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)

Inchinko-to (TJ-135) is a herbal medicine consisting of three kinds of crude drugs, and in Japan it is administered mainly to patients with cholestasis. The present study evaluated the effects of TJ-135 on concanavalin A (con A)-induced hepatitis in mice in vivo and con A-induced cytokine production in vitro. When mice were pretreated with oral TJ-135 for 1 week before intravenous con A injection, the activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) were significantly decreased 8 h after con A administration (-82%, -96% and -66% respectively). In histological investigations, sub-massive hepatic necrosis accompanying inflammatory cell infiltration was not observed in mice pretreated with TJ-135. Serum levels of interleukin-12 (IL-12), interferon-gamma (IFN-gamma) and IL-2 were significantly lower in mice pretreated with TJ-135 compared with controls, while IL-10 levels were higher in these mice. Intrasplenic IL-12 levels were significantly lower in mice pretreated with TJ-135, while intrasplenic IL-10 levels were higher in these mice. In vitro, IL-10 production by splenocytes was increased by the addition of TJ-135 to the culture medium, whereas the production of IL-12 and IFN-gamma was inhibited. These results suggest that con A-induced hepatitis was ameliorated by pretreatment with TJ-135. With regard to the mechanism of these effects of TJ-135, we speculate that TJ-135 inhibits the production of inflammatory cytokine and enhances the production of anti-inflammatory cytokines. Therefore administration of TJ-135 may be useful in patients with severe acute hepatitis accompanying cholestasis or in those with autoimmune hepatitis.
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PMID:Effects of the Japanese herbal medicine 'Inchinko-to' (TJ-135) on concanavalin A-induced hepatitis in mice. 1105 23

Possible molecular mechanisms underlying changes in catalytical properties of alcohol dehydrogenase (ADH) and lactate dehydrogenase (LDH) were studied at toxic hepatitis. The development of toxic hepatitis is accompanied by significant changes in the activity of ADH and LDH assayed in subcellular fractions and kinetic characteristics of these enzymes. This can result in an increase cellular level of acetylaldehyde and lactate which promotes the development of liver cirrhosis.
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PMID:[Molecular mechanisms of metabolic adaptation in pathological changed liver during toxic hepatitis ]. 1155 17

The precipitating factors of idiopathic pulmonary fibrosis (IPF) have not been elucidated. Recently, a novel DNA virus named TTvirus (TTV) was discovered in a patient with post-transfusion hepatitis of unknown aetiology TTV is a circular, single-stranded DNA virus of 3.8 kB. To evaluate the relationship between TTV and IPF, the sera of 33 patients with IPF were tested for the presence of TTV DNA by semi-nested polymerase chain reaction. TTV DNA was detected in 12 (36.4%) IPF patients. The serum lactate dehydrogenase (LDH) level was significantly higher in the IPF patients withTTV than in those without TTV (802 +/- 121 vs. 530 +/- 49 IU l(-1), p < 0.05). Six (50%) of 12 patients in theTTV DNA-positive group died during the observation period, while only six (28.6%) of 21 patients in theTTV DNA-negative group died. The 3-year-survival rate was significantly lower in the TTV DNA-positive group than in theTTV DNA-negative group (58-3% vs. 95.2%, P <0-02). Replicative intermediate forms of TTV DNA were detected in the lung specimen from a TTV-infected IPF patient. TTV infection influences the disease activityand prognosis of IPF in some cases. Further studies are required to elucidate the clinical significance of TTV in IPF.
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PMID:Infection of TT virus in patients with idiopathic pulmonary fibrosis. 1177 89

To characterize the toxicity of phosphorothioate antisense oligodeoxynucleotides ([S]ODNs) in vivo, the mice received intravenously 26-mer bcr-abl antisense oligodeoxynucleotides (1 mg/mice/day) for 9 consecutive days. The organs and tissues were removed on the indicated days (+1, +7, +30) after the treatment. Our investigation revealed middle elevation of aminotransferases activity, lactate dehydrogenase level, total protein level and globulin level, decrease of glucose, albumin and blood urea nitrogen level in the peripheral blood. The mild anaemia and thrombocytopenia were observed too. The most significant treatment-related findings in the antisense treated mice were splenomegaly, reactive hepatitis and atrocytosis of kidney. These findings together with previous results demonstrate little and temporary toxicity effects mainly in organs known from cumulating of [S]ODNs.
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PMID:[Adverse effects of parenteral administration of antisense oligonucleotides]. 1186 87

A 68-year old Japanese male with alcohol related rhabdomyolysis, hepatitis, and hematological disorders is presented. Biochemical data showed markedly elevated levels of serum hepatobiliary enzymes, lactate dehydrogenase and myoglobin, and decreased levels of serum sodium and phosphate. The serum creatine kinase level was approximately 40 times higher than the normal upper limit with 97% of MM fraction. Clinical manifestations of rhabdomyolysis, such as myalgia, muscle weakness and acute renal failure, were not recognized. Hematological examinations revealed mild neutropenia, lymphopenia, monocytopenia and thrombocytopenia but no anemia or macrocytosis. Initial treatment of an intravenous infusion of saline (30 mL/Kg body weight) and subsequent low sodium diet was successfully completed without severe complications. All the abnormal laboratory data were normalized within three weeks of his hospitalization. We suggest that hyponatremia and hypophosphatemia may be involved in the development of rhabdomyolysis, hepatitis and hematological disorders.
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PMID:Rhabdomyolysis, hepatitis and multiple hematological disorders associated with alcohol abuse: a case report. 1293 2

Antigenic mimicry has been proposed as a major mechanism by which viruses could trigger the development of immune thrombocytopenic purpura (ITP). However, because antigenic mimicry implies epitope similarities between viral and self antigens, it is difficult to understand how widely different viruses can be involved by this sole mechanism in the pathogenesis of ITP. Here, we report that in mice treated with antiplatelet antibodies at a dose insufficient to induce clinical disease by themselves, infection with lactate dehydrogenase-elevating virus (LDV) was followed by severe thrombocytopenia and by the appearance of petechiae similar to those observed in patients with ITP. A similar exacerbation of antiplatelet-mediated thrombocytopenia was induced by mouse hepatitis virus. This enhancement of antiplatelet antibody pathogenicity by LDV was not observed with F(ab')2 fragments, suggesting that phagocytosis was involved in platelet destruction. Treatment of mice with clodronate-containing liposomes and with total immunoglobulin G (IgG) indicated that platelets were cleared by macrophages. The increase of thrombocytopenia triggered by LDV after administration of antiplatelet antibodies was largely suppressed in animals deficient for gamma-interferon receptor. Together, these results suggest that viruses may exacerbate autoantibody-mediated ITP by activating macrophages through gamma-interferon production, a mechanism that may account for the pathogenic similarities of multiple infectious agents.
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PMID:Exacerbation of autoantibody-mediated thrombocytopenic purpura by infection with mouse viruses. 1520 64

A 45-year-old patient was sent to our department because of highly elevated transaminases and elevated lactate dehydrogenase. His medical history was unremarkable and he took no medication on regular basis. Physical examination did not detect any abnormalities. There was no evidence for viral hepatitis, Epstein-Barr virus or cytomegalovirus, autoimmune hepatitis, Budd-Chiari syndrome, haemochromatosis or Wilson's disease. During the interview he admitted that for 'prophylactic reasons' he had been drinking the juice of Noni (Morinda citrifolia), a Polynesian herbal remedy made from a tropical fruit, during the preceding 3 weeks. This gave rise to the suspicion of herbal toxicity, which was confirmed by a liver biopsy. After ceasing the ingestion of Noni, transaminase levels normalized quickly and were within normal ranges 1 month after the first presentation. To our knowledge, this is the first report of hepatotoxicity caused by this herbal remedy, which has been highly praised in the tabloid press.
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PMID:Herbal hepatotoxicity: acute hepatitis caused by a Noni preparation (Morinda citrifolia). 1660 61

Viral infections are involved in the pathogenesis of blood autoimmune diseases such as hemolytic anemia and thrombocytopenia. Although antigenic mimicry has been proposed as a major mechanism by which viruses could trigger the development of such diseases, it is not easy to understand how widely different viruses might induce these blood autoimmune diseases by this sole mechanism. In mice infected with lactate dehydrogenase-elevating virus (LDV), or mouse hepatitis virus, and treated with anti-erythrocyte or anti-platelet monoclonal autoantibodies at a dose insufficient to induce clinical disease by themselves, the infection sharply enhances the pathogenicity of autoantibodies, leading to severe anemia or thrombocytopenia. This effect is observed only with antibodies that induce disease through phagocytosis. Moreover, the phagocytic activity of macrophages from infected mice is increased and the enhancing effect of infection on autoantibody-mediated pathogenicity is strongly suppressed by treatment of mice with clodronate-containing liposomes. Finally, the disease induced by LDV after administration of autoantibodies is largely suppressed in animals deficient for gamma-interferon receptor. Together, these observations suggest that viruses may trigger autoantibody-mediated anemia or thrombocytopenia by activating macrophages through gamma-interferon production, a mechanism that may account for the pathogenic similarities of multiple infectious agents.
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PMID:Enhancement of autoantibody pathogenicity by viral infections in mouse models of anemia and thrombocytopenia. 1589 20

The hepatoprotective activity of aerial parts of Tridax procumbens was investigated against d-Galactosamine/Lipopolysaccharide (d-GalN/LPS) induced hepatitis in rats. d-GalN/LPS (300 mg/kg body weight/30 microg/kg body weight)-induced hepatic damage was manifested by a significant increase in the activities of marker enzymes (aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase and gamma glutamyl transferase) and bilirubin level in serum and lipids both in serum and liver. Pretreatment of rats with a chloroform insoluble fraction from ethanolic extract of Tridax procumbens reversed these altered parameters to normal values. The biochemical observations were supplemented by histopathological examination of liver sections. Results of this study revealed that Tridax procumbens could afford a significant protection in the alleviation of d-GalN/LPS-induced hepatocellular injury.
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PMID:Hepatoprotective activity of Tridax procumbens against d-galactosamine/lipopolysaccharide-induced hepatitis in rats. 1592 95

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


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