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)

We report here on a case of non-Hodgkin's lymphoma in which liver involvement was the predominant clinical manifestation. A healthy 44-year-old man presented with upper abdominal pain, hepatosplenomegaly, thrombocytopenia, elevated AST, ALT and bilirubin, and marked elevation of lactate dehydrogenase and alkaline phosphatase. The abdominal CT scan showed only diffuse hepatosplenomegaly and uneven contrast enhancement of the spleen without any definite mass of the liver and spleen. US-guided aspiration biopsy of liver and the histologic examination confirmed a diagnosis of non-Hodgkin's lymphoma, the diffuse large B cell type. Bone marrow biopsy showed the infiltration of malignant lymphoma cells. PET-CT showed an increased FDG uptake of the liver, spleen and long bones. The patient was treated with combination regimen of cyclophosphamide, doxorubicin, vincristine and prednisone chemotherapy. Even in the absence of a mass lesion or lymphadenopathy, primary hepatic or hepatosplenic lymphoma should be considered in differential diagnosis of hepatitis or liver cirrhosis, especially for patients with diffuse hepatosplenomegaly and markedly elevated LDH.
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PMID:[A case of primary hepatic lymphoma mimicking hepatitis]. 1617 55

We have studied the protective effect of chitosan on isoniazid- and rifampicin-induced hepatotoxicity with respect to the changes in the levels of diagnostic marker enzymes (in serum), lipid components and lipid peroxidation (in serum and liver). The oral administration of antitubercular drugs caused a significant elevation in the levels of diagnostic marker enzymes and cholesterol, triglycerides, free fatty acids and lipid peroxidation in serum and liver of experimental rats. There was a slight decline in the level of phospholipids in liver tissue also observed. Co-administration of chitosan significantly prevented the antitubercular drugs-induced elevation in the levels of serum diagnostic marker enzymes (alanine amino transferase, aspartate amino transferase, lactate dehydrogenase, acid phosphatase and alkaline phosphatase) in experimental groups of rats. It exerted a significant antilipidemic effect against isoniazid- and rifampicin-induced hepatitis by maintaining the levels cholesterol, triglycerides, free fatty acids and phospholipids in serum and liver at near normalcy. A tendency to prevent the isoniazid- and rifampicin-induced lipid peroxidation was also observed. The results of the present study indicated that the hepatoprotective effect of chitosan might be ascribable to its antilipidemic effect and/or antioxidant property.
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PMID:Effect of chitosan supplementation on antitubercular drugs-induced hepatotoxicity in rats. 1633 69

Macrophage activating syndrome (MAS) is a rare hematological disorder associated with uncontrolled systemic T-cell activation. Persistent fever, fatigue and hepatosplenomegaly are frequent clinical manifestations, whereas hyperferritinemia, elevated serum lactate dehydrogenase levels and cytopenia are key criteria for the diagnosis of MAS. The nature of liver pathology in MAS has been partially elucidated but destructive biliary lesions have been rarely described. This report illustrates four cases of MAS developing marked cholestasis, leading to one case of biliary cirrhosis necessitating liver transplantation. Histologically, liver involvement was characterized in all cases by acute lobular hepatitis, marked hepatocyte apoptosis and small bile duct injury similar to the vanishing bile duct syndrome. Immuno-histological studies showed that the inflammatory changes and bile duct lesions were dominated by the presence of activated macrophages and T-cells, in particular CD8+ lymphocytes, and in part NK-cells. These findings suggest that in MAS, various T-cell triggers such as infection, autoimmune disease and malignancy might result in the release of cytokines, which in turn activate macrophages to trigger a systemic acute phase response and local tissue damage. This communication suggests that a macrophage, T- and NK-cell network is operational in the pathogenesis of the cholangiocyte, hepatocyte and sinus endothelial cell damage in MAS.
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PMID:Macrophage activating syndrome is associated with lobular hepatitis and severe bile duct injury with cholestasis. 1661 13

In traditional oriental medicine, Yin-Chen-Hao decoction is used for the remedy of liver diseases such as hepatitis, fatty liver, hepatocirrhosis and jaundice. However, despite extensive pharmacological study, the molecular mechanism of the anti-inflammatory effect of Yin-Chen-Hao decoction is poorly understood. In this study, we have investigated the pharmacological action on the mechanism of concanavalin A-induced T cell-dependent hepatitis in mice. Concanavalin A administration resulted in a severe liver injury. This was shown through increased levels of serum transaminase and lactic dehydrogenase, and increased liver DNA fragmentation and caspase-3 activity. Pretreatment with the aqueous extract from Yin-Chen-Hao decoction dose-dependently inhibited the elevation in transaminase and lactic dehydrogenase activity, and reduced liver DNA fragmentation and caspase-3 levels. There was an improvement in histological changes including inflammatory infiltration, hepatocyte necrosis and degeneration, and Kupffer cell hyperplasia. In addition, Yin-Chen-Hao decoction significantly inhibited tumour necrosis factor-alpha (TNF-alpha) production in-vitro and in-vivo. Moreover, the activation of nuclear factor kappa B (NF-kappaB), which regulates TNF-alpha production, was blocked by Yin-Chen-Hao decoction in-vitro and in-vivo. In conclusion, Yin-Chen-Hao decoction was capable of regulating T-cell-mediated liver injury in-vivo. This event may have depended on the decrease of TNF-alpha production through the inhibition of NF-kappaB activation.
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PMID:Aqueous extract of Yin-Chen-Hao decoction, a traditional Chinese prescription, exerts protective effects on concanavalin A-induced hepatitis in mice through inhibition of NF-kappaB. 1664 Aug 37

A retrospective cohort study involving 29 Japanese patients with autoimmune hepatitis (AIH) was performed to clarify factors that predict the efficacy of prednisolone and the occurrence of various serious adverse effects. Independent predictors were identified by logistic analysis and with use of the Cox proportional hazard model. Responses to prednisolone were noted in 28 patients, who were classified into the complete remission group (52%) or the relapse group (48%). Multivariate analysis identified alanine aminotransferase, alkaline phosphatase, and immoglobulin G levels as independent predictors of relapse. The adverse effects most frequently observed were diabetes mellitus (37.9%), psychiatric/ neurologic symptoms (34.5%), and circulatory symptoms (34.5%). Predictive factors included lactate dehydrogenase, albumin, and fasting blood glucose levels for diabetes mellitus, alkaline phosphatase and C-reactive protein for psychiatric/ neurologic symptoms, and autoimmune hepatitis score and lactate dehydrogenase for circulatory symptoms. Selection of an optimal treatment method for individual patients may be possible after the risks of relapse and adverse effects have been estimated.
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PMID:Efficacy and safety of prednisolone in patients with autoimmune hepatitis. 1664 9

The hepatoprotective effects of whey protein on two injections of D-galactosamine (300 mg/kg, i.p.) were investigated in rats fed a modified AIN-93M diet formulated with a protein source of casein or whey for 16 d. The whey protein-containing diet clearly suppressed an increase in plasma alanine and aspartate aminotransferase activity, lactate dehydrogenase and bilirubin, which are hepatitis markers, and also hyaluronic acid, a fibrosis marker. In addition, it suppressed histopathological signs of portal fibrosis, bile duct proliferation, and perivenular sclerosis. These results suggest that supplementation with whey protein can help prevent the development of hepatitis and portal fibrosis.
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PMID:Hepatoprotective effects of whey protein on D-galactosamine-induced hepatitis and liver fibrosis in rats. 1671 38

Hepatitis is caused by hepatitis viruses, but hepatitis or hepatocellular enzyme abnormalities is sometimes associated with infection by the hepatiticomimetic viruses. The direct and indirect effects of infection with hepatiticomimetic viruses were examined in two human hepatocyte systems. Poliovirus, adenovirus, and herpes simplex virus (HSV) induced cytopathology in Hep G2 cells. Measles virus caused no change in hepatocytes. Poliovirus infection did not affect cellular protein synthesis, and the peak of hepatocellular enzyme release coincided with the peak of virus release. The increase in adenovirus protein synthesis correlated with the decrease of transferrin synthesis, and enzyme release was not prominent. HSV induced viral protein synthesis with enhanced processing and inhibition of synthesis of alpha1-antitrypsin. The peak of enzyme release was later than the peak of virus release. In primary hepatocytes, poliovirus, adenovirus, and induced extensive cytopathology and enzyme release, and VZV caused cytopathology and significant but minute enzyme release. The ratio of lactate dehydrogenase to aspartate aminotransferase release was larger in poliovirus infection in both hepatocytes than in HSV or VZV infection. Although poliovirus and adenovirus are released by cytolysis and HSV and VZV are secreted by exocytosis of cytoplasmic vacuoles, enzyme release was independent of the type of virus release. Adenovirus showed strong cytotoxicity but did not modify the membrane nor cause enzyme release. Enzyme release was associated with modification of the surface membrane due to apoptosis with poliovirus and necrosis with HSV. Consequently hepatocellular injury by viral infection did not reflect the amount or pattern of hepatocellular enzyme release.
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PMID:Infection and direct injury in human hepatocyte explants and a hepatoblastoma cell line due to hepatiticomimetic (non-hepatitis) viruses. 1731 34

A 23-year-old woman presented to our polyclinic complaining of itching, generalized dermatitis, and jaundice. She was in her 31st gestational week and had developed pruritus and the dermatitis since the first month of pregnancy; her jaundice started about a month before presentation. Her history included similar complaints in a previous pregnancy, which resulted in premature birth of a baby with a permanent brain defect. One of her sisters had had jaundice and itching in her 27th gestational week and delivered a healthy baby; a second sister had experienced itching and dermatitis in her second trimester and delivered a healthy baby. Physical examination of the patient showed that her eyes were jaundiced (Figure 1); skin examination revealed generalized erythematous excoriated papules, symmetrically distributed all over her body (Figure 2 Figure 3). Laboratory analyses revealed the following results: leukocyte count, 14.30/mm(3) (3.8-10.3/mm(3)); erythrocyte sedimentation rate, 25 mm/h (<20 mm/h); aspartate aminotransferase, 44 U/L (5-40 U/L); alanine aminotransferase, 63 U/L (5-40 U/L); lactate dehydrogenase, 1158 U/L (220-450 U/L); total bilirubin, 6.88 mg/dL (<1.10 mg/dL); and direct bilirubin, 3.27 mg/dL (<0.35 mg/dL). Urinalysis results were positive for bilirubin and urobilinogen. Positive serologic findings included rubella immunoglobulin G, 93 AU/mL (<15) and cytomegalovirus, 188 AU/mL (<10); negative findings included herpes simplex virus type 2 and hepatitis. Histopathologic examination of material collected from the left breast via punch biopsy showed parakeratosis, acanthosis, and perivascular lymphocyte infiltration in dermal vessels. Treatment with 2 g/d cholestyramine and a topical corticosteroid was effective in the patient, who was diagnosed with intrahepatic cholestasis of pregnancy and prurigo of pregnancy based on the clinical, histopathologic, and laboratory findings. To the authors' knowledge, this is the first such reported case in the literature.
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PMID:Intrahepatic cholestasis occurring with prurigo of pregnancy. 1797 52

Trichloroethylene (TCE) can induce non-dose-related hepatitis, possibly classified as delayed-type hypersensitivity (immune-mediated hepatitis), as well as dose-related toxic liver injury. However, the difference in pathophysiology between the two kinds of hepatitis remains unknown. This study aimed to characterize the liver injury associated with hypersensitive skin reactions induced by TCE in guinea pigs. As a model of dose-related acute toxic liver injury, the animals were treated with intradermal injection (ii) (0, 167, 500, 1500 or 4500 mg/kg of TCE) or dermal patch (dp) (0 or 900 mg/kg of TCE). The guinea pig maximization test (GPMT) was also carried out as a model of immune-mediated liver injury, in which the total TCE dosage was below 340 mg/kg. In the group of TCE 4500 mg/kg (ii), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) increased (p<0.01), while total protein and globulin decreased (p<0.05). Evident fatty degeneration, hepatic sinusoid dilation and inflammatory cell infiltration were observed. No significant change was found in animals treated with TCE of doses below 500 mg/kg (ii) or 900 mg/kg (dp). In the GPMT, sensitization rates of TCE-induced dermal allergy were 66%. ALT, AST, lactate dehydrogenase and the relative liver weight increased significantly (p<0.05) while albumin, IgA and gamma-glutamyl transpeptidase decreased significantly (p<0.05). Lesions of ballooning changes were observed in liver pathology. Thus, TCE could cause both acute-type toxic liver injury and immune-mediated liver injury, the so-called delayed-type hypersensitivity at doses below the dosage for toxic liver injury. Interestingly, the histopathological features were quite different: fatty degeneration was most prominent in the former, and ballooning in the latter.
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PMID:Characterization of liver injury associated with hypersensitive skin reactions induced by trichloroethylene in the guinea pig maximization test. 1840 61

Injection of D-galactosamine and lipopolysaccharide (DGaIN/LPS) is useful as an experimental model of acute hepatic damage. Juvenile rats were used for investigation. The hepatoprotective activity of aqueous garlic (Allium sativum) extract (AGE) at a dose of 300 mg/kg body weight for 14 days, intraperitoneal (i.p.) prior to the induction of DGalN/LPS, was investigated against DGalN/LPS-induced hepatitis in rats. DGalN/LPS (300 mg/kg body weight/30 microg/kg body weight, i.p.), induced hepatic damage that was manifested by a significant increase in the activities of marker enzymes [alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and gamma glutamyl transferase (gamma GT)], bilirubin, lipid peroxides (LPO), tumor necrosis factor (TNF-alpha) and myeloperoxidase (MPO) activity level in serum. Also, the lipid profile in serum and liver homogenate including total cholesterol, triglycerides, free fatty acids and phospholipids were significantly deteriorated. The antioxidant enzyme activities (superoxide dismutase, SOD; reduced glutathione, GSH; catalase, CAT and glutathione peroxidase, GPX) in liver homogenate were significantly decreased in the DGalN/LPS. Pretreatment of rats with AGE reversed these altered parameters near to normal control values. Results of this study revealed that AGE could afford a significant protection in the alleviation of DGalN/LPS-induced hepatic damage.
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PMID:Aqueous garlic extract attenuates hepatitis and oxidative stress induced by galactosamine/lipoploysaccharide in rats. 1857 Feb 25


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