Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Splenomegaly is a common finding in beta-thalassemia; however, its hemodynamic features and its potential correlations with high output state and hepatic disorders, both also frequent in thalassemia, have not yet been assessed in these patients. Eight beta-thalassemia patients with the indication for splenectomy and no symptoms or signs of heart disease, aged 25.6+/-5.5 years, were studied. Preoperative assessment included hematological profile, liver biology, hepatitis virus serology, and echocardiography. During splenectomy, splenic artery blood flow and splenic vein pressure were directly measured and liver biopsies were taken. Preoperative echocardiographic data were compared with those of 34 healthy controls. The preoperative cardiac index was significantly elevated in patients (4.8+/-1.3 vs 3.4+/-1.1 l/min per m2 in controls, p<0.001). Splenic blood flow, although increased, was not particularly high, being 285+/-56 ml/min or 0.13+/-0.04 ml/min per g of splenic mass, representing 4.1+/-0.9% of total cardiac output (CO). Splenic vein pressure was considerably elevated (29.7+/-5.5 cmH2O). Hepatic fibrosis, iron deposition, and extramedullary foci were found in all eight biopsies. Serology was positive in five of eight cases. beta-thalassemia patients with extensive splenomegaly requiring splenectomy are characterized by high output state, increased splenic blood flow, which probably makes a limited contribution to CO elevation, and portal hypertension, manifest by increased splenic vein pressure and hepatic histopathological abnormalities.
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PMID:Hemodynamic assessment of splenomegaly in beta-thalassemia patients undergoing splenectomy. 1533 97

The GI endoscopy can be divided into upper GI tract endoscopy (esophago-, gastro-, entero-, fistulo- and cholangioscopy) and lower GI tract endoscopy (recto-, sigmoido-, colonoscopy) from practical point of view and the characteristic of used equipment. A lot of therapeutic methods for GI tract is associated with each of these procedures. GI tract endoscopy doesn't play significant part in diagnosis of acute and chronic C hepatitis. Significance of endoscopy procedures decidedly increases in the case of progressive liver fibrosis and liver cirrhosis associated with HCV infection., where changes in GI tract are observed to 87% patients. These changes can be divided into: 1) not associated with portal hypertension, 2) these ones caused by portal hypertension. The most observed changes not associated with portal hypertension involve: reflux esophagitis, esophageal candidiasis; different variants of gastritis, gastric and duodenal ulcer. To the changes connected with portal hypertension, which are possible for endoscopy assessment, belongs esophageal and gastric varices, portal gastro-, entero-, colopathy, and gastric antral vascular ectasiae (GAVE). However to-day endoscopy has got not only diagnostic significance but also enables: estimation of pharmacotherapy efficiency, the primary and secondary prophylaxis of bleedings from GI varices as well as therapy of GI bleeding in this group of patients.
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PMID:[Endoscopy in the diagnosis of chronic hepatitis C--diagnosis and therapy depending on the phase of diseases progression and liver regeneration]. 1555 69

49 patients with viral hepatitis were studied on the correlationship between liver fibrosis and the level of serum precollagen type III (PC III), pre-collagen III pre-peptide (P III P), Laminin (LN), hyaluronic acid (HA) and collagen type IV (IV-C), as well as relationship between them and the expression of LN, IV-C, a-smooth muscle actin (a-SMA) and cytokeration (CK) in the liver tissues examined by immunohistochemistry. Results showed that the level of PC III, P III P, LN, HA and IV-C in the groups of liver cirrhosis and chronic severe hepatitis were higher than that in the groups of acute and chronic hepatitis. High correlation was found between the level of these markers (especially the level of the IV-C) and the degree of fibrosis in the group of chronic hepatitis. So were the expression of LN, IV-C, a-SMA and CK in the liver tissue. The results also showed that the liver fibrosis correlated with inflammatory reaction in the liver. So the authors suggested that more attention should be paid to the inflammatory reaction of the liver for prevention and treatment of liver fibrosis.
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PMID:[Clinical and pathological study on liver fibrosis in viral hepatitis]. 1561 38

In the era of antiretroviral therapy (ART), liver disease has emerged as an important cause of death among persons with human immunodeficiency virus (HIV)/hepatitis C virus (HCV) coinfection. The objective of this study was to estimate the burden of liver disease and evaluate determinants of liver fibrosis and necroinflammatory activity among HIV/HCV coinfected patients receiving ART. We studied 112 randomly selected and 98 referred HCV-infected patients undergoing care in the Johns Hopkins University HIV clinic. Liver disease was characterized clinically and histologically. Of the 210 individuals studied--64% of whom had received ART within 2 years of liver disease assessment--33% had no fibrosis (F0), and 26% had bridging fibrosis or cirrhosis (> or =F3). The median necroinflammatory activity score was 3 (range, 0-9 of 18). ART was not associated with fibrosis; however, significantly less hepatic necroinflammatory activity was observed among persons who had received highly active antiretroviral therapy longer (P = .02) and more effectively (defined by HIV RNA suppression; P < .01). Twelve percent of individuals had previous ART-associated liver enzyme elevations (grades 3-4), but liver fibrosis was not more severe if the liver enzyme elevation resolved. On the other hand, liver fibrosis was more severe in persons with persistent liver enzyme elevations (grades 1-4). In conclusion, despite widespread exposure to ART and documented instances of ART-related hepatitis, we found no evidence that ART caused serious histological liver disease. Recognition of bridging fibrosis and cirrhosis in some but not most patients underscores the importance of identifying and treating liver disease in HIV/HCV coinfected persons.
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PMID:The effect of antiretroviral therapy on liver disease among adults with HIV and hepatitis C coinfection. 1561 37

The significance of apoptosis in liver injury or liver fibrosis in viral hepatitis is yet unknown. The authors investigated the hepatocyte apoptosis and the correlation between the apoptosis and the liver injury in 22 liver biopsy specimens from the patients with hepatitis. Specimens were put onto slides to detect DNA strand breaks in situ with nick end labeling method using terminal deoxynucleotide transferase and bio-11-dUTP (TUNEL). The results showed that most of TUNEL-positive hepatocytes which have the features of apoptosis were apoptotic hepatocytes. There was TUNEL-positive reaction in few of the hepatocytes with ballooning degeneration. The degree of apoptotic hepatocytes in the chronic hepatitis was stronger than that in the acute hepatitis. This suggested that the degree of apoptotic hepatocytes correlated with the chronicity of hepatitis.
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PMID:[In situ detection of DNA strand breaks associated with apoptosis in viral hepatitis]. 1561 12

We report the case of a 56 year-old woman with post-transfusion chronic hepatitis C who presented with a severe ALT flare up associated with a rapid progression of liver fibrosis during interferon alpha 2b therapy. Several hypotheses were considered to explain the etiology of this ALT flare: there was no viral super infection by other hepatotropic viruses, no toxic hepatitis, no metabolic disease, and no other specific liver diseases could be identified. HLA typing showed a specific profile A1 B8 DR3 (risk factor of auto-immunization during interferon alpha therapy) with antinuclear antibodies and anti smooth muscle antibodies. This case suggests that auto-immunization induced by interferon alpha should be investigated in case of ALT flare that is not followed by an HCV breakthrough.
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PMID:[Autoimmunization induced by interferon alpha therapy in chronic hepatitis C]. 1565 45

The molecular mechanisms of acute hepatitis C virus (HCV) infection, end-stage hepatitis (cirrhosis), and hepatocellular carcinoma have been extensively studied, but little is known of the changes in liver gene expression during the early stages of liver fibrosis associated with chronic HCV infection, that is, the transition from normal liver (NL) of uninfected patients to the first stage of liver fibrosis (F1-CH-C). To obtain insight into the molecular pathogenesis of F1-CH-C, we used real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) to study the mRNA expression of 240 selected genes in liver tissue with F1-CH-C, in comparison with NL. The expression of 54 (22.5%) of the 240 genes was significantly different between F1-CH-C and NL; 46 genes were upregulated and 8 were downregulated in F1-CH-C. The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11). Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)). Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10). Thus, a limited number of signaling pathways, and particularly the transcriptional network regulated by interferons, are dysregulated in the first stage of HCV-induced liver fibrosis. Some of the genes identified here could form the basis for new approaches aimed at refining IFN-based therapies for chronic HCV infection.
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PMID:Molecular profiling of early stage liver fibrosis in patients with chronic hepatitis C virus infection. 1566 Nov 46

Hepatic stellate cells have been considered the most important cell-type involved in hepatic fibrogenesis. Proliferation and differentiation of hepatic stellate cells into myofibroblast-like cells has been related to the development of liver fibrosis. The alpha-actin expressed by hepatic stellate cells was considered a marker of their activation to myofibroblast-like cell. The aim of this study is to evaluate the changes in morphology, distribution, percentage and alpha-smooth muscle actin expression of hepatic stellate cells in normal and cirrhotic livers, and to correlate activated hepatic stellate cells with the progression of fibrosis. Human liver biopsies (n=121) were divided in five groups: 1) normal livers (controls); 2) cirrhosis post-HCV hepatitis; 3) cirrhosis post-HBV hepatitis; 4) non viral related cirrhosis; 5) recurrent HCV hepatitis after orthotopic liver transplantation. Samples immunostained with anti alpha-smooth muscle actin antibody by immunoperoxidase method were semi-quantitatively evaluated. Liver fibrosis was quantified by computer image analysis on specimens stained with Masson's trichrome. In normal adult livers stellate cells were very rarely stained for alpha-smooth muscle actin. In cirrhotic livers, a strongly enhanced percentage of stellate cells expressing alpha-smooth muscle actin was detected in cirrhotic fragments with respect to the control group, with a significant correlation between alpha-smooth muscle actin positive stellate cells and the volume fraction of fibrosis. Moreover, liver biopsies of recurrent hepatitis revealed an increased number of activated stellate cells compared to normal livers, and intermediate volume fraction of fibrosis. These results confirmed that a direct correlation existed between activated stellate cells and the progression of fibrosis. Alpha-smooth muscle actin confirmed to be a reliable marker of hepatic stellate cells activation also in precocious stages of the disease.
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PMID:Activated hepatic stellate cells in liver cirrhosis. A morphologic and morphometrical study. 1571 57

In untreated hepatitis virus (HCV)-positive renal transplant patients, the rate of liver fibrosis progression is low. In contrast, in those treated by ribavirin monotherapy, liver fibrosis score increased significantly after only 1 year of ribavirin monotherapy. The aim of this study was to identify the factors that might contribute to accelerate liver fibrosis progression in this population. Eleven patients were included in the study. Intrahepatic transforming growth factor (TGF)-beta, interferon (IFN)-gamma, and interleukin (IL)-10 mRNA quantification determined by real-time reverse transcription-polymerase chain reaction (RT-PCR) were similar before and after ribavirin therapy. The number of amino acid substitutions observed in the hypervariable region (HVR)-1 of the HCV genome between baseline and 1 year after ribavirin monotherapy was low, i.e., 3 (1-11) amino acid substitutions, suggesting the absence of a high selection pressure induced by ribavirin. In contrast, due to ribavirin-induced hemolysis, there was a significant increase in serum ferritin levels (P = 0.02) and in intrahepatic iron deposition (P = 0.04). Transferrin level and total iron-binding capacity decreased significantly during ribavirin monotherapy (P = 0.004). The increased liver fibrosis observed in renal transplant patients receiving ribavirin monotherapy could be related to ribavirin-induced anemia. Severe chronic hemolysis is responsible for iron overload, liver iron deposition, and an acceleration in the progression of liver fibrosis.
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PMID:Factors accelerating liver fibrosis progression in renal transplant patients receiving ribavirin monotherapy for chronic hepatitis C. 1577 76

The impact of treatment on progression of fibrosis in autoimmune hepatitis (AIH) is unknown. We assessed the changes in liver fibrosis before and after treatment among these patients. Nineteen AIH patients who had paired liver biopsies were studied. Of these, seven had been treated with 6 months of cyclosporine A and the rest with 6 months of prednisolone for induction of remission. Thereafter all had been maintained on azathioprine. Biopsy specimens before and after treatment were reviewed by one pathologist and scored by the Ishak method. Mean fibrosis stages before and after treatment were compared. Also, factors predicting significant fibrosis (stage > or =3) and cirrhosis (stage > or =5) at presentation were assessed. Mean interval between biopsies was 3.38 years. Mean fibrosis stage decreased from 4.53 to 2.16 following treatment (P < 0.001). Mean decrement in inflammatory grade was 8 scores (range, 4-10) in patients in whom fibrosis improved, and 2 scores (range, 0-4) in patients in whom fibrosis did not decrease after treatment (P < 0.001). ALT-to-platelet ratio was the best predictor of significant fibrosis and also cirrhosis. Fibrosis commonly improves after immunosuppressive treatment in AIH. ALT-to-platelet ratio can predict accurately the presence of significant fibrosis and cirrhosis in AIH.
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PMID:Impact of immunosuppressive treatment on liver fibrosis in autoimmune hepatitis. 1581 Jun 40


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