatic stones, biliary cirrhosis, chronic cholangitis of the large bile ducts and a peculiar proliferation of small dilated bile ducts at the periphery of the portal tracts led to the diagnosis of secondary biliary cirrhosis and cholangitis, possibly linked to ductal plate malformation, including congenital hepatic fibrosis associated with a minor form of Caroli's disease. Ex vivo portogram and histology showed the paucity of portal vein branches and the hypertrophy of the peribiliary vascular plexus. This hypertrophy, which has been reported in livers with presinusoidal hypertension, is another indirect argument to suggest the diagnosis of congenital hepatic fibrosis.