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)

Serum specimens from 42 normal dogs and 42 with untreated malignant tumours were assayed for the presence of antibodies to human adenovirus types 5, 21 and 31 and to infectious canine hepatitis (ICH) virus. Radioimmunoassays using human adenovirus antigens showed that 71 per cent (30/42) of all dogs with tumours, but only 19 per cent (8/42) of all normal dogs, were positive for human adenovirus antibody. Canine sera reactive with antigens of one human adenovirus type in radioimmunoassays were also reactive with antigens of the other two types. Dogs bearing malignant lymphoma or squamous cell carcinoma tumours had higher levels of antibody against adenovirus type 5 antigens. Human adenovirus type 5 was neutralised by sera from four tumour-bearing and two normal dogs, while sera from two normal and five tumour-bearing dogs were positive in immunodiffusion tests with human adenovirus antigens. Levels of ICH antibody in sera of normal adult dogs and adult dogs with tumours were not markedly different when measured by radioimmunoassays. Likewise, sera from these two groups of dogs had similar ranges of ICH neutralising antibody titres. In contrast, levels of ICH antibody detected by the serological assays in sera from non-pet, non-vaccinated pups were either markedly low or absent. Possible explanations for the observed increased levels of human adenovirus antibody in sera of tumour-bearing canine pets are discussed.
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PMID:Human adenovirus antibody in sera of normal and tumour-bearing dogs. 23 77

A characteristic alkaline phosphatase (orthophosphoric monoester hydrolase, alkaline pH optimum, EC 3.1.3.1) was detected in the sera of most patients with infectious mononucleosis, acute and chronic lymphatic leukaemia, non-Hodgkin's lymphoma, Burkitt's lymphoma and nasopharyngeal carcinoma. The enzyme was also present in the sera of nine out of 26 patients with cancer of the cervix. N-APase in these cases counted 30-100% of the total alkaline phosphatase activity. N-APase was absent from the sera of healthy individuals and of patients with acute and chronic granulocytic leukaemia, breast cancer, colon cancer, rheumatoid arthritis, ulcerative colitis, systemic lupus erythematosis, hepatitis and obstructive jaundice. Only three of 22 patients with Hodgkin's disease showed n-apase activity in the serum. In infectious mononucleosis the presence of N-APase activity was well correlated with the clinical course. In 13 cases studied, the clinical improvement was associated with the decrease or disappearance of N-APase activity. N-APase activity could not be detected in white cells of acute myeloid leukaemic patients, nor in the cells of myeloid blastic crisis of chronic granulocytic leukaemia. It was present in the cells of lymphoid blastic crisis of chronic granulocytic leukaemia.
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PMID:N-alkaline phosphatase: a potential disease marker for lymphoproliferative disorders. 43 2

Six patients who were referred to the liver unit on account of jaundice are described. A different initial diagnosis has been made in each case, these being fulminant hepatic failure, severe hepatitis with renal failure, toxoplasma hepatitis, extrahepatic obstruction, sclerosing cholangitis, and liver abscess. After delays of four weeks to 12 months from the time of first symptoms all six patients were eventually found to have advanced Hodgkin's disease (stage 4). In four patients the diagnosis was made during life, but in two only at autopsy. In four lymphoma tissue was finally demonstrable in the liver, but in two liver biopsy showed only minor non-specific changes despite grossly abnormal liver function tests. Three of the six patients were treated with chemotherapy, and two of these recovered sufficiently to leave hospital. With the encouraging survival figures now being obtained in Hodgkin's disease, an awareness of the varied hepatic manifestations of the disease may allow treatment to be instituted at an earlier stage.
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PMID:Liver disease as presenting manifestation of Hodgkin's disease. 48 87

Exposure of mice to 1000 ppm of vinyl chloride (VC), 6 hr/day, 5 days/week, caused some acute deaths with toxic hepatitis and marked tubular necrosis of the renal cortex. Starting the sixth month, mice exposed to 1000, 250, or 50 ppm of VC became lethargic, lost weight quickly, and died. Only a few mice exposed to 50 ppm survived for 12 months. Pulmonary macrophage count was elevated in some mice. There was a high incidence of bronchiolo-alveolar adenoma, mammary gland tumors including ductular adenocarcinoma, squamous and anaplastic cell carcinomas with metastasis to the lung, and hemangiosarcoma in the liver, and, to a lesser extent, in some other organs. The incidence of these tumors quickly increased, and the severity was in direct proportion to the levels of VC and the length of exposure. Malignant lymphoma involving various organs was observed in a few mice. Rats were more resistant to the toxic effects of VC. Exposure to 1000 ppm slightly depressed the body weight of the females. Exposures of 250 or 1000 ppm caused a number of deaths and hemangiosarcoma in the liver starting the ninth month. Most rats with hepatic hemangiosarcoma also developed hemangiosarcoma in the lung. Hemangiosarcoma occasionally occurred in other tissues of one or two rats exposed to 50 ppm or higher level of VC. Exposure of mice to 55 ppm of vinylidene chloride (VDC) also caused a few acute deaths and a few hepatic hemangiosarcomas. Inflammatory, degenerative, and mitotic changes occurred in the liver. No mouse exposed to VDC developed any mammary gland tumors. Several mice had bronchioloalveolar adenoma. Exposure of rats to 55 ppm of VDC slightly depressed the body weight. Hemangiosarcoma occurred in the mesenteric lymph node or subcutaneous tissue in two rats.
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PMID:Inhalation toxicity of vinyl chloride and vinylidene chloride. 56 2

Sporadic cases or radiation hepatitis have been reported following doses above 3500 rad delivered in 3-4 weeks to the liver. The authors report their experience of radiation hepatitis in two out of 117 consecutive lymphoma cases treated with total abdominal irradiation. These two patients developed clinically overt manifestations which lasted for a short period of time and fully recovered. The dose delivered to the whole liver was 3000 rad in six weeks, but in one an additional 1000 rad in five fractions were delivered to the left lobe in an attempt to boost the dose to the central axis lymphatic system up to 4000 rad. The low incidence of radiation hepatitis and its reversible course, when 3000 rad in six weeks are delivered to the whole liver, is emphasised.
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PMID:Acute transient radiation hepatitis following whole abdominal irradiation. 100 Aug 90

Transient bacteremia associated with percutaneous liver biopsy was studied by pour-plate blood cultures, which were obtained immediately before and after the procedure and 5, 10, 15, and 30 min later in 89 patients. Part of the liver tissue was also cultured in all patients. Histological diagnoses included hepatitis, cirrhosis, cholangitis, fatty liver, granulomata, metastatic liver disease, lymphoma, and miscellaneous disorders. All blood cultures obtained before liver biopsy were sterile. Bacteremia was demonstrable in 12 patients (13.48%). In most of these patients, blood cultures were positive for as long as 15 min after liver biopsy; all cultures were negative at 30 min. Among the bacteria associated with 12 episodes of bacteremia were Escherichia coli, Klebsiella, Bacteroides, enterococci, diphtheroids, Staphylococcus aureus, alpha-hemolytic Streptococcus, and Streptococcus pneumoniae. The patients with positive liver biopsies had a higher incidence of bacteremia (83.3%) than did the patients whose liver biopsies were sterile (8.r%); this difference is stastically significant (P smaller than 0.01). Thus, liver biopsy can be associated with transient bactermia.
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PMID:Transient bacteremia associated with percutaneous liver biopsy. 109 72

In a 47-year-old male patient a tonsillar swelling was pointed out in May, 1991. Lymph node biopsy revealed that he had malignant lymphoma (diffuse large cell type). He had no hepatic dysfunction on admission, but because of positive hepatitis B (HB) antigen and negative HB antibody, he was diagnosed as an asymptomatic HB carrier. The staging examination showed that he had stage IIA lymphoma. Treatment with the COP-BLAM regimen was initiated on June 8. But the level of serum GOT and GPT increased to 286 IU/l and 392 IU/l, respectively. Serum DNA polymerase also increased to 9492 cpm. Interferon-alpha (3 x 10(6) units daily) was administered intramuscularly from June 8. Serum DNA polymerase decreased to zero on September 2, and his HBe antibody became positive indicating seroconversion. COP-BLAM chemotherapy without prednisolone was initiated from September 9 and complete remission was achieved. He was discharged from our hospital on September 25. It has been frequently reported that asymptomatic HB antigen carriers developed fulminant hepatitis during the course of chemotherapy. Our case suggests that it is necessary to continue chemotherapy in order to attain seroconversion by early use of interferon-alpha, when lymphoma patients display aggravated hepatic dysfunction and increased DNA polymerase levels.
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PMID:[Successful interferon-alpha treatment of hepatitis B developing during chemotherapy of malignant lymphoma]. 143 50

Hepatomegaly and deranged liver functions are common findings in reactive haemophagocytic syndrome (RHS). We report the findings of 12 fatal cases of RHS in which histological materials of the liver are available for study. The underlying diseases of these patients included lymphoma/leukaemia (6 cases), disseminated undifferentiated carcinoma of the ovary (1 case), disseminated nasopharyngeal carcinoma complicated by tuberculosis (1 case), adenovirus pneumonia (1 case), pneumococcal pneumonia (1 case), typhoid fever (1 case), and possible drug intoxication (1 case). Ten patients had involvement of the liver by the underlying disease process which contributed to the marked hepatic derangement. Non-specific reactive hepatitis, sinusoidal dilatation and steatosis resulting from systemic or local effects of the associated diseases and the haemophagocytosis also added to the high incidence of liver abnormalities. A diffuse Kupffer cell hyperplasia with haemophagocytosis is characteristic of the syndrome, as all the cases showed increased numbers of bland-looking histiocytes within the hepatic sinusoids and haemophagocytosis which was moderate to marked in 8 cases and mild in 4. Thus the finding of Kupffer cell hyperplasia with prominent haemophagocytosis in liver biopsy is indicative of an element of RHS and warrants clinical monitoring. Differential diagnoses of haemophagocytosis in liver are also discussed.
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PMID:Liver changes in reactive haemophagocytic syndrome. 147 7

Sarcoidosis and malignant lymphoma can occur in the same patient; sarcoidosis appears first, the malignant lymphoma follows later. The case histories of three patients illustrate what Brinker first coined as the "sarcoidosis-lymphoma syndrome". In two patients a pulmonary sarcoidosis stage I was diagnosed over 30 years respectively 4 years prior to the histological diagnosis of highly malignant Non-Hodgkin lymphoma. The third patient suffered from generalized sarcoidosis with splenomegaly, , granulomatous hepatitis and interstitial lung disease, in addition to which a lymphoproliferative syndrome was diagnosed. Comparing the pathogenesis of malignant lymphoma and sarcoidosis, parallels such as T-cell dysfunction, which probably facilitates malignant transformation of B-cells, become apparent. In both diseases the transforming gene could be the Ebstein-Barr virus.
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PMID:[The "sarcoidosis-lymphoma syndrome"--a lymphocyte dysregulation?]. 149 11

Radiographically, the liver may appear normal even if severely diseased. Ultrasonography can be an important adjunct in the evaluation of diffuse parenchymal hepatic disease. Diffuse liver disease appears ultrasonographically as a change in liver echogenicity from normal when compared with the renal cortex or spleen. Diffuse liver disease can be characterized as either hyperechoic due to fatty change, steroid hepatopathy, and cirrhosis or hypoechoic due to congestion, suppurative hepatitis, and lymphoma. Ultrasonographic diagnosis of diffuse liver disease should be substantiated by biopsy and histopathologic evaluation.
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PMID:Ultrasonography of diffuse liver disease. A review. 158 44


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