Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the most prevalent forms of hepatitis in intravenous heroin addicts, 389 addicts consecutively admitted to outpatient treatment clinics throughout California were tested for antibodies to hepatitis A (anti-HAV), B core (anti-HBc), B surface (anti-HBs), C (anti-HCV), D (anti-HDV), and B surface antigen (HBsAg). The majority were also tested for serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, lactic dehydrogenase, total bilirubin, globulins, albumin, and platelet count. The seroprevalence of each marker was: anti-HAV (40.7%); anti-Hbc (73.6%); anti-HBs (46.7%); anti-HCV (93.6%); anti-HDV (9.6%), and HBsAg (3.5%). No single case was positive for IgM, anti-HAV, or for both HBsAg and anti-HDV, indicating the presence of recent hepatitis A or hepatitis D infection. Abnormal liver enzymes, serum proteins, total bilirubin, and platelet count were found to be normal in 5.3 to 44.8% of anti-HCV cases indicating persistent infection. Among anti-HCV cases, elevated total bilirubin or a low platelet count was invariably associated with one or more liver enzyme and protein abnormalities. We conclude that while acute hepatitis may be frequent and caused by various viral types, hepatitis C is the primary form of chronic hepatitis found in intravenous heroin addicts. Almost half of hepatitis C cases demonstrate liver function abnormalities indicating persistent infection that has the potential to be contagious and progress to cirrhosis, liver failure, and hepatocellular carcinoma.
 ...
PMID:Seroprevalence of hepatitis A, B, C, and D markers and liver function abnormalities in intravenous heroin addicts. 855 78

The liver is commonly involved in patients with typhoid fever. However, severe hepatic derangement simulating acute viral hepatitis is rare. Our aim was to characterize the clinical picture, biochemical features, and prognosis of Salmonella hepatitis. Retrospective case-control analysis of medical records included 27 patients with Salmonella hepatitis and 27 inpatients with acute viral hepatitis from 1973 to 1993. Travel history, clinical picture, a standard battery of 18 biochemical tests, complete blood counts, disease complications, duration of hospital admission, and final outcome were analyzed. Eleven patients with Salmonella hepatitis (40%) travelled abroad within 1 month of illness. A greater proportion of Salmonella hepatitis patients developed fever > 104 degrees (44% vs. 4%, respectively; P < .0001), and had relative bradycardia (42% vs. 4%, respectively; P < .002) than viral hepatitis patients. Salmonella hepatitis was associated with lower peak serum alanine transaminase (ALT), aspartate transaminase, and higher peak serum alkaline phosphatase (296 vs. 3,234 U/L, 535 vs. 2,844 U/L, and 500 vs. 228 U/dL, respectively; P < .0001, <.0003, and <.004). The admission ALT/lactic dehydrogenase (LDH) ratio, when levels of both enzymes were expressed as multiples of upper limit of normal value for each, was significantly lower in Salmonella hepatitis. All Salmonella hepatitis cases had a ratio < 4, and all viral hepatitis cases had a ratio > 5, P < .0001. Left shift of white blood cells was more common in Salmonella hepatitis (83% vs. 37%; P < .004). Patients with Salmonella hepatitis had a longer hospitalization (14.8 vs. 6.5 days, respectively; P < .0001). All 54 patients survived their illness. The clinical picture of Salmonella hepatitis is frequently indistinguishable from viral hepatitis. The admission ALT/LDH ratio is the best discriminator between both entities. Other clues that raise the possibility of Salmonella hepatitis include high fever, relative bradycardia, and left shift of WBCs. Despite long hospitalization, Salmonella hepatitis responds to proper antibiotic therapy and has an excellent prognosis.
 ...
PMID:Salmonella hepatitis: analysis of 27 cases and comparison with acute viral hepatitis. 878 16

Fas is an apoptosis-signaling receptor molecule expressed in vivo on thymocytes, liver, heart, and ovary. In vivo administration of the anti-Fas Jo2 antibody in mice induces severe apoptotic liver damage leading to fulminant hepatitis and death. Linomide, a quinoline 3-carboxamide, inhibits apoptosis of B and T cells induced by various stimuli including viruses, superantigens, and glucocorticoids. Mice treated with linomide survived the lethal effect of anti-Fas antibody, did not accumulate ceramide in hepatocytes, and recovered liver structure and function within 96 h of anti-Fas injection, as confirmed by histology and glutamic oxalacetic transaminase, glutamic pyruvic transaminase, and lactate dehydrogenase levels. Surviving mice showed severe depletion of cortical thymocytes, but medullar thymic cells expressing high CD3 and Fas levels also survived the treatment with anti-Fas in the presence of linomide. Heart, lung, and ovary showed no signs of apoptosis promoted by Fas ligation. These results suggest that linomide prevents cell death triggered by Fas ligation and can be useful for therapeutic intervention in fulminant hepatitis.
 ...
PMID:Linomide prevents the lethal effect of anti-Fas antibody and reduces Fas-mediated ceramide production in mouse hepatocytes. 878 88

Intraperitoneal injection of pathogen-free B10.A mice with mouse hepatitis virus (MHV)-A59 resulted in a short subclinical infection which was terminated by a rapid antiviral immune response. The infection resulted in a rapid, but transient, about 10-fold increase in the number of macrophages and total cells in the peritoneum of the mice. This increase was preceded by a complete depletion of the peritoneum of the subpopulation of macrophages that supports a productive infection by lactate dehydrogenase-elevating virus (LDV). The depletion of LDV-permissive macrophages was a long-term effect; at 50 days post-infection with MHV, the proportion of LDV-permissive macrophages in the peritoneum had reached only 20% of that observed in the peritoneum of uninfected mice, whereas the total number of macrophages in the peritoneum had returned to normal. Furthermore, MHV infection resulted in a long-term alteration in the proliferative response of spleen T cells to concanavalin A (ConA) and in their ability to produce interferon gamma; several times higher concentrations of ConA were required to induce a maximum proliferative response in spleen T cell populations from 5-week MHV-infected B10.A mice than in spleen T cell populations from infected companion mice but the former produced 5 times more interferon gamma than the T cells from uninfected mice.
 ...
PMID:Mouse hepatitis virus infection of mice causes long-term depletion of lactate dehydrogenase-elevating virus-permissive macrophages and T lymphocyte alterations. 883 97

Ten muskrats (Ondatra zibethicus) each were infected with 17,000 eggs (long-term study) and eight muskrats each were infected with 8,000 eggs (short-term study) of Capillaria hepatica (Nematoda). Food intake, body weight, and selected clinicopathological parameters were measured every 2 days for 28 days in the short-term study and every 14 days for 184 days in the long-term study. Muskrats in the short-term study had moderate to severe necrotizing granulomatous hepatitis associated with mild anorexia and weight loss, varying degrees of leukocytosis with eosinophilia and elevation of serum alanine and aspartate aminotransferases. No significant changes in packed cell volume, hemoglobin, total plasma protein, albumin, blood urea nitrogen, bilirubin, lactate dehydrogenase or alkaline phosphatase were found among animals from the short-term study. Muskrats in the long-term study had severe necrotizing granulomatous hepatitis associated with marked anorexia, weight loss and 60% mortality over 39 days post-inoculation (PI); animals that survived for 184 days did not return to pre-inoculation body weights despite returning to normal food intake. Hepatic lesions at 184 days PI consisted of minimal to severe liver replacement by C. hepatica eggs. No statistically significant differences in values of clinical parameters between inoculated animals and a non-inoculated control group from the long term study were found.
 ...
PMID:Clinicopathological features and histopathology of experimental hepatic capillariasis in muskrats (Ondatra zibethicus). 902 99

A 27-year-old male suffered from Epstein-Barr virus (EBV)-related liver dysfunction with persistent hypogammaglobulinemia. IgG titers to EBV antigens were significantly high, while other hepatitis markers were negative. Liver biopsy disclosed active intralobular inflammation. Two years later, he manifested persistent fever, leukopenia, effusions and hypoproteinemia, and his general condition worsened progressively. The peripheral blood small lymphocytes predominantly expressed natural killer (NK)-like phenotypes (CD2+, CD7+, CD16+, CD56+). Hepatosplenomegaly and marked elevation of serum lactic dehydrogenase were observed. He died of respiratory failure at the age of 29. At autopsy, the liver (2190 g), spleen (860 g), small bowel and mesenteric lymph nodes showed massive infiltration of large atypical lymphoid cells in close association with hemophagocytic histiocytes. Involvement was mildly noted also in the bone marrow, lungs, gall-bladder and kidneys. The atypical cells belonged to CD30+ activated NK-type cells expressing CD2, cytoplasmic CD3 epsilon, CD7, CD45RO, CD56, HLA-DR and HLA-DQ. T cell receptors (TCR), surface CD3, CD4, CD5 and CD8 were not expressed. Epstein-Barr virus-related small nuclear RNA (EBER1) and Epstein-Barr virus-associated nuclear antigen 1 were detected in the nuclei of a significant number of atypical cells, while EBV-related latent membrane protein-1 was negative. EBER1 was also identified in the nuclei of non-neoplastic small lymphocytes at both biopsy and autopsy. Monoclonal integration of the EBV genome into the lymphoma cells was shown by Southern blot analysis. Clonal rearrangement of TCR was undetectable. Roles of chronic active EBV infection in the development of NK cell-type malignancy resembling malignant histiocytosis are discussed.
 ...
PMID:Epstein-Barr virus (EBV)-induced CD30+ natural killer cell-type malignancy resembling malignant histiocytosis: malignant transformation in chronic active EBV infection associating hypogammaglobulinemia. 921 26

It is well known that cytomegalovirus infection is often accompanied by hepatitis, but there have been few comparative studies with respect to clinical features of cytomegalovirus-associated hepatitis and other acute viral hepatitides. In the present study, clinical and pathological features of 11 acute sporadic cytomegalovirus hepatitis infections in previously healthy adults were compared with those of 45 acute sporadic viral hepatitis, including type A, type B and type C. As a result, the characteristics of cytomegalovirus hepatitis were a long-lasting fever, splenomegaly, atypical lymphocytosis, a mild transaminasemia, a low ratio of alanine aminotransferase level to lactate dehydrogenase level, and mild hepatic histopathological changes.
 ...
PMID:Clinical and histological features of cytomegalovirus hepatitis in previously healthy adults. 924 26

Administration of alpha-naphthylisothiocyanate (ANIT) to rats causes acute liver injury characterized in part by hepatocellular damage and marked neutrophil infiltration, effects that resemble drug-induced cholangiolitic hepatitis in people. ANIT-induced liver injury is neutrophil dependent. Moreover, ANIT can activate neutrophils in vitro. Since neutrophil-derived proteases can mediate hepatocellular killing, we hypothesized that ANIT stimulates neutrophils to release proteolytic enzymes that are cytotoxic to hepatic parenchymal cells. To test this hypothesis, neutrophils were isolated from Sprague-Dawley rats and incubated with ANIT for 6-24 h. ANIT (6-50 microM) was not toxic to neutrophils as indicated by the lack of lactate dehydrogenase release into the incubation medium. The conditioned medium from ANIT-treated neutrophils (ANCM) was collected, centrifuged, added to isolated hepatocytes, and incubated for 8, 16, or 24 h. Conditioned medium collected from neutrophils exposed to 25 or 50 microM ANIT for 16-24 h caused hepatocellular damage as indicated by the release of alanine aminotransferase into the culture medium. The concentration of ANIT in ANCM was nondetectable (0.5 microM). Analysis of ANCM indicated the presence of both cathepsin G and elastase activities. Inhibitors of these enzymes afforded protection against ANCM-induced hepatocellular injury. These results indicate that ANIT causes neutrophils to release toxic proteases which cause hepatocellular damage in vitro.
 ...
PMID:Alpha-naphthylisothiocyanate causes neutrophils to release factors that are cytotoxic to hepatocytes. 946 76

Influence of a new sorbent based on the AU-L lignin on the hepatic enzyme spectrum has been investigated in rats with experimental toxic hepatitis. The intact animals were in control group. There was a shift in lactate dehydrogenase (LDH) isoenzymic spectrum to the LDH5 side, glucose-6-phosphate dehydrogenase (G-6-PDH) activity increased to 144.7% against the control. Aspartate aminotransferase (AsT) activity reduced 2 times and alanine aminotransferase (ALT) activity enhanced 1.3 times, LDH2 activity increased 2.8 times in the liver of rats with toxic hepatitis which received sorbent for 7 days versus the untreated animals. The LDH4 and LDH5 fractions activity lowered to the level of the intact animals. G-6-PDH activity continued to increase, aminotransferase activity reduced up to the level less than control. The aerobic shifts in the LDH isoenzymic spectrum in which LDH4 and LDH5 fractions' activity completely returned to the control level evidence for glycolysis conversion to the aerobic type that apparently was promoted by positive effects of enterosorbent.
 ...
PMID:[Effect of enterosorption effects on hepatic enzyme spectrum in experimental toxic hepatitis]. 947 96

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40 degrees C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission: his serum glutamic oxaloacetic transaminase was 3.203 IU/ml, serum glutamic pyruvic transaminase was 3.825 IU/ml, lactic dehydrogenase was 2.840 IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19-day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody. HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. However, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.
 ...
PMID:[Acute renal failure in non-fulminant acute hepatitis without hepatitis A, B or C virus infection]. 951 78


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>