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)

In order to evaluate geographical differences in the liver pathology of ducks infected with duck hepatitis B virus (DHBV), ducks in Chiba and Shimane, Japan, and Shanghai, China, were investigated. The numbers (DHBV positive/negative) and the maximum age of the ducks examined were 18/10 at 19 mo, 15/1 at 3 yr 4 mo, and 72/27 at 18 mo, respectively. DHBV infection was induced experimentally in ducks from Chiba and Shimane but was present congenitally in those from Shanghai. Ducks were examined regarding liver function tests, conventional histology, immunohistology, electron microscopy, and molecular hybridization for DHBV DNA in the serum and liver. There was no significant difference between DHBV-positive and -negative ducks in bilirubin and transaminase and alkaline phosphatase activities in the sera. Histologically, while the livers of ducks from Chiba and Shimane did not show necroinflammatory (hepatitis) activity, those from Shanghai frequently did (52.5%). Necroinflammatory activity of the Shanghai ducks was present almost equally in both DHBV-positive and -negative livers. The livers of Shanghai ducks but not the other two areas often (8.3%) had ground-glass inclusions which corresponded ultrastructurally to numerous virus particles in the dilated cisternae of the proliferated endoplasmic reticulum. No advanced liver disease, such as cirrhosis or hepatocellular carcinoma, was observed. There was no significant difference in the amount of DHBV DNA in the sera or in its pattern in the liver tissue among ducks of the three areas. In addition, the livers of Chiba ducks frequently had amyloidosis, while those of Shanghai ducks were contaminated with parasites. In conclusion, DHBV infection did not appear to provoke significant hepatitis activity or advanced liver disease in the examined ducks of all three areas, and the DHBV-positive livers from Shanghai ducks showed a different morphological appearance from those of the other two areas. This variation might reflect the difference in the strain of ducks, subtypes of DHBV, environmental factors, or a combination of these influences.
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PMID:Geographical pathology of duck livers infected with duck hepatitis B virus from Chiba and Shimane in Japan and Shanghai in China. 334 10

We recently presented preliminary data indicating the presence of antibodies against acetaldehyde adducts in sera of over 70% of alcoholic patients. To assess the respective roles of liver disease and alcohol consumption as well as the specificity of this immune response, 141 patients in various stages of alcoholic and nonalcoholic liver diseases were tested by a hemagglutination assay. Sixty-three (73%) of 86 alcoholics had antibody titers above control levels (p less than 0.0001). Alcohol consumption of these individuals was significantly higher (p less than 0.001) than that of those alcoholics with normal titers. Twenty-two patients (39%) with nonalcoholic liver diseases also had elevated levels of antibodies against acetaldehyde adducts (p less than 0.0005); of these, 8 had primary biliary cirrhosis (7 in Stages III and IV), 9 had chronic active hepatitis (6 with cirrhosis) and 5 had acute (virus- or drug-induced) hepatitis. Antibody titers did not correlate with levels of transaminase or alkaline phosphatase activity, nor with bilirubin, and albumin. However, in 52 alcoholics and in nonalcoholic patients with biopsy-confirmed liver disease, the highest titers were seen in the more advanced stages of liver damage. Thus, in addition to alcohol consumption, severity of liver disease may play a role in the appearance of circulating antibodies against acetaldehyde adducts.
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PMID:The role of alcoholism and liver disease in the appearance of serum antibodies against acetaldehyde adducts. 337 72

Candida hepatitis, usually a manifestation of disseminated candidiasis in immunocompromised patients, is difficult to diagnose antemortem. We studied six patients with proven hepatic candidiasis to assess features helpful in deriving a correct diagnosis. Five patients were immunosuppressed as a result for treatment for leukemia; one was immunosuppressed due to renal transplantation. All had sustained fevers greater than 101 degrees F, elevated alkaline phosphatase levels, and multiple hepatic and splenic defects--presumably abscesses--on abdominal CT scan. Twelve liver biopsies (nine needle, three wedge) were examined. Biopsies from four patients contained identifiable Candida organisms within suppurative granulomas; a biopsy from a fifth patient grew Candida albicans in cultures. In the sixth patient, the first biopsy was culture positive for Candida albicans, and the second biopsy, a fine-needle aspirate, contained Candida organisms and purulent material. In all of the nondiagnostic biopsies, as well as in regions of the diagnostic biopsies around the suppurative granulomas, mass-associated obstructive changes were noted. These included pericentral sinusoidal dilatation and cholestatic inflammation characterized by periportal ductular proliferation with surrounding neutrophils and edema. We conclude that in the appropriate clinical setting, these mass-associated histologic findings are suggestive of adjacent Candida abscesses. Definite diagnosis requires either the identification of Candida organisms within inflammatory hepatic lesions or positive culture of Candida from the liver biopsy.
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PMID:Candida hepatitis. Histopathologic diagnosis. 341 94

Patients with jaundice and hyperbilirubinemia over 34 mumol/l have been examined by different methods in order to assess the diagnostic value of the methods. 340 patients were examined clinically and by laparoscopy, 168 patients and 92 healthy persons were examined by 10 laboratory indices, 639 patients--by ultrasonography, 95 patients--by scintigraphy, 116 patients--by computer tomography, 83 patients--by endoscopic retrograde cholangio-pancreatography (ERCPG), 17 patients--by percutaneous transhepatic cholangiography (PTC), 70 patients--by directed liver biopsy. In the patients with cholestasis the 5'-nucleotidase, alkaline phosphatase, glutamyl transpeptidase (lipoprotein X is positive in 92% of the patients) and cholesterol are increased most. The extrahepatic obstructions are diagnosed by ultrasonography in 94.8% of the patients (the biliary ducts are dilated), in 88.7% of the patients the localization of the obstruction and in 74.7% of the patients the cause of the obstruction are found. In parenchymal jaundice the sonography reveals the disease which has caused jaundice in 62.1% of the patients. The scintigraphy gives correct diagnosis in 50% of the patients with hepatitis and jaundice, in 78% of the patients with cirrhosis and jaundice and in 87.5% of the patients with liver cancer. The computer tomography reveals the obstructive jaundice in 94.7% of the patients and the focal processes in the liver in 96.7% of the patients. The ERCPG gives a clear picture of the biliary ducts in 72.28% and of the pancreatic duct in 83.13% of the patients with jaundice, simultaneously the biliary and the pancreatic ducts--in 45.78% of the patients and correct diagnosis in 83.1% of the patients examined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Differential diagnosis of jaundice]. 343 27

The interpretation of total alkaline phosphatase in paediatric patients is complicated by the wide range of normal values in the various age groups. Selected separations of isoenzymes in cases of rickets, hepatitis, cirrhosis, congenital atresia of the bile duct, during cytostatic or anticonvulsant therapy in 32 paediatric patients demonstrate the clinical relevance of isoenzyme determination.
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PMID:[Significance and selected examples for using determinations of isoenzyme of alkaline phosphatase in pediatrics]. 347 94

A model for immunologically T cell-mediated hepatitis was established in mice infected with lymphocytic choriomeningitis virus (LCMV). The severity of hepatitis was monitored histologically and by determination of changes in serum levels of the enzymes alanine aminotransferase (ALT), aspartate aminotransferase (AST), glutamate dehydrogenase (GLDH), and alkaline phosphatase (AP). Kinetics of histological disease manifestations, increases of liver enzyme levels in the serum, and cytotoxic T cell activities in livers and spleens all correlated and were dependent upon several parameters: LCMV-isolate; LCMV-WE caused extensive hepatitis, LCMV-Armstrong virtually none. Virus dose. Route of infection; i.v. or i.p. infection caused hepatitis, whereas infection into the footpad did not. The general genetic background of the murine host; of the strains tested, Swiss mice and A-strain mice were more susceptible than C57BL or CBA mice; BALB/c and DBA/2 mice were least susceptible. The degree of immunocompetence of the murine host; T cell deficient nu/nu mice never developed hepatitis, whereas nu/+ or +/+ mice always did. B cell-depleted anti-IgM-treated mice developed immune-mediated hepatitis comparably or even more extensively than control mice. Local cytotoxic T cell activity; mononuclear cells isolated from livers during the period of overt hepatitis were two to five times more active than equal numbers of spleen cells. Adoptive transfer of nylon wool-nonadherent anti-Thy-1.2 and anti-Lyt-2 plus C-sensitive, anti-L3T4 plus C-resistant lymphocytes into irradiated mice preinfected with LCMV-WE caused a rapid time- and dose-dependent linear increase of serum enzyme levels. This increase was caused by adoptive transfer of lymphocytes if immune cell donors and recipient mice shared class I, but not when they shared class II histocompatibility antigens. The donor cell dose-dependent increase of these enzymes was first measurable 6-18 h after transfer with 2 X 10(8) cells or 3 X 10(6) cells, respectively. The time-dependent increase caused by the adoptive transfer of 1-2 X 10(8) cells was strictly linear during a period of up to 25-40 h. These results indicate single-hit kinetics of liver cell death and suggest that effector T cells destroy infected liver cells via direct contact rather than via soluble toxic mediators. The results may represent the best in vivo correlate of the in vitro 51Cr-release assay that has been analyzed so far, and strongly support the view that antiviral cytotoxic T cells are directly cytolytic in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:T cell-mediated hepatitis in mice infected with lymphocytic choriomeningitis virus. Liver cell destruction by H-2 class I-restricted virus-specific cytotoxic T cells as a physiological correlate of the 51Cr-release assay? 348 5

We report the case of a patient in whom troleandomycin-induced hepatitis was followed by prolonged anicteric cholestasis. Jaundice occurred after administration of troleandomycin for 7 days and was associated with hypereosinophilia. Jaundice disappeared within 3 months but was followed by prolonged anicteric cholestasis marked by pruritus and high levels of alkaline phosphatase and gammaglutamyltransferase activities. Finally, pruritus disappeared within 19 months, and liver tests returned to normal 27 months after the onset of hepatitis. This observation demonstrates that prolonged cholestasis can follow troleandomycin-induced acute hepatitis.
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PMID:Prolonged cholestasis after troleandomycin-induced acute hepatitis. 349 78

We report a patient in whom cyproheptadine-induced hepatitis was followed by prolonged cholestasis marked by elevation of serum alkaline phosphatase levels, gammaglutamyltransferase and bile acid levels, and disappearance of small bile ducts. Chlorpromazine and imipramine, which can induce a similar acute hepatitis followed by protracted cholestasis, have a close chemical structure (i.e., a tricyclic ring). We suggest that this structure might be involved in this type of hepatotoxicity.
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PMID:Prolonged cholestasis after cyproheptadine-induced acute hepatitis. 355

Brachytherapy by embolization with radiotherapeutic microspheres following intraarterial infusion of a radiosensitizer represents an attempt to combine several selective modalities into a more potent, focused attack on regionally confined tumors. In pursuit of this goal, we examined the ability of foxhounds with surgically implanted hepatic arterial (HA) delivery systems to tolerate a clinically relevant dosage of HA yttrium-90 (Y-90) by microsphere administration either alone or preceded by a 28-day constant HA infusion of either 5-bromo-2'-deoxyuridine (BUDR) or a control solution. Five dogs received BUDR (10 mg/kg/day) and five a control buffer infusion for 28 days immediately prior to the administration of Y-90-coated 15 micron resin microspheres (equivalent of 5000 rads to the entire liver) to each dog on day 31. In all animals, blood counts, bilirubin, amylase, appetite, weight, and behavior remained unchanged. Dogs receiving the microspheres after buffer infusion alone exhibited no hepatic enzyme alanine aminotransferase or alkaline phosphatase elevation. Alanine aminotransferase and alkaline phosphatase levels both rose during the third week of BUDR infusion, and while subsequent microsphere administration further increased enzyme levels, these levels had largely normalized by necropsy on day 82. At necropsy, the type and degree of hepatic toxicity among the animals receiving radioactive microspheres was comparable to that previously described in patients receiving external beam hepatic irradiation at conventional doses (2000-3000 rads). Also noted was a radiation-induced cholecystitis (due in large part to the gallbladder's total reliance on the hepatic artery for blood supply). One resin microsphere dog exhibited a small quantity of microspheres in the lungs causing focal radiation-induced granulomas suggesting the need to assess shunting of microspheres through the liver in clinical studies. Thus, HA Y-90 microspheres with BUDR can produce acceptable, nonlethal, and tolerable toxicities in this dog model suggesting that clinical studies of this combination are not likely to be contraindicated by synergistic toxicity. Although HA BUDR did not contribute significantly to the toxicity of the Y-90 microspheres, HA BUDR by itself administered uninterrupted for 4 weeks may, like HA FUDR (clinically), cause chemical hepatitis/cholangitis. The unexpected fragmentation of the resin spheres (albeit without myelosuppression) has led us to begin studies with a recently developed nondisruptible glass microsphere (ThereSphere) in which the Y-90 is part of the glass matrix and cannot leach.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of hepatic arterial yttrium-90 microsphere administration alone and combined with regional bromodeoxyuridine infusion in dogs. 358 Oct 69

The hepatoprotective antioxidant bioflavonoid cianidanol has beneficial therapeutic and immunomodulatory effects in chronic hepatitis. Its action on natural killer (NK) cell activity has not yet been studied in hepatitis B virus (HBV) infection. In the present study, the in vitro and in vivo effects of the drug on NK cell activity have been determined in six patients with chronic HBV hepatitis and in ten healthy control subjects. Two methods were used: an enzyme release assay and a cytotoxicity test based on the assessment of endogenous alkaline phosphatase activity of the target cells. The in vitro effect of the drug was assessed using cianidanol at 10(-6), 10(-5) and 10(-4) M concentrations. For in vivo studies, HBV hepatitis patients were treated with cianidanol at a daily dose of 3.0 g cianidanol for seven days and were investigated before and after the treatment. Chronic HBV hepatitis patients showed a moderate decrease in NK cell activity compared to the controls, but after the cianidanol therapy their NK cell activity significantly rose to 68.0% +/- 9.5% (p less than 0.01). Cianidanol in vitro inhibited the NK cell activity both in hepatitis and healthy groups when using K-562 target cells and the lactic acid dehydrogenase enzyme release assay, but did not influence or even slightly enhance the NK activity when human embryonic fibroblast cells and alkaline phosphatase assay were used for the test. After the 7-day in vivo treatment, the in vitro inhibitory action of the drug was diminished or absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of cianidanol on natural killer cell activity in patients with chronic B virus hepatitis. 359 73


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