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)

The aim of this study was to evaluate the effect of astilbin on concanavalin A (Con A)-induced hepatitis, a T cell-dependent model of liver injury. Con A administration resulted in a severe liver injury in mice, with a strong increment in spleen cell adhesion and liver infiltration of T cells, as well as in tumour necrosis factor (TNF)-alpha production. Against this liver injury, astilbin significantly inhibited the elevation in transaminase activity, reduced the TNF-alpha production, and improved the histological changes, including inflammatory infiltration, hepatocyte necrosis and degeneration and Kupffer cell hyperplasia. In addition, astilbin inhibited the adhesion of spleen cells and purified T lymphocytes isolated from the liver-injured mice to fibronectin, laminin and type IV collagen.Moreover, the adhesion of human Jurkat T cells to endothelial cell line ECV-304 was also inhibited by astilbin. These results suggest that the improvement of the T cell-mediated liver injury by astilbinmay be related to the reduction in TNF-alpha production and in T cell adhesion to extracellular matrices and endothelial cells.
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PMID:Astilbin prevents concanavalin A-induced liver injury by reducing TNF-alpha production and T lymphocytes adhesion. 1510 95

We investigated correlations between laboratory test results and multicentric development of hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC) in 202 patients who underwent liver resection. Two types of HCC were considered to meet multicentricity criteria: in one, at least one tumor was well-differentiated, with at least one other being less differentiated; in the other, all tumors included well-differentiated HCC with or without less differentiated components. Forty-five patients had multicentric HCC. Platelet counts were lower in patients with multicentric HCC than in others. Serum concentrations of type IV collagen 7s domain and alpha-fetoprotein, histologic hepatitis activity score, and histologic hepatic fibrosis score were higher in patients with multicentric HCC. By multiple logistic regression analysis, low platelet count was an independent risk factor for multicentric HCC. The proportion of patients with multicentric HCC was significantly higher among patients with low platelet counts (below 10(5)/mm(3)) than in patients with a higher count. Thus, HCC patients with a platelet count below 10(5)/mm(3) may require particularly careful examination for multicentricity.
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PMID:Correlation between low platelet count and multicentricity of hepatocellular carcinoma in patients with chronic hepatitis C. 1558 30

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

Halothane as a cause of hepatitis is rare and may be overlooked when evaluating a patient with sudden onset jaundice. A 34-year-old lady, a nurse, presented to the liver clinic with sudden onset non-pruritic jaundice. Viral and collagen serological tests were all normal, malaria and sickling tests were negative, but transaminases were elevated. She reported inadvertent exposure to halothane in surgical theatre where she works. She improved on conservative management, then had a re-exposure to halothane after three weeks and developed a similar clinical picture, which improved on conservative management. In an area endemic of malaria, hepatitis and haemolysing conditions like sickle cell anaemia, the diagnosis of halothane hepatitis requires high index of suspicion. The mechanism of halothane-induced hepatic damage in this patient is very likely idiosyncratic. This is because of the modest dose at first exposure and more severe clinical picture at re-exposure.
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PMID:Halothane induced hepatitis: case report. 1571 33

The question addressed here is: does the bile duct reactive component of hepatitis C disease progress during the progression of the disease to cirrhosis? The question is important because if the answer to the question is yes, then an important correllated question is: does the bile duct reactive component contribute to the fibrotic change which leads to cirrhosis? The first question is addressed in the present study of a series of liver biopsies taken at the four stages of liver fibrosis in patients with hepatitis C. Sixty-four patients with hepatitis who had been biopsied for staging purposes were reviewed retrospectively. The liver biopsies were routinely stained with antibodies for liver cells, bile duct cells, activated stellate cells and cells in S phase of the cell cycle and histochemical stains for collagen and basement membrane. Selective biopsies were stained for stem cells and oval cells. There was a progressive increase in metaplastic bile ductules but the increase did not reach a significant level until stages III and IV of fibrosis. There was a positive correlation between the number of ductules formed and the stage of liver fibrosis. The incidence of proliferating metaplastic ductules was low and did not change significantly during the progression of the stage of the fibrosis. Stains for oval cells and stem cells were negative. It is concluded that the answer to the question posed is: bile ductule reaction does increase during the development of cirrhosis caused by hepatitis C but the increase is due to bile ductular metaplasia, not due to proliferation.
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PMID:The role of bile duct reactive change in the pathogenesis of liver fibrosis due to hepatitis C. 1604 6

Infliximab, a chimeric monoclonal antibody that binds the tumor necrosis factor alpha (TNFalpha), is used in the treatment of rheumatoid arthritis (RA) and Crohn's disease (CD). Previous cases of significant secondary liver disease associated with infliximab treatment have been reported in patients with RA, CD, and psoriatic arthritis. Two additional patients with RA who developed a serious liver disease associated with infliximab treatment are reported here. A 39-year old RA patient was admitted with cholestatic liver disease after 8 months of treatment with infliximab. She had no history of hepatic diseases, exposure to hepatotoxic or illicit drugs, or alcohol abuse. A liver biopsy showed severe ductal proliferation with collapse and enucleation of the hepatocytes. Despite aggressive treatment with oral prednisolone, she developed hepatic failure. On the 45th day, a liver transplant was performed. The second patient, a 54-year old RA patient, was diagnosed with autoimmune hepatitis after 12 infliximab infusions. She fulfilled autoimmune hepatitis type 1 criteria. A liver biopsy disclosed an altered lobulillar structure with chronic inflammation and the formation of collagen bands. She was treated with prednisolone and azatioprine and a complete recovery was noted 1 month later. These cases should alert rheumatologists to the possibility of new adverse reactions (liver injury) associated with the use of TNFalpha blockers in an autoimmune setting.
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PMID:Serious liver disease induced by infliximab. 1654 95

Liver fibrosis commonly occurs in patients with hepatitis C virus (HCV) infection as a consequence of the chronic liver damage, thus leading to the development of liver cirrhosis. When hepatic stellate cells (HSCs) become active, they play an essential role in liver fibrogenesis. In this study, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), commonly elevated in chronic C hepatitis, stimulate the production of matrix metalloprotease-9 (MMP-9) by human hepatocytes at a transcriptional and translational level, but the addition of recombinant interferon-alpha2b (rIFN-alpha2b) hampers this effect. Furthermore, a human HSC line is activated in vitro by incubation with human MMP-9 in the presence of collagen I, and this effect is blocked by the MMP inhibitor BB94. A similar activation was observed when incubating HSCs with conditioned medium of hepatocytes previously stimulated with IL-1beta and TNF-alpha but not when using conditioned medium of hepatocytes costimulated with IL-1beta or TNF-alpha together with rIFN-alpha2b. In conclusion, our results show that hepatocytes stimulated by inflammatory cytokines participate in the activation of HSCs via MMP-9 production and that antiviral therapy modulates such activation.
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PMID:Antifibrogenic effect of IFN-alpha2b on hepatic stellate cell activation by human hepatocytes. 1668 58

Hepatic fibrosis is an outcome of many chronic liver diseases, such as viral and autoimmune hepatitis, and of alcohol consumption and biliary obstruction. Prolonged liver injury results in hepatocyte damage, which triggers activation of hepatic stellate cells (HSC) and recruitment of inflammatory cells into the liver. The HSC play a critical role in fibrogenesis. They produce collagen type I and secrete pro-fibrogenic cytokines and inhibitors of matrix-degrading enzymes (tissue inhibitor of matrix metalloproteinase), causing the production of extracellular matrix deposition over degradation. However, many clinical and experimental studies suggest that this process can be reversed, including the apoptosis of activated HSC. Thus, HSC represent an appealing target for antifibrotic therapy. This review will focus on some aspects of etiology and molecular pathogenesis of liver fibrosis and the reversal of fibrosis.
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PMID:Hepatic stellate cells and the reversal of fibrosis. 1695 81

NKT cells are a subset of regulatory lymphocytes characterized by co-expression of the NK cell receptor-CD161 and an invariant TCR-alpha chain (Valpha14-Jalpha28). They are most abundant in the liver, spleen, and bone marrow. NKT lymphocytes have been implicated in the regulation of autoimmune processes in both mice and humans. Activation of NKT lymphocytes leads to rapid amplification of either IFNgamma or IL4, endowing these cells with the capability to mediate both pro-inflammatory and anti-inflammatory immune responses. Activation of this subset of cells is associated with significant liver damage in the Concanavalin A immune mediated hepatitis model. Administration of CD1d ligand has a protective role in collagen-induced arthritis in mice. Disease amelioration was associated with a shift in the immune balance from a pathological Th1 type response towards a protective Th2 type response. In humans, patients with SLE, scleroderma, diabetes, multiple sclerosis, and rheumatoid arthritis have lower numbers of peripheral NKT cells. NKT lymphocytes promote tumor rejection in experimental models of tumor immunotherapy. In contrast, NKT lymphocyte-related anti-tumor activity is associated with pro-inflammatory Th1-type immune responses. NKT cells were shown to have a role in suppression of hepatocellular carcinoma (HCC) via immune regulation towards tumor derived antigens, and adoptive transfer of dendritic cells pulsed ex vivo with the same antigens. NKT lymphocytes are activated by interaction of their TCR with glycolipids presented by CD1d, a nonpolymorphic, MHC class I-like molecule expressed by antigen presenting cells, and also by hepatocytes. Several possible ligands for NKT cells have recently been suggested including CD1d bound Glucocerebroside. Glucocerebroside (GC, beta-glucosylceramide), a naturally occurring glycolipid, is a metabolic intermediate in the anabolic and catabolic pathways of complex glycosphingolipids. Its synthesis from ceramide is catalyzed by the enzyme glucosylceramide synthase. Inherited deficiency of glucocerebrosidase, a lysosomal hydrolase, results in Gaucher's disease. Patients with Gaucher's disease have altered humoral and cellular immune profiles and increased peripheral blood NKT lymphocytes. CD1d-bound glucocerebroside does not activate NKT cells directly, and may inhibit activation of NKT cells by alpha-GalCer. On the other hand, glucosylceramide-synthase deficiency was shown to lead to defective ligand presentation by CD1d, with secondary inhibition of NKT cell activation. Recent studies have suggested that a number of glycolipids, including GC, have an immune modulatory effect in several immune mediated disorders. The ability to alter NKT lymphocyte function in various settings and the potential application of natural glycolipids for treatment are discussed.
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PMID:Glycolipids as immune modulatory tools. 1710 Jun 36

We aimed to investigate the frequency of rheumatic diseases in patients suffering from autoimmune thyroid diseases (ATD). Sixty-five patients (56 F, 9 M), who were followed by diagnosis of ATD, were questioned and examined for the presence of rheumatic disease. Basic laboratory tests and antithyroid antibodies, antinuclear antibody and rheumatoid factor (RF) levels were also measured by appropriate methods. Various rheumatic diseases were detected in 40 (62%) of patients with ATD. The most frequent rheumatic conditions were fibromyalgia, recurrent aphthous stomatitis, osteoarthritis, keratoconjunctivitis sicca and xerostomia and carpal tunnel syndrome which were detected in 20 (31%), 13 (20%), 10 (15%), 9 (14%) and 8 (12%) of patients, respectively. Autoimmune diseases, except Sjogren's syndrome, which were detected in ten patients with ATD, are as follows-vitiligo: two; autoimmune hepatitis: two; oral lichen planus: one, ulcerative colitis: one, inflammatory arthritis in four patients (two of them had rheumatoid arthritis, one had psoriasis and psoriatic arthritis and one had mixed collagen tissue disease). RF was positive in two patients, one of them had rheumatoid arthritis and FANA was positive in six (9%) patients; all of them had hypothyroidism. The frequency of rheumatic diseases seems to be higher in patients suffering from ATD. Initial evaluation and a regular checking for rheumatic diseases in patients suffering from ATD were recommended.
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PMID:Frequency of rheumatic diseases in patients with autoimmune thyroid disease. 1710 43


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