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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis C virus (HCV) is the main cause of parenteral non-A, non-B hepatitis and serum can be tested for the virus itself by reverse-transcription polymerase chain amplification. What of the level of this viraemia? To find out if quantitative study of HCV RNA might be useful clinically we took advantage of participation in trials of interferon-alpha in patients with chronic HCV infection and applied a new assay, branched DNA (bDNA) signal amplification. Paired serum and liver biopsy specimens from 47 patients with confirmed chronic HCV infection and evidence of HCV RNA in their serum were studied. The quantitative bDNA assay (detection limit 350,000 equivalents/mL [eq/mL]) was positive in 34 sera (sensitivity 72%). Patients who acquired HCV infection by blood transfusion had a higher viraemia (median 2,701,000 eq/mL, n = 29) than health workers and intravenous drug users (635,000 eq/mL, n = 13; p < 0.01). Patients with a sustained complete response to interferon-alpha therapy had lower pre-treatment viraemia levels (median at bDNA cut-off, n = 11) than complete responders who relapsed after the drug was stopped (1,613,000 eq/mL, n = 15; p < 0.01) and non-responders (3,066,000 eq/mL, n = 20; p < 0.01). High viraemia levels were not related to the histological diagnosis but were associated with lobular inflammation, lymphoid aggregates, and bile-duct lesions. These findings indicate that mode of acquisition is an important determinant of HCV viraemia and that patients with low HCV viraemia levels are more likely to respond to interferon in a sustained fashion.
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PMID:Significance of serum hepatitis C virus RNA levels in chronic hepatitis C. 810 50

We reviewed the clinical records of 140 consecutively evaluated patients with chronic hepatitis C infection. One hundred twenty-four patients (89%) contracted infection through blood transfusion or intravenous drug use. The liver biopsy specimens of 83 patients (43 blood transfusion cases and 40 intravenous drug abuse cases) were examined without knowledge of the mode of disease transmission. The mean histological activity index score was significantly higher in the blood transfusion group (10.2 +/- 4.2) than in the intravenous drug use group (6.9 +/- 4.5) (p = 0.001). The transfusion group had more periportal bridging necrosis (p = 0.0015) and fibrosis (p = 0.0016) than did the intravenous drug use group, whereas significant differences between lobular degeneration and portal inflammation were not achieved across the two groups. The distribution of final biopsy interpretations also differed significantly between the two groups (p < 0.001), with chronic active hepatitis more frequent in the transfusion group. Moreover, lymphoid aggregates and bile duct damage were more common in patients with chronic hepatitis due to blood transfusion. Multivariate analysis showed that the mode of viral transmission was the most powerful predictor of histological activity index score when tested against patient gender, duration of disease or age at biopsy. One year after completion of this study, 9 of 70 transfused patients and 1 of 54 intravenous drug users had died of liver disease or are awaiting liver transplantation at this writing (p = 0.03). We conclude that transfusion-acquired hepatitis C is associated with more aggressive histological inflammatory activity than hepatitis resulting from intravenous drug use.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pathology of hepatitis C as a function of mode of transmission: blood transfusion vs. intravenous drug use. 824 58

A 29-year-old male patient presented with acute liver failure from non-A, non-B and non-C hepatitis, necessitating orthotopic liver transplantation. After operation he developed progressive pancytopenia on the basis of aplastic anemia, which was probably hepatitis associated. After therapy with GM-CSF had failed, he underwent allogeneic BMT from his HLA genotypically identical brother following a conditioning regimen of CY 50 mg/kg x 4 and 500 cGy total lymphoid irradiation. He engrafted promptly but transfusion dependency did not resolve until CMV viremia was treated with ganciclovir. The patient is alive and well 2 years after BMT.
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PMID:Successful allogeneic bone marrow transplantation in an adult with aplastic anemia following orthotopic liver transplantation for non-A, non-B, non-C hepatitis. 827 44

The oronasal median infectious doses of reovirus serotypes 1, 2, and 3 were established in infant and weanling Sencar mice on the basis of disease expression and seroconversion. Infant mice were susceptible to infection with low doses of all three serotypes, whereas weanling mice were comparatively resistant to infection. Uniform transmission of virus to cagemates or mothers of infants did not occur, indicating low contagiousness of all three virus serotypes. The comparative susceptibility of 2-day-old Sencar mice to disease was examined following oronasal inoculation with reovirus 1, 2, or 3. Tissues were collected on days 3, 5, 7, 9, 14, 16, and 21 after inoculation for virus isolation, histologic examination, and serologic analysis. Disease patterns in infant mice were distinctly different among reovirus serotypes. Reovirus 3 induced severe disease, with focal myocarditis, hepatitis, diffuse encephalitis, and generalized lymphoid depletion, whereas reovirus 1 induced a similar pattern, but much milder disease. In contrast, reovirus 2 induced mild transient enteritis without lesions in other organs. Sera from experimentally infected mice were tested in virus serotype-specific enzyme immunoassays. Cross reactivity of antibody among the three virus serotypes was found, but antibody titers were always highest with the homologous antigen. These studies confirm that infant laboratory mice are susceptible to infection with all three serotypes of virus; weanling mice are comparatively resistant to infection and disease; the viruses induce different patterns of disease in infant mice; and infecting virus serotypes can be distinguished serologically by enzyme immunoassay.
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PMID:Infectivity, disease patterns, and serologic profiles of reovirus serotypes 1, 2, and 3 in infant and weanling mice. 827 20

Liver biopsies from 63 patients with hepatitis C virus (HCV) infection have been studied. 31 were asymptomatic and had been detected by a variety of screening programs, and most of the other 32 had complained of vague symptoms only. In 57 patients a confident estimate of the duration of infection was able to be made (ranging from 12 months to over 38 years) and 73% of these had been infected for over 5 years. The most common histological pattern observed was a low-grade panacinar hepatitis. This affected 74.6% of all biopsies, and 43% of this group had been infected for over 10 years. Severe chronic active hepatitis and/or cirrhosis occurred in only 8% of the whole series, and in 16.7% of those infected for over 10 years. This incidence of serious sequelae in chronic HCV infection is much lower than previously reported, probably reflecting the methods of patient selection, and may represent more accurately the natural history of the disease in this community. The occurrence of a number of characteristic histological features (lymphoid follicles and aggregates, steatosis, Kupffer cell prominence, and apoptotic or acidophilic bodies) was confirmed, the constellation of which is highly suggestive of HCV infection. It is suggested that apoptosis may play an important role in the perpetuation of HCV as a chronic infection.
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PMID:Histological patterns of prolonged hepatitis C infection. 835 26

We produced hepatitis in guinea pigs by immunization with acetaldehyde adducts and ethanol treatment. Human hemoglobin-acetaldehyde adducts were prepared without any reducing agents and affinity purified with polyclonal antibodies against acetaldehyde adducts. Female guinea pigs were immunized with the adducts and were simultaneously given ethanol for 40 days. These treatments induced hepatic necrosis with infiltration of mononuclear cells in the hepatic lobules. The formation of the lymphoid follicle was also observed in severe cases. These changes were accompanied by the elevation of serum AST and lactic dehydrogenase activities and titers of circulating antibodies against acetaldehyde adducts. By contrast, the combination of ethanol and immunization with unmodified hemoglobin produced only fatty change of the liver, and animals immunized with the adducts alone had minimal inflammatory changes of the liver. Peripheral blood lymphocytes obtained from the animals with hepatitis were shown to be stimulated by acetaldehyde adducts to a significantly greater degree than those from control animals who received nothing, ethanol alone or ethanol and unmodified hemoglobin. These results suggest that the immune response to acetaldehyde adducts may be involved, at least partly, in the pathogenesis of inflammation observed in alcoholic liver disease.
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PMID:Experimental hepatitis induced by ethanol after immunization with acetaldehyde adducts. 842 34

Fourteen mares and their foals were attended at parturition. After mare-foal bonding, 8 colostrum-deprived (CD) foals were removed from their dams, deprived of colostrum, and provided with an alternative milk source for the first 24 h of life. The mares were milked out every 2-4 h during this period to remove colostrum, after which the CD foals were returned to their mares and allowed to nurse. Six colostrum-fed (CF) foals were allowed to suck colostrum in the normal manner. Foal serum IgG concentration was determined by single radial immunodiffusion (means, CD = 0 mg/dl; CF = 1,508 mg/dl). Accepted methods were used to minimise infections in the neonatal foals. Of the 8 CD foals, 7 demonstrated clinical signs of sepsis. Septicaemia was confirmed in 5 of the 7 septicaemic CD foals by ante-mortem blood culture or by culture of tissue at necropsy. Organisms isolated included: Actinobacillus equuli, Escherichia coli, undifferentiated coliforms, Pseudomonas spp., and Actinomyces pyogenes. Clinically ill foals were treated with antimicrobial drugs, intravenous fluid therapy, flunixin meglumine, and anti-endotoxin hyperimmune serum. Three septicaemic CD foals survived. Four of 7 septicaemic CD foals died or were destroyed. Post-mortem lesions included bacterial embolic pneumonia, glomerulonephritis/nephritis, lymphoid depletion/atrophy, splenic and lymphoid necrosis, hepatitis, septic arthritis, and systemic bacterial embolism. None of the CF foals became septicaemic. One CF foal had foal heat diarrhoea and 1 CF foal had a serum IgG concentration of 160 mg/dl (i.e. failure of passive transfer), but both foals were otherwise normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A prospective study of septicaemia in colostrum-deprived foals. 822 85

Hepatitis C virus (HCV) represents the major etiologic agent of non-A, non-B hepatitis. The pathological changes in hepatitis C are characterized by the histologic triad of lymphoid aggregates in portal tracts, epithelial damage of small bile ducts, and micro- and macro-vesicular steatosis. HCV antigens are demonstrable in the cytoplasm of infected hepatocytes by immunohistochemical staining with mono- or polyclonal antibodies, particularly when frozen tissues are employed. Detection of HCV RNA sequences in fixed liver tissues by in situ hybridization appears to be a more sensitive method than immunohistochemical staining. These studies are important to determine the viral load and expression pattern of HCV in the infected liver. The mechanism of hepatocyte and bile duct injury in HCV infection appears to be related to the host immune response to the virus, although direct viral cytopathogenicity may also pay a role.
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PMID:Pathobiology of hepatitis C. 860 Jun 81

Hepatitis C viral recurrence after orthotopic liver transplantation is almost universal. Hepatitis C induced graft failure may occur, but the clinical and histologic profiles are not well defined. The aim of this study was to describe the pattern of early graft failure in patients with recurrent hepatitis C after liver transplantation. Thirty patients with hepatitis C underwent liver transplantation from October 1989 through September 1994. Four patients were excluded because of death (2 patients), graft failure unrelated to hepatitis C (1 patient), and lost to follow-up (1 patient). Hepatitis C recurred in 24 of the 26 remaining patients. In 4 patients with hepatitis C virus recurrence and cholestasis, graft failure developed at 5.25, 11.0, 11.0, and 18.5 months. The medical records and liver biopsies were reviewed. In all 4 patients, a histologic pattern characterized by centrilobular ballooning degeneration developed and progressed to involve more than two-thirds of the lobules. Moderate to severe cholestasis and bridging fibrosis were present in all grafts at explant. Two patients had portal inflammation on 3-month biopsies consistent with viral hepatitis. All patients had mild macrovesicular steatosis, but only 1 patient had significant lymphoid aggregates. No patient had evidence of hepatic artery thrombosis. One patient had potential drug-induced cholestasis. One patient had 3 episodes of rejection that were not believed to contribute to graft loss. All 4 patients developed clinical features of hepatic failure and were retransplanted. Two patients had early recurrence of graft failure. We conclude that a pattern of progressive centrilobular ballooning degeneration, bridging fibrosis, and cholestasis occurs in some patients with hepatitis with early graft failure, similar to fibrosing cholestatic hepatitis seen in some transplant patients with recurrent hepatitis B.
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PMID:Clinical and histologic patterns of early graft failure due to recurrnet hepatitis C in four patients after liver transplantation. 860 70

The incidence and severity of recurrent hepatitis C virus (HCV) infection in liver transplant recipients vary widely, and the long-term sequelae of recurrent infection are not known. To better define the biology of recurrent HCV in liver transplant patients, we reviewed the histology of recurrent HCV in serial biopsies of 19 patients with pretransplant polymerase chain reaction (PCR) evidence of HCV infection. All posttransplant (post-TX) biopsies (n = 81) were reviewed, and RNA was extracted from at least one paraffin-embedded biopsy from each patient. RNA was analyzed for HCV by nested, reverse transcription-PCR (RT-PCR) using primers for the 5' non-coding region of HCV as well as for albumin (as an internal control). All post-TX biopsies tested (12-1,677 days post-TX) were positive for HCV RNA by RT-PCR, while normal control biopsies were negative. Fifteen of 19 patients developed recurrent chronic hepatitis typical of HCV. Many of these patients showed a progression from early biopsies with acute lobular hepatitis to later biopsies with chronic hepatitis with portal lymphoid aggregates. An acute lobular hepatitis typified by sinusoidal lymphocytosis, acidophil bodies, and lobular disarray was seen an average of 135 days post-TX, with a range of 39-279 days. The time post-TX between this and earlier non-hepatitis biopsies was significantly different (p < 0.0004, Student's t test). Chronic hepatitis with portal lymphoid aggregates was seen an average of 356 days post-TX, with a range of 89-1,365 days. The time post-TX was significantly longer than for acute lobular hepatitis (p < 0.03, Student's t test). Fifty-three percent of HCV TX patients progressed from acute lobular hepatitis to chronic hepatitis with lymphoid aggregates within 1 year of TX, and 79% showed these changes within 4 years. Six patients had progressive fibrosis; one die of liver failure and two became cirrhotic. Recurrent HCV appears to progress from an acute lobular hepatitis to chronic hepatitis with lymphoid aggregates in the majority of patients. Significant scarring occurred in 32% of patients and 16% developed end-stage liver disease from recurrent HCV. These later findings suggest that the long-term course of recurrent HCV in liver allografts may not be as indolent as first thought.
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PMID:Histologic progression of recurrent hepatitis C in liver transplant allografts. 865 53


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