Liver[JOURNAL]
Sun
200 papers
Electrophysiological and neuropsychological tests for the diagnosis of subclinical hepatic encephalopathy and prediction of overt encephalopathy.
Saxena N, Bhatia M, Joshi YK … +3 more , Garg PK, Dwivedi SN, Tandon RK
Liver · 2002 Jun · PMID 12100568 · Publisher ↗
BACKGROUND: Subclinical hepatic encephalopathy (SHE) features in 30-84% of patients with cirrhosis of the liver. Its clinical significance with regards to progression to overt encephalopathy has however, not been establi...
BACKGROUND: Subclinical hepatic encephalopathy (SHE) features in 30-84% of patients with cirrhosis of the liver. Its clinical significance with regards to progression to overt encephalopathy has however, not been established. AIMS: The present study was conducted (i) to compare the diagnostic usefulness of neuropsychological tests with that of electrophysiological (EP) tests in detection of SHE, and (ii) to examine the natural course of SHE. METHODS: Seventy-five-nonencephalopathic cirrhotics (11 females, 64 males; mean (+/- SD) age 43.6 (+/- 11.7) years; mean (+/- SD) education 11(+/- 3) years) were studied using a battery of tests for intelligence and memory, the number connection test (NCT), and EP tests viz. electroencephalogram (EEG) and auditory P300 event related potentials (P3ERP). All the patients were followed up for a period of 6 months to 2 years for development of overt encephalopathy. RESULTS: Thirty-five out of 75(47%) patients were diagnosed to have SHE based on at least one abnormal test result. The P3ERP latencies detected SHE in maximum number of patients (23%) followed by EEG (21%). Nearly 59% of patients with SHE progressed to overt encephalopathy within a mean duration of 4 months. Multivariate analysis showed that prior episode of encephalopathy (RR = 6.3; 95% CI = 2.0-19.7), abnormality on EEG (RR = 7.5; 95% CI = 2.2-25.3), abnormal performance on psychometric battery of tests (RR = 35.2; 95% CI = 4.3-287.3), occurrence of gastrointestinal bleed (RR = 19.3; 95% CI = 4.1-88.9), occurrence of dehydration (RR = 10.7; 95% CI = 2.5-45.4) and infection (RR = 11.4; 95% CI = 2.0-64.4) had significantly higher risk for development of overt encephalopathy. CONCLUSIONS: EP methods were more sensitive in detection of SHE. Amongst all the tests used, presence of only an abnormal EEG was significantly associated with development of overt encephalopathy along with the precipitating factors.
Iron as a cofactor in chronic hepatitis C infection.
Sherrington CA, Olynyk JK
Liver · 2002 Jun · PMID 12100567 · Publisher ↗
Abstract loading — click title to view on PubMed.
Genetic changes in hypervariable region 1 as a possible mechanism for biochemical responders with interferon therapy.
Shindo M, Hamada K, Oda Y … +1 more , Okuno T
Liver · 2002 Apr · PMID 12028415 · Publisher ↗
Approximately 10% of chronic hepatitis C patients who were treated with interferon have a sustained normalization of aminotransferase levels after interferon therapy without HCV RNA clearance. We investigated genetic cha...
Approximately 10% of chronic hepatitis C patients who were treated with interferon have a sustained normalization of aminotransferase levels after interferon therapy without HCV RNA clearance. We investigated genetic change in hypervariable region 1 (HVR 1) to see if the mutation in this region is responsible for their sustained biochemical response and relapse thereafter. A total of 250 patients with chronic hepatitis C who were treated with interferon were studied for 8 to 11 years post therapy. Of these, 26 were biochemical responders (BR) whose ALT remained normal without viral clearance for more than 6 months after IFN therapy. HVR 1 was examined by direct sequencing of the PCR products, and found that no significant HVR 1 differences were observed in samples obtained pretreatment, posttreatment or during flares from these patients, suggesting that mutations in this region were not responsible for either the persistence of the HCV RNA or for the ALT relapses thereafter.
Relationship between protein kinase C alterations and nitric oxide overproduction in cirrhotic rat aortas.
Tazi KA, Barrière E, Moreau R … +2 more , Poirel O, Lebrec D
Liver · 2002 Apr · PMID 12028414 · Publisher ↗
BACKGROUND: Although nitric oxide (NO) overproduction and protein kinase C (PKC) alterations may play a role in systemic haemodynamic changes in cirrhotic rat aortas, the relationship between NO synthase (NOS) hyperactiv...
BACKGROUND: Although nitric oxide (NO) overproduction and protein kinase C (PKC) alterations may play a role in systemic haemodynamic changes in cirrhotic rat aortas, the relationship between NO synthase (NOS) hyperactivation and PKC hypoactivation is unknown. Therefore, the relationships between NOS and PKC activities were studied in cirrhotic rat aortas. METHODS: The effects of NOS inhibition by Nw-nitro-L-arginine (LNNA) on the contractile response to phorbol myristate acetate (PMA), a PKC activator, were studied. The effects of NOS inhibition and those of S-nitroso-N acetyl-DL-penicillamine (SNAP), an NO donor, on PKC activity were also evaluated. The effects of PKC activation and inhibition on total NOS and inducible NOS (iNOS) activities were measured. Nitric oxide synthase inhibition caused an increase in PMA-induced contraction and an increase in PKC activity in cirrhotic rat aortas. S-nitroso-N acetyl-DL-penicillamine induced downregulation of PKC activity. Total basal aortic NOS activity was significantly higher in cirrhotic rats than in control rats and activation of PKC by PMA induced a decrease in total aortic NOS activity. Protein kinase C downregulation caused an increase in both total aortic NOS and iNOS activities only in control rats, whereas only iNOS activity increased in cirrhotic rats. CONCLUSION: In cirrhotic rat aortas, NO overproduction plays a role in the decreased PKC activation that leads to reduced aortic contraction. Overactivation of aortic NOS in cirrhotic rats may be because of, in part, the reduced PKC activity.
Leptin deficiency reduces but does not eliminate the development of hepatic fibrosis in mice infected with Schistosoma mansoni.
Potter JJ, Mezey E
Liver · 2002 Apr · PMID 12028413 · Publisher ↗
AIMS/BACKGROUND: Leptin, a product of the obese (ob) gene, was demonstrated previously in activated hepatic collagen-producing stellate cells, but not in quiescent retinol-storing stellate cells. The role of leptin in fi...
AIMS/BACKGROUND: Leptin, a product of the obese (ob) gene, was demonstrated previously in activated hepatic collagen-producing stellate cells, but not in quiescent retinol-storing stellate cells. The role of leptin in fibrogenesis is unknown. This study investigated the possible influence of leptin in the pathogenesis of fibrosis by determination of the amount of fibrosis produced by Schistosoma mansoni infection in leptin deficient male ob/ob mice as compared to control mice. METHODS: The mice were infected percutaneously with cercaria of Schistosoma mansoni and the amount of liver fibrosis determined 12 weeks after infection. The amount of hepatic collagen deposited was quantified by morphometric analysis of liver sections stained with sirius red and by hydroxyproline content. RESULTS: The amount of histologically detectable fibrosis was greater in the infected controls than in the infected ob/ob mice. In the infected control mice, but not in the ob/ob mice, the fibrosis surrounding the granuloma was broad and extended beyond the portal tracts into the lobule with the formation of fibrous septa. CONCLUSIONS: This study shows that leptin is a potentiating, but not an essential factor, for the development of hepatic fibrosis, because leptin deficiency reduces but does not prevent the development of hepatic fibrosis.
Bone mineral metabolism and histomorphometry in rats with cholestatic liver disease.
Ackerman Z, Weinreb M, Amir G … +1 more , Pollak RD
Liver · 2002 Apr · PMID 12028412 · Publisher ↗
BACKGROUND: The etiology of osteopenia in cholestatic liver disease is uncertain. An animal model is needed in order to study the efficacy of therapeutic agents. AIMS: In order to characterise the bone disease in rats wi...
BACKGROUND: The etiology of osteopenia in cholestatic liver disease is uncertain. An animal model is needed in order to study the efficacy of therapeutic agents. AIMS: In order to characterise the bone disease in rats with cholestatic liver disease. METHODS: Four-month old male Sprague-Dawley bile duct-ligated (BDL) and sham-operated (SO) rats were studied. Twenty-eight days after surgery serum osteocalcin, a bone-formation marker, urinary deoxypyridinoline (DPD) cross-links, a resorption marker, and 25-hydroxyvitamin D3 were determined. Static and dynamic (tetracycline-based) histomorphometric analysis was performed on femurs and tibiae. RESULTS: All BDL rats developed biliary cirrhosis. Bile duct-ligated rats had lower bone mass, reflected in statistically significantly 13.5% lower femoral dry-weight, 16% lower femoral ash-weight, 42.7% lower tibial cancellous bone area and 19% lower trabecular thickness, compared with SO rats. Bile duct-ligated rats exhibited decreased bone formation manifested by statistically significantly 70% lower tetracycline double-labelling, 40% lower mineralising surface, 51% lower bone-formation rate and 47% lower osteocalcin compared with SO rats. Deoxypyridinoline levels were 20% lower in BDL rats. Bile duct-ligated rats had 52% lower serum 25-hydroxyvitamin D3 level, but no significant increase in cortical osteoid area. CONCLUSIONS: Bile duct-ligated rats develop osteopenia characterised by low bone-formation rate, and can be used for studying therapeutic agents for patients with cholestatic liver disease displaying similar bone changes.
Quantitative testing of liver function compared to prognostic scores in patients with primary biliary cirrhosis.
Herold C, Ganslmayer M, Deynet C … +2 more , Hahn EG, Schuppan D
Liver · 2002 Apr · PMID 12028411 · Publisher ↗
AIM: Primary biliary cirrhosis (PBC) is a slowly progressive liver disease which can lead to cirrhosis. We investigated if quantitative tests of liver function (QTLF) and serum levels of a surrogate marker of hepatic fib...
AIM: Primary biliary cirrhosis (PBC) is a slowly progressive liver disease which can lead to cirrhosis. We investigated if quantitative tests of liver function (QTLF) and serum levels of a surrogate marker of hepatic fibrogenesis (PIIINP) provide information in addition to established prognostic scores. METHODS: In 34 PBC patients PIIINP, PBC-relevant parameters, histological staging and QTLF at entry and at 2 years were determined and compared with the Christensen (CPS I, CPS II) and Mayo prognosis score. QTLF included aminopyrine breath test, galactose elimination capacity, sorbitol and indocyanine green clearance. RESULTS: Bilirubin, serum IgM and PIIINP were elevated at both time points, whereas albumin and prothrombin time remained normal. Clinical findings (ascites, cirrhosis, central cholestasis) and histological staging worsened after 2 years, as did the CPS II. However, QTLF, PIIINP, CPS I and the Mayo score revealed no significant changes. CONCLUSIONS: Only CPS II changed after 2 years, whereas CPS I and the Mayo score remained unaltered. QTLF and PIIINP did not provide any further information on progression of PBC, suggesting that QTLF cannot predict prognosis of PBC patients in a two-year interval and that CPS II is superior to CPS I and the Mayo score in short-term studies for PBC.
Enhanced expression of endothelial nitric oxide synthase and caveolin-1 in human cirrhosis.
Yokomori H, Oda M, Ogi M … +2 more , Sakai K, Ishii H
Liver · 2002 Apr · PMID 12028410 · Publisher ↗
BACKGROUND/AIMS: Nitric oxide is synthesized in diverse mammalian tissues by a family of calmodulin-dependent nitric oxide synthases (NOS). Caveolin, the principal structural protein in caveolae, interacts with endotheli...
BACKGROUND/AIMS: Nitric oxide is synthesized in diverse mammalian tissues by a family of calmodulin-dependent nitric oxide synthases (NOS). Caveolin, the principal structural protein in caveolae, interacts with endothelial NOS (eNOS) leading to enzyme inhibition by a reversible process modulated by Ca++ -calmodulin. The aim of the present study was to examine the localizations of eNOS and caveolin-1 at protein level in normal human liver tissue, and how the expressions are altered in cirrhotic liver. METHODS: Fresh liver specimens were obtained from hepatic surgeries. Normal portions resected from cases of carcinoma metastasized to the liver were used as control specimens, and cirrhotic portions resected from cases of hepatocellular carcinoma with hepatitis C-related cirrhosis were used as cirrhotic specimens. Anti-eNOS and anticaveolin-1 antibodies were used for immunohistochemistry and Western blotting. Immunoelectron microscopy was conducted on ultra thin sections using immunoglobulin-gold combined with silver staining. RESULTS: Immunohistochemistry revealed that both eNOS and caveolin-1 were sparsely expressed on hepatic sinusoidal lining in normal liver specimens, and these findings were confirmed by Western blot. Both immunohistochemistry and Western blotting demonstrated over-expression of eNOS and caveolin-1 in cirrhotic liver specimens. Morphometric analysis of immunogold particle labeling for eNOS and caveolin-1 was performed on immunoelectron micrographs. In normal liver tissue, hepatic stellate cells and sinusoidal endothelial cells (SEC) expressed low levels of caveolin-1, and SEC expressed a very low level of eNOS. In cirrhotic liver, both caveolin-1 and eNOS expressions were significantly increased by approximately four-fold on SEC compared to normal liver. CONCLUSION: In cirrhotic human liver, marked increase of caveolin-1 in perisinusoidal cells may promote caveolin-eNOS binding and reduce the activity of eNOS despite an increased eNOS expression, leading to impaired NO production and increased hepatic microvascular tone.
Expression of p57/Kip2 protein in extrahepatic bile duct carcinoma and intrahepatic cholangiocellular carcinoma.
Ito Y, Takeda T, Sasaki Y … +7 more , Sakon M, Yamada T, Ishiguro S, Imaoka S, Tsujimoto M, Monden M, Matsuura N
Liver · 2002 Apr · PMID 12028409 · Publisher ↗
BACKGROUND: Evaluation of the biological character of carcinomas requires understanding of cell cycle regulators. P57 (Kip2) belongs to the Cip/Kip family and is known to be one of the universal negative regulators of ce...
BACKGROUND: Evaluation of the biological character of carcinomas requires understanding of cell cycle regulators. P57 (Kip2) belongs to the Cip/Kip family and is known to be one of the universal negative regulators of cell cycle. METHODS: In the present study, therefore, we investigated p57 expression in 37 extrahepatic bile duct carcinomas (BDC) and 28 intrahepatic cholangiocellular carcinomas (CCC). RESULTS: The average p57 labeling index (LI) in BDC and CCC were 60.8 +/- 7.9 and 58.6 +/- 18.6, respectively, which were significantly lower (p = 0.0008 and p = 0.0408, respectively) than those in normal duct epithelia (73.1 +/- 7.9, 70.4 +/- 8.2). p57 LI was significantly lower in BDC and CCC cases with biological aggressive phenotypes such as poor differentiation (p = 0.0260 and p = 0.0069), lymph node metastasis (p = 0.0274 and p = 0.0214), high Ki-67 LI (p = 0.0164 and p = 0.0343) and cyclin D1 overexpression (p = 0.0359 and p = 0.0255). CONCLUSION: These findings suggest that decreased p57 expression is related to the increased activity of cell proliferation and also the progression of these carcinomas.
Progression of fibrosis in untreated patients with hepatitis C virus infection.
Lagging LM, Westin J, Svensson E … +5 more , Aires N, Dhillon AP, Lindh M, Wejstål R, Norkrans G
Liver · 2002 Apr · PMID 12028408 · Publisher ↗
BACKGROUND/METHODS: In order to evaluate the progression of liver fibrosis associated with Hepatitis C virus (HCV) infection, two liver biopsy specimens obtained prior to antiviral therapy from 98 patients with HCV were...
BACKGROUND/METHODS: In order to evaluate the progression of liver fibrosis associated with Hepatitis C virus (HCV) infection, two liver biopsy specimens obtained prior to antiviral therapy from 98 patients with HCV were scored and evaluated using statistical methods appropriate for ordered categorical data. RESULTS/CONCLUSIONS: Greater progression of fibrosis was seen with increasing time between the biopsies. Likewise, the change in fibrosis score was significantly more pronounced in the 11 patients whose first biopsy was obtained within the first year after acquiring HCV. A multivariate logistic regression analysis of possible explanatory factors for the fibrosis outcome showed that interface hepatitis in both biopsies, the time interval between the biopsies, and age at first biopsy were associated with change in the fibrosis score. In addition we found that higher age at the time of infection was associated with development of cirrhosis, that moderate intake of alcohol was associated with fibrosis progression, and that an inflammatory response in the form of moderate interface hepatitis in the first biopsy was not necessarily associated with greater progression of fibrosis if the second biopsy showed mild interface hepatitis. However, having moderate interface hepatitis later in the course of infection as reflected by the second biopsy may be detrimental. If moderate interface hepatitis early in the course of the disease is followed by less interface hepatitis later there is less fibrosis; and if moderate interface hepatitis persists, there is more fibrosis eventually.
Correlation of HBV DNA levels in serum and liver of chronic hepatitis B patients with cirrhosis.
Lee CZ, Huang GT, Yang PM … +3 more , Sheu JC, Lai MY, Chen DS
Liver · 2002 Apr · PMID 12028407 · Publisher ↗
AIM: We sought to evaluate whether serum HBV DNA levels correlates with the liver free HBV DNA levels in chronic hepatitis B. METHODS: Thirty-three consecutive chronic hepatitis B patients with cirrhosis were included in...
AIM: We sought to evaluate whether serum HBV DNA levels correlates with the liver free HBV DNA levels in chronic hepatitis B. METHODS: Thirty-three consecutive chronic hepatitis B patients with cirrhosis were included in this study. Twenty cases had detectable serum HBV DNA (> 1.8 pg/ml). All had detectable free liver HBV DNA. RESULTS: There was a strong correlation between the serum and liver HBV DNA levels (P = 0.0018, r = 0.717). Thirteen cases had undetectable serum HBV DNA. Among them, six cases still had detectable liver free HBV DNA. Eight cases were HBeAg-positive. Among them, seven cases were positive for both serum and liver HBV DNA, and one case was negative for both serum and liver HBV DNA. Twenty-five cases were HBeAg-negative and anti-HBe-positive. Among them, 13 cases were positive for serum HBV DNA, and 19 cases were positive for liver HBV DNA. No significant difference was noted for positivity of serum HBV DNA or liver free HBV DNA between HBeAg-positive and HBeAg-negative groups. The level of serum HBV DNA(491 +/- 772 pg/ml versus 203 +/- 447 pg/ml, p = 0.07) and liver free HBV DNA (33 +/- 81 pg/microg versus 6 +/- 15 pg/microg, p = 0.13) was also not statistically different. CONCLUSION: In conclusion, serum HBV DNA levels is strongly correlated with liver HBV DNA levels in chronic hepatitis B with cirrhosis. Liver free HBV DNA can still be detected in about half of the cirrhotic patients with undetectable serum HBV DNA. Serum HBeAg is not a good predictor of serum or liver HBV DNA levels in cirrhotic patients.
Thrombopoietin serum levels do not correlate with thrombocytopenia in hepatic schistosomiasis.
Souza MR, Aguiar LA, Goto JM … +3 more , Carvente CT, Toledo CF, Borges DR
Liver · 2002 Apr · PMID 12028406 · Publisher ↗
BACKGROUND: In severe forms of cirrhosis reduced liver synthesis of thrombopoietin (Tpo) can contribute to thrombocytopenia. In the hepatosplenic form of schistosomiasis, portal hypertension is the most evident clinical...
BACKGROUND: In severe forms of cirrhosis reduced liver synthesis of thrombopoietin (Tpo) can contribute to thrombocytopenia. In the hepatosplenic form of schistosomiasis, portal hypertension is the most evident clinical complication, although a deficiency of protein synthesis may be detected early. Our aim was to determine, for the first time in schistosomiasis, Tpo serum concentrations in patients with chronic forms of the disease. METHOD: Twenty-four patients with the pure form of schistosomiasis were studied; 13 had the hepatosplenic form (HE, with portal hypertension) and 11 had the hepatointestinal form (HI, without portal hypertension). Patients were HBsAg, anti-HBc and anti-HCV negative, and reported alcohol ingestion below 160 g/week. RESULTS: The Tpo serum concentration, determined in 10 healthy volunteers, varied from undetectable (< 15 pg/mL) to 489 pg/mL (median 208 pg/mL). The HE and HI groups differed (p = 0.004) in regard to the prothrombin index, thrombocytemia and gamma-glutamyltransferase but not in regard to Tpo (p = 0.622). No significant correlation was found between Tpo and the other parameters (p > 0.05). CONCLUSIONS: The results suggest that Tpo serum concentration does not mirror and/or has no significant participation in the mechanisms responsible for the thrombocytopenia observed in schistosomiasis patients with splenomegaly and portal hypertension.
Viral dynamics in chronic hepatitis B patients during lamivudine therapy.
Wolters LM, Hansen BE, Niesters HG … +3 more , Zeuzem S, Schalm SW, de Man RA
Liver · 2002 Apr · PMID 12028405 · Publisher ↗
RATIONALE AND AIM: Recently, we described a first-order decay model for the description of a decrease in viral load during treatment with lamivudine for a chronic hepatitis B virus infection (HBV). However, more frequent...
RATIONALE AND AIM: Recently, we described a first-order decay model for the description of a decrease in viral load during treatment with lamivudine for a chronic hepatitis B virus infection (HBV). However, more frequent sampling of viral load during the first month of treatment shows a bi-phasic viral decline. We therefore compared several mathematical models which are currently in use to describe the dynamics of various viruses and treatments. METHODS: HBV DNA positive chronic hepatitis B patients were treated with lamivudine 150-600 mg daily for four weeks. During the first two days, blood samples were drawn every 6 h, then daily during the first week and weekly during the following three weeks. HBV DNA was measured with the Digene Hybrid Capture II HBV DNA test and the sensitive Roche PCR assay, both calibrated on the Eurohep standard. RESULTS: Our HBV DNA data are most accurately described if we use the bi-phasic model previously described by Neumann et al. while introducing all consecutive data of all patients simultaneously (mixed effects model). This results in an effectiveness of blocking of viral replication of 93%, a half-life of free virus of 17 h and a half-life of infected hepatocytes of 7 day in patients treated with 150 mg of lamivudine. CONCLUSION: HBV dynamics during treatment with lamivudine can be explained by blocking of virion production with or without blocking of de novo infection. The bi-phasic model as described by Neumann et al. in combination with frequent blood sampling provides the most accurate fit and can be used to compare new nucleoside analogue profiles to lamivudine therapy.
Thrombopoietin serum levels are elevated in patients with hepatitis B/C infection compared to other causes of chronic liver disease.
Schöffski P, Tacke F, Trautwein C … +5 more , Martin MU, Caselitz M, Hecker H, Manns MP, Ganser A
Liver · 2002 Apr · PMID 12028404 · Publisher ↗
BACKGROUND/AIMS: Thrombocytopenia in patients with advanced liver disease may stem from a deficient hepatic thrombopoietin production. METHODS: We determined the relationship between thrombopoietin, thrombocytopenia, aet...
BACKGROUND/AIMS: Thrombocytopenia in patients with advanced liver disease may stem from a deficient hepatic thrombopoietin production. METHODS: We determined the relationship between thrombopoietin, thrombocytopenia, aetiology and extent of liver damage by incorporating serum thrombopoietin measurements in the pretransplant evaluation of 111 patients with liver disease. RESULTS: The extent of thrombocytopenia was related to the underlying cause of disease. The platelet count directly correlated with factor V, II, fibrinogen, and PTT, and a negative correlation was found for splenic size and Child's stage. The thrombopoietin concentrations were age-dependent, and no significant difference resulted between the median thrombopoietin level of liver disease patients with age-matched healthy controls. Thrombopoietin concentrations and platelet counts were not correlated. Although noncirrhotic patients had higher platelet counts than those with Child's A-C cirrhosis (p < 0.001, U-test), no such difference was found in thrombopoietin levels. Patients with hepatitis B and/or C had lower platelet counts compared to patients with nonviral diseases (p < 0.001), and their median thrombopoietin concentrations were significantly higher (p < 0.001). CONCLUSION: We conclude that thrombocytopenia in patients with liver disease is unlikely to be explained only based on a deficient hepatic production of thrombopoietin. Patients with chronic viral hepatitis have significantly elevated thrombopoietin levels; the involved pathomechanisms require further study.
Hepatic Met-enkephalin immunoreactivity is enhanced in primary biliary cirrhosis.
Bergasa NV, Liau S, Homel P … +1 more , Ghali V
Liver · 2002 Apr · PMID 12028403 · Publisher ↗
BACKGROUND/AIMS: In contrast to the normal adult liver, the fetal human and rat livers, and the liver of rats with cholestasis secondary to bile duct resection (BDR) express the preproenkephalin (ppENK) mRNA, which codes...
BACKGROUND/AIMS: In contrast to the normal adult liver, the fetal human and rat livers, and the liver of rats with cholestasis secondary to bile duct resection (BDR) express the preproenkephalin (ppENK) mRNA, which codes for the endogenous opioid peptide Met-enkephalin. In addition, Met-enkephalin immunoreactivity (MEIR) is detected in hepatocytes and in proliferating bile ductules in the cholestatic rat liver. These data suggest that cholestasis is associated with the resurgence of cells that produce Met-enkephalin. To explore further the status of opioids in cholestasis, we studied the expression of MEIR in liver tissue. METHODS: The MEIR was sought in paraffin-preserved liver tissues from patients with primary biliary cirrhosis (PBC) (n = 10). RESULTS: The MEIR was detected in all the PBC livers. Its intensity varied from weak to strong on hepatocytes and bile ducts and the strongest expression appeared as coarse granules. The MEIR was either absent or only faintly expressed by some hepatocytes from disease and nondisease control biopsies, but absent from bile ducts. CONCLUSION: These results suggest that the human liver in cholestasis may be a source of endogenous opioids.
Autoimmune cholangiopathy associated with systemic lupus erythematosus.
Heyman SN, Spectre G, Aamar S … +3 more , Rubinger D, Pappo O, Ackerman Z
Liver · 2002 Apr · PMID 12028402 · Publisher ↗
We report a 39-year-old female who presented over 11 years with autoimmune cholangiopathy associated with kaleidoscopic manifestations of systemic lupus erythematosus (SLE), including, arthritis, skin changes, pleuritis,...
We report a 39-year-old female who presented over 11 years with autoimmune cholangiopathy associated with kaleidoscopic manifestations of systemic lupus erythematosus (SLE), including, arthritis, skin changes, pleuritis, diffuse proliferative glomerulonephritis, lymphadenopathy, splenomegaly, hyperglobulinemia, and major depression. While antimitochondrial antibodies (AMA) were absent, antinuclear (ANA) and anti-DNA antibodies were detected in high titres associated with hypocomplementemia. The patient also had vitamin B12 deficiency and antiphospholipid antibodies. The patient required steroids and repeated courses of cyclophosphamide for the management of lupus nephritis, and ursodeoxycholic acid (ursolite) administration resulted in amelioration of cholestatic laboratory abnormalities. This unusual case report and review of literature illustrate that immune liver disease may be an important clinical manifestation of SLE, especially autoimmune cholangiopathy.
Intrahepatic expression of the hepatic stellate cell marker fibroblast activation protein correlates with the degree of fibrosis in hepatitis C virus infection.
Levy MT, McCaughan GW, Marinos G … +1 more , Gorrell MD
Liver · 2002 Apr · PMID 12028401 · Publisher ↗
BACKGROUND: Activated hepatic stellate cells (HSCs), recognised by their alpha smooth muscle actin immunoreactivity, are primarily responsible for liver fibrosis. However, the presence of alpha smooth muscle actin positi...
BACKGROUND: Activated hepatic stellate cells (HSCs), recognised by their alpha smooth muscle actin immunoreactivity, are primarily responsible for liver fibrosis. However, the presence of alpha smooth muscle actin positive HSCs is not always associated with the development of liver fibrosis. Recently, other markers of human HSCs including the gelatinase fibroblast activation protein (FAP) and glial fibrillary acidic protein have been identified. AIMS: We examined the relationship between the expression of these HSC markers and the severity of liver injury in patients with chronic hepatitis C virus infection. METHODS: Liver tissue from 27 patients was examined using immunohistochemistry. Linear correlation analysis was used to compare staining scores with the stage and grade of liver injury. RESULTS-CONCLUSIONS: FAP expression, seen at the tissue-remodelling interface, was strongly and significantly correlated with the severity of liver fibrosis. A weaker correlation was seen between glial fibrillary acidic protein expression and fibrosis stage. This contrasted with the absence of a relationship between alpha smooth muscle actin and the fibrotic score. A correlation was also observed between FAP expression and necroinflammatory score. In summary, FAP expression identifies a HSC subpopulation at the tissue-remodelling interface that is related to the severity of liver fibrosis.
The detection of HBV antigens and HBx-transcripts in an Indian fibrolamellar carcinoma patient: a case study.
Dadke D, Jaganath P, Krishnamurthy S … +1 more , Chiplunkar S
Liver · 2002 Feb · PMID 11906624 · Publisher ↗
Fibrolamellar carcinoma (FLC) of the liver is a rare variant of hepatocellular carcinoma (HCC). Here we report the case of a 12-year-old Indian male with typical FLC with no apparent hepatitis B virus (HBV) infection and...
Fibrolamellar carcinoma (FLC) of the liver is a rare variant of hepatocellular carcinoma (HCC). Here we report the case of a 12-year-old Indian male with typical FLC with no apparent hepatitis B virus (HBV) infection and a non-cirrhotic liver. The patient, though seronegative for HBsAg, showed expression of HBcAg in both the liver and tumour tissue. RT-PCR analysis revealed the presence of full-length HBx-transcripts in both liver/tumour tissue, along with truncated HBx-transcripts only in the tumour tissue. The lymphocytes in both peripheral and liver/tumour compartments showed a proliferative response to either/or HBcAg and HBxAg, which could be further augmented on addition of rIL-2. This is the first study to show not only the presence of HBcAg in the liver/tumour tissue but also prior exposure of the FLC patient's lymphocytes to HBV antigens. Also, the presence of the full-length and truncated HBx-transcripts in the tumour tissue, a proposed tumorigenic marker for hepatocarcinogenesis in chronic HBV patients, suggests an oncogenic role of HBV in this rare variant of HCC.
Long-term asymptomatic biochemical cholestasis after fulminant or subfulminant liver failure is associated with extensive postnecrotic collapse with regeneration of the liver.
Ngassa M, Van Beers BE, Geubel AP
Liver · 2002 Feb · PMID 11906623 · Publisher ↗
Fulminant or subfulminant liver failure usually leads to liver failure or to recovery. In rare instances, patients who recover exhibit prolonged asymptomatic biochemical cholestasis which coincides with the development i...
Fulminant or subfulminant liver failure usually leads to liver failure or to recovery. In rare instances, patients who recover exhibit prolonged asymptomatic biochemical cholestasis which coincides with the development into the parenchyma of large postnecrotic collapse with regeneration. This hitherto poorly recognized form of recovery may now be assessed by noninvasive techniques such as magnetic resonance imaging. We report the case of three patients who recovered from fulminant or subfulminant liver failure and in whom investigation of long-term biochemical cholestasis led to that unusual diagnosis.
Single nucleotide insertion in the 5'-untranslated region of hepatitis C virus with clearance of the viral RNA in a liver transplant recipient during acute hepatitis B virus superinfection.
Sergi C, Arnold JC, Rau W … +2 more , Otto HF, Hofmann WJ
Liver · 2002 Feb · PMID 11906622 · Publisher ↗
Hepatitis C virus (HCV) infection is an important etiology in patients undergoing orthotopic liver transplantation (OLT) world-wide. Antiviral therapy-related clearance of HCV RNA may occur both in patients with chronic...
Hepatitis C virus (HCV) infection is an important etiology in patients undergoing orthotopic liver transplantation (OLT) world-wide. Antiviral therapy-related clearance of HCV RNA may occur both in patients with chronic HCV infection and in transplanted patients for HCV-related liver cirrhosis, but the role of the 5'-untranslated region (UTR) of HCV containing the internal ribosome entry site (IRES), which directs the translation of the viral open reading frame has not hitherto been evaluated. We studied the 5'-UTR in an HCV-infected recipient of a liver graft that showed spontaneous clearance of HCV RNA during an acute hepatitis B virus (HBV) superinfection. Sequencing of the 5'-UTR of HCV showed a nucleotide A insertion at position 193 of the IRES.
About
- Frequency
- Sun
- Papers found
- 200
- RSS feed
- Subscribe