Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serums containing the "e" antigen of hepatitis B virus were subjected to electrophoresis in polyacrylamide gel. An extra band appeared in the lactate dehydrogenase isozyme pattern, but this band was undetectable in serums containing antibodies to the e antigenic determinant. Prior separation of the lactate dehydrogenase isozyme-5 fraction by chromatography of serum on minicolumns of diethylaminoethyl-Sephadex-A50 improved electrophoretic identification of the extra band. Neutralization with antibodies to the e antigen as well as by antibodies to the homologous d or y component of the hepatitis B surface antigen removed the extra band; antibodies to the lactate dehydrogenase isozyme-5 removed both the normal and the extra enzymatic band of isozyme-5. This feature of the e antigen provides an assay system for laboratory diagnosis of potential clinical usefulness and suggests its possible role in pathogenesis of hepatocellular injury.
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PMID:Hepatitis B "e" antigen: an apparent association with lactate dehydrogenase isozyme-5. 7 21

Regular 4-weekly follow-up controls of serum lactate dehydrogenase activity in 23 renal transplant recipients revealed a constant rise in serum LDH activity during the early postoperative months. During the first post-transplant month serum LDH activity increased from 150.0 +/- 48.2 mE/ml to 195.5 +/- 84.8 mE/ml, serum enzyme activity being highest (329.1 +/- 143.2 mE/ml) 6 months after surgery. Since serum creatinine levels remained relatively constant, it seems unlikely that renal rejection played a major pathogenic role in the production of increased LDH activity. Since the pattern of lactate dehydrogenase isoenzymes was ithin normal limits, the pathogenesis of increased LDH serum activity following renal transplantation is not yet clear. Possible causes such as liver damage due to hepatitis B, macrocytosis induced by immunosuppressive therapy and myopathy to steroids are discussed.
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PMID:[Serum lactate dehydrogenase activity after renal transplantation (author's transl)]. 33 55

Since October 1987, 80 patients underwent open-heart surgery without donor-blood transfusion. 50 (Group I) out of these 80 cases were selected to be paired with 50 patients (Group II) who underwent open-heart surgery with homologous blood transfusion in the same period. Twelve cases (Group III) underwent open-heart surgery without homologous blood transfusion but were transfused after surgery. To decrease the homologous blood requirements, ultra-filtration system as well as conservation and autotransfusion of autologous blood was employed. Peripheral blood count, blood chemistry for liver and renal function were analyzed and compared among these three groups. Although hematocrit of Group I was lower than that of Group II until the third postoperative day, there was no difference after the seventh postoperative day. The platelet count was more in Group I than in Group II or III on the first and the seventh postoperative day. The level of lactate dehydrogenase was higher in Group II than in Group I. Total bilirubin was more elevated in Group II than in Group I on the first and the fourteenth postoperative day. Direct bilirubin was also higher in Group II than in Group I till fourteenth postoperative day. Five cases in Group II fulfilled the criteria of the serum hepatitis. Blood urea nitrogen and creatinine were less in Group I than in Group II. The duration of the intra-tracheal intubation was shorter in Group I than in Group II or III. There was no difference in postoperative dosage or duration of catecholamines among three groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Open-heart surgery without donor-blood transfusion--a clinical study]. 148 33

We report the development of severe hepatotoxicity in a patient on zidovudine therapy who received 3.3 g of acetaminophen in less than 36 hours. Three days later, the patient's serum aspartate aminotransferase level was 5,724 U/L, alanine aminotransferase was 3,124 U/L, lactate dehydrogenase was 12,675 U/L, alkaline phosphatase was 84 U/L, and total bilirubin was 20 mumol/L. These values substantially improved over the ensuing 4 days. Serologic results for hepatitis B, hepatitis A, and cytomegalovirus were all negative. The pattern and time sequence of transaminase elevation in this patient are consistent with acute acetaminophen hepatotoxicity, especially since zidovudine-induced hepatotoxicity is described as producing cholestasis rather than acute hepatitis. We hypothesize that our patient's susceptibility to acetaminophen-dependent hepatotoxicity may have been augmented by competitive utilization of glucuronidation by other drugs such as zidovudine and/or trimethoprim-sulfamethoxazole with subsequent increased cytochrome P450-dependent metabolism of acetaminophen. Additionally, due to malnutrition and/or to human immunodeficiency virus infection per se, our patient may have had decreased hepatic reserves of glutathione with which to conjugate the toxic acetaminophen product of the P450 system. Although severe acetaminophen-associated hepatotoxicity has not previously been reported in patients receiving zidovudine, we suggest that clinicians be aware of this potential interaction and counsel malnourished patients, especially those with concomitant hepatic disease, to exercise caution when taking both these medications.
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PMID:Severe hepatotoxicity in a patient receiving both acetaminophen and zidovudine. 836 34

A total of 92 patients with previously untreated intermediate- or high-grade non-Hodgkin's lymphoma attending the University Department of Medicine, Queen Mary Hospital, Hong Kong, were treated with the m-BACOD chemotherapy regimen (methotrexate, bleomycin, doxorubicin, cyclophosphamide, vincristine and dexamethasone). Additional involved-field radiotherapy was given to 32 (35%) patients. Myelosuppression was the major toxicity, and 5 (5%) treatment-related deaths occurred due to pneumonia, bleomycin sensitivity, doxorubicin cardiotoxicity and reactivation of hepatitis B infection. The overall complete response (CR) rate was 65/92 (71%) and the relapse rate was 22/65 (34%). The disease-free survival of the 65 CR patients at 2 years was 52% and the overall survival of all 92 patients at 3 years was 56%. The CR rate of stage I and II patients was significantly better than that of those with stage III and IV disease (87% vs 59%; P = 0.01), and the CR rate of stage III patients was superior to that of those with stage IV disease (86% vs 50%; P = 0.05). The overall survival of stage III and IV patients was significantly worse than that of subjects with stage I and II disease (31% vs 73%; P = 0.02). Multivariate analysis revealed that the independent prognostic variables significantly determining the CR rate and survival included the clinical stage and the serum lactate dehydrogenase level. From this study, the results of treatment with the m-BACOD regimen in patients with advance disease appeared to be similar to those obtained using the conventional CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone).
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PMID:m-BACOD chemotherapy for intermediate- and high-grade non-Hodgkin's lymphoma. 171 34

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

The tissue oxygen concentration, the serum antioxidant system state and the serum malondialdehyde (MDA) concentration were studied in patients with hepatitis B. The good correlations were studied in patients with hepatitis B. The good correlations between MDA concentration in patients serum and the oxygen concentration in tissues (R-0.79), and the cytoplasmic enzymes activity (R-0.75 for lactate dehydrogenase; R-0.75 for alanine transferase) were found. On the other hand, it was shown an antioxidant activity decrease of ceruloplasmin-transferrin system in patients serum. It is proposed, that the tissue hypoxia and the decrease of the serum antioxidant activity are the general factors leading to the MDA accumulation in the serum of patients with hepatitis B.
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PMID:[Caused of intensified lipid peroxidation in the blood of patients with viral hepatitis B]. 226 21

A human hepatoma cell line, associated with thorotrast exposure, from an hepatitis B marker-negative patient was established as a permanent cell line (Mz-Hep-1) in tissue culture. Histology of the primary tumor, as well as phase contrast, transmission and scanning electron microscopy of the cultured cells showed typical characteristics of liver cells. Mz-Hep-1 cells secreted complement components (C2, C3, C4), carcinoembryonic antigen, lactate dehydrogenase, chymotrypsin, haptoglobin and retinol-binding protein and expressed HLA-, transferrin-, blood group B-related determinants and complement component C5 and carcinoembryonic antigen on their cell surface. Mz-Hep-1 cells represent the first human hepatoma cell line, which is strongly associated with a carcinogen.
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PMID:Hepatocellular carcinoma after thorotrast exposure: establishment of a new cell line (Mz-Hep-1). 241 35

A unique type of Ag-specific hypersensitivity was induced by challenging the Ag-sensitized mice at the ear. It was elicited within 1 h after the Ag challenge, and thus was distinct from either the delayed-type hypersensitivity (DTH) which developed in 24 h or the immune complex-mediated hypersensitivity which evolved in 4 to 6 h. This hypersensitivity was referred to as early-type hypersensitivity (ETH). The time required for these types of hypersensitivity to develop after immunization was also different; DTH required 4 to 6 days, ETH 9 to 11 days, whereas plasma protein-induced immune complex-mediated hypersensitivity needed 18 to 21 days. The ETH could be induced by a smaller amount of Ag than DTH, and unlike DTH could be transferred by either immune sera or T cell-derived culture factor which was small m.w. Although the ETH developed later than DTH after sensitization, it lasted longer once developed and the pattern of response was inversely related to DTH. Furthermore, the denatured hepatitis B surface Ag induced DTH but not ETH, in contrast to native hepatitis B surface Ag that induced both, suggesting that the epitopes recognized by TETH cells were distinct from those recognized by TDTH cells. The ETH could be induced by most Ag tested including poly(Glu60Ala10Tyr10, L-lactic dehydrogenase, insulin, chicken egg white lysozyme, polymerized human serum albumin, horse gamma-globulin, transferrin, fibrinogen, and plasminogen, but not by purified protein derivative. Because poly(Glu60Ala10Tyr10, L-lactic dehydrogenase, egg white lysozyme and insulin were under the Ir gene control and the inducibility of ETH was Ag dependent and was closely correlated with that of DTH, the expression of ETH also must be regulated by Ir gene. The histopathologic changes in ETH consisted of capillary congestion and edema. The vasopermeability was increased and there was the leakage of plasma proteins into the tissue. Based on these data, we concluded that the ETH reported in this study was a novel type of Ag-specific hypersensitivity.
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PMID:An antigen-specific hypersensitivity which does not fit into traditional classification of hypersensitivity. 247 37

The hematotoxicity of benzene exposure has been well known for a century. Benzene causes leukocytopenia, thrombocytopenia, pancytopenia, etc. The clinical and hematologic picture of aplastic anemia resulting from benzene exposure is not different from classical aplastic anemia; in some cases, mild bilirubinemia, changes in osmotic fragility, increase in lactic dehydrogenase and fecal urobilinogen, and occasionally some neurological abnormalities are found. Electromicroscopic findings in some cases of aplastic anemia with benzene exposure were similar to those observed by light microscopy. Benzene hepatitis-aplastic anemia syndrome was observed in a technician with benzene exposure. Ten months after occurrence of hepatitis B, a severe aplastic anemia developed. The first epidemiologic study proving the leukemogenicity of benzene was performed between 1967 and 1973 to 1974 among shoe workers in Istanbul. The incidence of leukemia was 13.59 per 100,000, which is a significant increase over that of leukemia in the general population. Following the prohibition and discontinuation of the use of benzene in Istanbul, there was a striking decrease in the number of leukemic shoe workers in Istanbul. In 23.7% of our series, consisting of 59 leukemic patients with benzene exposure, there was a preceding pancytopenic period. Furthermore, a familial connection was found in 10.2% of them. The 89.8% of our series showed the findings of acute leukemia. The possible factors that may determine the types of leukemia in benzene toxicity are discussed. The possible role of benzene exposure is presented in the development of malignant lymphoma, multiple myeloma, and lung cancer.
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PMID:Hematotoxicity and carcinogenicity of benzene. 267 98


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