International Hepatology Communications最新文献

{"title":"Changes in rat liver microsomal enzyme activities induced by injection of rat liver growth factor into male rats","authors":"Rafael García-Cañero,&nbsp;Javier Pérez de Diego,&nbsp;Carolina Trilla,&nbsp;Miguel de Foronda,&nbsp;Juan José Díaz-Gil,&nbsp;Rosa M. Cereceda,&nbsp;Maricarmen Guijarro","doi":"10.1016/S0928-4346(96)00335-0","DOIUrl":"10.1016/S0928-4346(96)00335-0","url":null,"abstract":"<div><p>Microsomal cytochromes P450 and b₅ and enzyme activities linked to P450 isoforms <span><math><mtext>IA1</mtext><mtext>2</mtext></math></span>, <span><math><mtext>IIB1</mtext><mtext>2</mtext></math></span>, IIC11 and IIIA were assessed over a 72 h period in male Wistar rats after intraperitoneal injection of a single dose of 4 μg/100 g body weight of rat liver growth factor (r-LGF) and compared with those of partially hepatectomized and sham-operated animals. The injection provoked a marked decrease in the activities of cytochrome P450 isozymes <span><math><mtext>IIB1</mtext><mtext>2</mtext></math></span>, IIC11 and IIIA and about a 50% reduction in cytochrome P450 and b₅ contents during the first 48 h postinjection, which were slowly restored to the levels observed in control or sham-operated animals. The findings in partially hepatectomized rats were similar. These results suggest that, alone, the rat liver growth factor selectively mimics the effects of the initial stages of in vivo liver regeneration in certain hepatic microsomal detoxifying enzymes.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00335-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76209775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New Inuyama classification; new criteria for histological assessment of chronic hepatitis","authors":"Fumihiro Ichida ,&nbsp;Takao Tsuji ,&nbsp;Masao Omata ,&nbsp;Takafumi Ichida ,&nbsp;Kyouichi Inoue ,&nbsp;Tomoteru Kamimura ,&nbsp;Goutarou Yamada ,&nbsp;Kunihiko Hino ,&nbsp;Osamu Yokosuka ,&nbsp;Hiroshi Suzuki","doi":"10.1016/S0928-4346(96)00325-8","DOIUrl":"10.1016/S0928-4346(96)00325-8","url":null,"abstract":"","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00325-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80995426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alcohol hepatic toxicity in rat: evidence of the utility of gastric ethanol metabolism","authors":"Lucia Battiston ,&nbsp;Michèle Moretti ,&nbsp;Patrizia Tulissi ,&nbsp;Massimiliano Fanni-Canelles ,&nbsp;Gabriele Pozzato","doi":"10.1016/S0928-4346(96)00330-1","DOIUrl":"10.1016/S0928-4346(96)00330-1","url":null,"abstract":"<div><p>Since a fraction of ingested ethanol (EtOH) is metabolized by gastric mucosa, different amounts of alcohol should reach the liver, when the same dose is administered by oral or intravenous route. Accordingly, we demonstrated that the hepatic depletion of glutathione induced by EtOH is lower when it is administered orally rather than intraperitoneally (i.p.). In the present study we investigated, after EtOH load, the time-course of common serum liver damage tests and of α-glutathione-<em>S</em>-transferase (αGST) levels as a new indicator of hepatocellular injury in rats. The tests were also performed in Cimetidine-treated rats. Oral EtOH administration was followed by a less pronounced decrease and by a quicker recovery of hepatic glutathione than after i.p. route. After oral EtOH load, Cimetidine, a potent inhibitor of gastric alcohol-dehydrogenase, produced a decrease of hepatic glutathione significantly (<em>P</em> &lt; 0.005) more pronounced than in controls. Serum αGST increased significantly (<em>P</em> &lt; 0.05) 6 h after i.p. EtOH administration, whereas no modifications were found after oral EtOH load. Common liver damage tests did not show any modification. In Cimetidine-treated rats, oral EtOH load was followed by an increase of serum αGST similar to that after i.p. administration. This study demonstrates the beneficial effects of gastric EtOH metabolism on the liver. The lack of gastric alcohol metabolism resulted not only in decreased content and delayed recovery of liver glutathione, but in potential hepatocellular damage.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00330-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86797330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ursodeoxycholic acid decreases the serum transaminase levels of chronic liver disease patients treated with glycyrrhizin","authors":"Hironori Mitsuyoshi,&nbsp;Toshiaki Nakashima,&nbsp;Koji Inaba,&nbsp;Hiroki Ishikawa,&nbsp;Yoshikuni Sakamoto,&nbsp;Ninko Matsumoto,&nbsp;Takeshi Okanoue,&nbsp;Kei Kashima","doi":"10.1016/S0928-4346(96)00334-9","DOIUrl":"10.1016/S0928-4346(96)00334-9","url":null,"abstract":"<div><p>The effects of ursodeoxycholic acid (UDCA) on the liver function test values were investigated in patients with chronic hepatitis (CH) and liver cirrhosis (LC) in whom treatment with glycyrrhizin (SNMC) for more than 6 months had failed to improve serum transaminase levels. Twenty-six patients treated with Stronger neo minophagen C (SNMC), 60 ml, i.v., three times/week) for more than 6 months were given UDCA (Urso, 600 mg/day) in addition (SNMC + UDCA group) and 22 patients were given UDCA (Urso, 600 mg/day) alone (UDCA group). The mean AST, ALT, γ-GTP and total bile acid (TBA) values during the 3 months before UDCA treatment and the 3 months after the start of UDCA treatment were compared in each case. The results showed that AST, ALT and γ-GTP were improved by 28, 34 and 46%, respectively in the 24 patients with CH, type C in the SNMC + UDCA group, and 27, 30 and 39%, respectively in the 14 patients with CH, type C in the UDCA group. UDCA was also effective in improving AST and ALT in the patients in the SNMC + UDCA group who were resistant to interferon therapy. The percentages of improvement in AST, ALT and γ-GTP in the 10 LC patients were lower than in the CH patients in both SNMC + UDCA and UDCA group. In conclusion, UDCA is useful in decreasing the serum transaminase levels of patients with CH, even when they are being treated with SNMC.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00334-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76727710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell killing effect of heparin-binding EGF-like growth factor Pseudomonas exotoxin on human hepatoma cells","authors":"Minoru Ono ,&nbsp;Michael Klagsbrun ,&nbsp;Yutaka Kohgo","doi":"10.1016/S0928-4346(96)00333-7","DOIUrl":"10.1016/S0928-4346(96)00333-7","url":null,"abstract":"<div><p>Heparin-binding, EGF-like growth factor (HB-EGF) is a potent mitogen for smooth muscle cell, fibroblast, and it also stimulates hepatocyte proliferation. We generated several chimeric toxins by fusing the cDNA sequence of HB-EGF and the mutant of <em>Pseudomonas</em> exotoxin, PE^4EKDEL (PE) that lacks the binding ability to a specific receptor. HB-EGF-PE was generated by fusing the DNA fragment encoding the full length mature HB-EGF polypeptide to the N-terminus of PE^4EKDEL, while HB-PE was generated by fusing the 45 N-terminal heparin-binding sequence to PE^4EKDEL. HB-EGF-PE was capable of binding both to the EGF receptor and heparin sulfate proteoglycans (HSPGs), whereas HB-PE was capable of binding only to HSPGs on the target cells. Human hepatoma cells, SK-Hepl, Hep-G2 and PLC/PRF/5 were killed in a very low concentration, of HB-EGF-PE with the ID₅₀ of 0.1–0.5 ng/ml. HB-PE could also kill SK-Hepl with the ID₅₀ of 50 ng/ml, whereas it was resistant to PE. Both exogenous EGF and heparin inhibited the cytotoxicity of HB-EGF-PE. These results indicated the existence of two alternative pathways for the internalization of the chimeric toxins defined by two different targets, EGFR and HSPGs.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00333-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74926412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of liver cell polarity by retinoic acid in vitro: bile canaliculi formation","authors":"Annie Claude ,&nbsp;Samuel W. French","doi":"10.1016/S0928-4346(96)00336-2","DOIUrl":"10.1016/S0928-4346(96)00336-2","url":null,"abstract":"<div><p>The mechanisms which regulate liver cell polarity and the formation of the bile canaliculi are unknown. Retinoic acid may, like dexamethasone, regulate cell polarity through its effects on the development of the bile canaliculus. We examined these effects on hepatocytes in primary culture by observing the formation of bile canaliculi and the pericanalicular sheath. The hypothesis is that retinoic acid induces organizational changes in cellular polarity in hepatocytes in vitro. To test this hypothesis, we added <em>trans</em>-retinoic acid 10⁻⁵ M to monolayers of hepatocyte cultures derived from preweanling rats. After 48 h the organization of the cytokeratin intermediate filament cytoskeleton was visualized by immunofluorescence on partially extracted preparations, by unembedded whole mount electron microscopy and gel electrophoresis on detergent extracted preparations. Quantitative measurements of the bile canaliculi were performed. Under the influence of retinoic acid, the number and size of bile canaliculi formed were significantly increased and formed a more complex architecture such as branching. The bile canaliculi were functional as demonstrated by the fluorescein diacetate dye uptake and excretion. In conclusion, retinoic acid enhanced cell polarity as indicated by the increase in the size and complexity of the bile canaliculi and the pericanalicular sheaths.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00336-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76529820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antithrombin III stimulates prostaglandin I2 production by cultured rat hepatic sinusoidal endothelial cells","authors":"Hiromasa Ohira,&nbsp;Katsutoshi Obara,&nbsp;Masahito Kuroda,&nbsp;Jun Tojo,&nbsp;Hironobu Ochiai,&nbsp;Masae Kokubun,&nbsp;Masayuki Miyata,&nbsp;Tomoe Nishimaki,&nbsp;Reiji Kasukawa","doi":"10.1016/S0928-4346(96)00332-5","DOIUrl":"10.1016/S0928-4346(96)00332-5","url":null,"abstract":"<div><p>We examined the production of prostanoids, specifically prostaglandin (PG) I₂ and thromboxane (TX) A₂, in cultured rat hepatic sinusoidal endothelial cells treated with antithrombin (AT) III. When cells were treated for 3 h with various concentration of AT III, production of 6-keto-PGF_1α (a stable metabolite of PG I₂) increased significantly and in a dose-dependent manner, compared with production by untreated cells. In terms of kinetics, significant increases were noted at 3 h (20.13 ± 1.38 pg/ml), 4 h (21.23 ± 0.63 pg/ml) and 24 h (36.58 ± 4.93 pg/ml) with AT III (300 μg/ml) stimulation, compared with production by the untreated cells (10.29 ± 1.21, 10.34 ± 1.66 and 22.64 ± 2.59 pg/ml, respectively). Moreover, this production was significantly reduced with increasing concentrations of heparin. On the other hand, TX B₂ (a stable metabolite of TX A₂) production was unaffected by AT III treatment. These data suggest that AT III may ameliorate the liver damage or disturbances in the sinusoidal microcirculation by stimulating the PG I₂ production of hepatic sinusoidal endothelial cells.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00332-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77969397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interferon treatment of chronic hepatitis C patients with normal or near normal alanine-amino-transferase levels: might it be harmful rather than useful?","authors":"G. Idéo ,&nbsp;A. Bellobuono ,&nbsp;S. Tempini ,&nbsp;G. Bellati ,&nbsp;L. Romanò ,&nbsp;A.R. Zanetti","doi":"10.1016/S0928-4346(96)00320-9","DOIUrl":"10.1016/S0928-4346(96)00320-9","url":null,"abstract":"<div><p>The efficacy of α-interferon (αIFN) in chronic hepatitis C (CHC) with normal or near normal alanine-amino-transferase (ALT) levels is not well known. Aim of this study was to evaluate the biochemical and virological response to αIFN therapy in CHC with persistently normal or near normal ALT levels. Sixteen HCV RNA positive patients affected by biopsy-proven CHC, of whom eight with persistently normal ALT levels and eight with ALT less than 1.5 times the upper reference value, monitored monthly for 6 months before treatment, were treated with recombinant α2b IFN 3 MU/t.i.w. for 6 months. Serum ALT levels were evaluated monthly during and for at least 6 months after the end of treatment. Serum HCV RNA (by nested reverse transrcription-polymerase chain reaction (RT-PCR))was tested before, at the end of treatment and at the end of follow-up. HCV genotyping was performed in pretreatment sera, according to the method of Okamoto. Serum HCV RNA titre was evaluated before and at the end of treatment. Of the eight patients with normal ALT, only two (one with genotype 1a and one with 2a) cleared serum HCV RNA and maintained normal ALT levels during treatment and follow-up. All the remaining six patients were persistently HCV-RNA positive: two showed a reduction in HCV RNA titre at the end of therapy, two had no variation and two developed an increase of viraemia; two patients (both with HCV type 1b) had flare-ups during treatment and four (two type 1b, two type 2a) had relapses after the end of treatment. All the eight patients with near normal ALT remained HCV-RNA positive: three showed a reduction in HCV RNA titre, two no variation and three an increase of viraemia at the end of therapy; two patients (both infected with HCV type 1b) had flare-ups during treatment, two maintained ALT levels less than 1.5 times the upper reference limit and four normalized ALT levels during treatment but relapsed after the end of therapy. αIFN treatment induced the clearance of serum HCV RNA only in <span><math><mtext>2</mtext><mtext>16</mtext></math></span> patients; <span><math><mtext>9</mtext><mtext>16</mtext></math></span> patients showed no variation or increase of viraemia at the end of therapy; a flare-up of ALT during therapy or follow-up was frequently observed (<span><math><mtext>8</mtext><mtext>16</mtext></math></span>). In conclusion, αIFN treatment seems to be of little efficacy for patients with chronic hepatitis C with normal or near normal ALT levels, and may be harmful for those infected with genotype 1b.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00320-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78985666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A case of chronic active hepatitis C presenting severe myocarditis during interferon-β therapy","authors":"Shigeo Maruyama ,&nbsp;Chisato Hirayama ,&nbsp;Kenji Oyama ,&nbsp;Atsushi Sagayama ,&nbsp;Hideshi Omura ,&nbsp;Shyuzo Ohata ,&nbsp;Hiroshi Kuzuo ,&nbsp;Nobuyuki Oyake ,&nbsp;Yasushi Horie","doi":"10.1016/S0928-4346(96)00326-X","DOIUrl":"10.1016/S0928-4346(96)00326-X","url":null,"abstract":"<div><p>A 47-year-old woman was diagnosed as having chronic active hepatitis C in February, 1995. She was administered 6 MU of interferon (IFN) β daily, beginning on March 8. After 6 weeks of the treatment she complained of chest pain and she entered a state of shock 1 h after administration of IFN. On the electrocardiogram, negative conversion of the T wave at leads: II, III, AVF and V3-6 was seen. Since myocardial ischemia was suspected, catecholamine and nitroglycerin were administered; the symptoms abated, however the electrocardiogram on the fifth day indicated junctional rhythm. The patient was diagnosed as having myocarditis based on the findings of strongly positive C-reactive protein and elevated erythrocyte sedimentation rate together with the features seen on electrocardiograms, echocardiograms and myocardial scintigrams. After the IFN-β treatment was discontinued, the clinical symptoms, electrocardiographic and echocardiographic findings improved. The myocarditis in this case was interpreted as being due to the treatment of IFN-β, because the patient presented no evidence of previous heart disease.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00326-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80983462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transjugular intrahepatic portosystemic shunting improves splanchnic hemodynamics and renal Na excretion in cirrhosis with refractory ascites","authors":"Shuichi Sezai ,&nbsp;Mitsuhiro Terada ,&nbsp;Masayoshi Ito ,&nbsp;Yukihiro Sakurai ,&nbsp;Kazuaki Kamisaka ,&nbsp;Takashi Abe ,&nbsp;Fumiaki Ikegami ,&nbsp;Masanori Hirano","doi":"10.1016/S0928-4346(96)00319-2","DOIUrl":"10.1016/S0928-4346(96)00319-2","url":null,"abstract":"<div><p>To clarify the pathogenesis of ascites in patients with liver cirrhosis, we explored the effects of transjugular intrahepatic portosystemic shunting in six cirrhotic patients with refractory ascites. The portal pressure decreased from 39 ± 7 cmH₂O before treatment to 32 ± 5 cmH₂O immediately after the procedure. Liver function transiently deteriorated after the procedure, but recovered within 1 week. Urinary Na excretion increased 1 week after treatment. In five patients, ascites improved within 3 weeks. Along with the decrease of portal congestion, there was an improvement of esophageal varices, and an increase of gastric mucosal blood flow, and an inhibition of the renin-angiotensin-aldosterone system in all of the patients after 2–4 weeks. Manageable shunt encephalopathy occurred in three patients. These findings strongly suggest the pivotal role of increased portal pressure in the formation of ascites in patients with liver cirrhosis.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0928-4346(96)00319-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74278094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}