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

The incidence and morbidity of viral and Toxoplasma gondii infections were studied in 40 children who underwent liver transplantation between December 1983 and February 1988. The incidence of primary and reactivated cytomegalovirus (CMV) infection was 19% and 47%, respectively; primary infection caused clinical disease in all five cases affected and was fatal in one. Primary Epstein-Barr virus (EBV) infection occurred in 10 (26%) recipients but caused only mild disease. No reactivated EBV infection was recorded and no lymphoproliferative disorders associated with EBV were found after a maximum of four years' follow up. Adenovirus infection occurred in seven (18%) patients; this was associated in one case with fatal pneumonia and fulminant hepatitis, but otherwise with only mild respiratory disease. Primary T gondii infection was detected in one patient who remained asymptomatic. Other viruses causing infection included herpes simplex, varicella zoster, and respiratory syncytial virus. Surveillance for these infections and the long term sequelae should be included in the follow up of all children who undergo transplantation.
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PMID:Viral and toxoplasma gondii infections in children after liver transplantation. 215 47

HBsAg positive sera of 70 patients with lymphoproliferative disorders were tested for hepatitis Be antigen (HBEAg) and antibodies to hepatitis B virus serum immunoglobulins: IgG, IgM and IgA were measured systematically in the whole group before and after acquisition of HBV infection. Sera of 37 patients with neoplastic disorders and of control group were also tested for antibodies to rubella virus (LRV). HBeAg was found in serum of 2 asymptomatic carriers of HBsAg, anti-HBs in serum of 2/70 patients who eliminated HBsAg from their serum within 3 months, anti-HBc were found in serum samples of all transient or persistent HBsAg positive patients. Substantial rise of IgG concentration was determined in the whole infected group irrespective of the clinical course. The percentage of patients without anti-RV was lower in HBsAg positive than in HBsAg negative patients. The differences in reactions to RV between cancer patients and control group were not significant. General impairment of humoral immunity or more specific defects are discussed as factors determining relative or absolute deficiency of anti-HBs and persistence of HBsAg in patients with lymphoproliferative disorders.
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PMID:Immunological aspects of HBs antigenemia in patients with hematological malignancies. 647 66

Epstein-Barr virus is a ubiquitous virus associated with a variety of different diseases and disorders. The manifestations of Epstein-Barr virus-associated diseases or disorders within the liver, which involve a broad spectrum of histologic and clinical features, ranging from hepatitis through lymphoproliferative disorders to lymphoma, are presented. An important aspect of Epstein-Barr virus expression and infection is the biology of the Epstein-Barr virus. Documentation of infection can be performed using serology to detect the interaction of Epstein-Barr virus with the immune system, and the detection of EBV proteins and use of molecular biologic techniques to identify the presence of EBV RNA, and DNA sequences. Of particular utility are in situ hybridization, Southern blot analysis, and polymerase chain reaction as diagnostic methods to identify specific RNA or DNA sequences. Epstein-Barr virus-associated diseases and disorders including infectious mononucleosis, sporadic fatal infectious mononucleosis, X-linked proliferative disorder (Duncan's disease), post-transplant lymphoproliferative disorders, lymphoma, and AIDS are discussed. The histopathologic findings present in liver associated with each disease are presented with illustrative examples. Handling the tissue and interaction with clinical services are also discussed as a method for appropriate diagnosis of Epstein-Barr virus-driven processes affecting the liver.
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PMID:Manifestations of Epstein-Barr virus-associated disorders in liver. 817 24

Epstein-Barr virus (EBV) infection may complicate orthotopic liver transplantation, and can lead to hepatitis with subsequent graft failure and to benign and malignant lymphoproliferative disorders. Early diagnosis allows for prevention or treatment of complications. Histopathologic features of EBV infection in the liver vary and may be difficult to recognize. To delineate the morphologic features that allow for recognition we studied 61 biopsy specimens from 37 patients, correlating the results of EBV-DNA demonstration after polymerase chain reaction with histopathology of formalin-fixed, hematoxylin-eosin-stained liver biopsy specimens. DNA was extracted from fresh liver biopsy samples, and polymerase chain reaction was carried out with EBV primers (capsid protein gp220) using standard techniques and 25-cycle amplification. Epstein-Barr virus-related sequences after polymerase chain reaction were detected by DNA blot assay. Histopathologic features were classified into three categories on the basis of the semiobjective determination of the number and distribution of immunoblasts and other immature lymphocytes in portal tracts and sinusoids: highly suggestive (three biopsy specimens), indeterminant (one biopsy specimen), and negative (57 biopsy specimens). Only the three highly suggestive biopsy specimens had high levels of EBV-DNA. We conclude that the histopathologic features of EBV infection after orthotopic liver transplantation can be relied on to establish the diagnosis.
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PMID:Epstein-Barr virus infection in liver transplantation patients: correlation of histopathology and semiquantitative Epstein-Barr virus-DNA recovery using polymerase chain reaction. 827 78

Review of liver biopsy or autopsy material from 33 patients with severe combined immunodeficiency or combined immunodeficiency and four patients with DiGeorge syndrome revealed a wide range of hepatic pathology. The most common abnormality was graft-versus-host disease (16 patients), followed by viral infection (4 patients had adenovirus hepatitis, 3 had cytomegalovirus hepatitis). Centrilobular fibrosis with or without veno-occlusive disease was seen in five patients. Three patients had nonspecific hepatitis, four had changes attributed to total parenteral nutrition, and two had lymphoproliferative disorders involving the liver. Both patients with lymphoproliferative disorders had received transplants. Two patients had resolving necrosis probably secondary to non-A, non-B hepatitis. One had atypical mycobacterial infection. Hemosiderosis was a common nonspecific abnormality, seen in nine patients. All patients with hepatic graft-versus-host disease had received transplants or nonirradiated blood products. Hepatic graft-versus-host disease varied in severity from hepatic necrosis with destruction of both large and small bile ducts in a transfusion-associated case to subtle damage to interlobular bile ducts. Even minimal bile duct changes correlated with the clinical impression of graft-versus-host disease in these patients. Late chronic graft-versus-host disease was not seen in any patient, although acute graft-versus-host disease sometimes occurred late after transplant.
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PMID:Pathology of the liver in severe combined immunodeficiency and DiGeorge syndrome. 837 33

Over the past 30 years, liver transplantation has evolved from an experimental therapy to a routine procedure and most pathology textbooks have now a section dedicated to the pathology of liver transplant. Although there remain problems of biopsy interpretation due to the numerous post-transplant complications which can occur singly or in association, the major changes have been well characterized and are reviewed here, a particular attention being given to those features which are unique to or distinctive of the liver allograft. These include the outcome of donor fatty liver, reperfusion damage, massive haemorrhagic necrosis and the patterns of rejections, in particular the rarity and delayed onset of hyperacute rejection and the selective involvement of the small interlobular bile ducts and vascular endothelia in both acute and chronic graft rejection. "Functional" cholestasis with hepatocyte ballooning, cholangiolar cholestasis associated with sepsis and lesions of the larger bile ducts which may result from preservation, immune and/or ischaemic injury and closely resemble the changes observed in primary sclerosing cholangitis are also considered. Later in the post-transplant course, changes due to de novo or recurrent hepatitis have to be distinguished from those of late cellular rejection, protracted biliary complications, lymphoproliferative disorders, disease recurrence, in particular autoimmune chronic hepatitis, primary biliary cirrhosis and sclerosing cholangitis, differential diagnoses which often require interpretation of allograft changes in conjunction with all laboratory and clinical data available.
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PMID:Pathology and biopsy diagnosis of the transplanted liver. 860 Jun 91

Epstein-Barr virus is an ubiquitous member of the human herpes virus family. A specific antigen structure of the Epstein-Barr virus was discovered in the last decade. It was possible to diagnose some unusual clinical manifestations of EBV infections and its clinical course by different serologic analyses (immunofluorescent tests, immunoenzyme assay and polymerase chain reaction). This is very important in cases of atypical primary infections (hepatitis, meningoencephalitis), chronic mononucleosis and lymphoproliferative disorders and nasopharyngeal carcinoma. Famciclovir, a new antiviral agent (peroral form of penciclovir) may play an important role in the therapy of these infections.
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PMID:[New findings on the etiopathogenesis and clinical manifestations of Epstein-Barr virus infections]. 869 94

Hepatitis C virus has been proven to be the major cause of NANB hepatitis, cirrhosis and hepatocellular carcinoma worldwide. Based on the genome similarities between HCV and flavivirus or pestivirus, this agent has been included within the family Flaviviridae as a separate genus. Among the analogies between HCV and the other members of the same family there is the possibility of infecting blood cells. In particular, significant evidence obtained through studies performed in vivo and in vitro support the concept that HCV is not only a hepatotropic but also a lymphotropic virus. This suggests that, in addition to playing a role in inducing hepatic diseases (both of a non-tumoral and a neoplastic nature), HCV infection may also play a role in extrahepatic pathologies. The striking association observed between HCV infection and some autoimmune-lymphoproliferative disorders of either benign or neoplastic nature is consistent with this hypothesis. However, in analogy with what has been observed in the case of liver disease, the mechanisms involved in the pathogenesis of HCV-related extra-hepatic manifestations have to be more deeply analysed and clarified.
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PMID:Hepatitis C virus as a lymphotropic agent: evidence and pathogenetic implications. 873 Apr 74

Infection with hepatitis C virus (HCV) may affect not only the liver but also various nonhepatic tissues and organs and may combine with many etiologically unrelated diseases and morbid conditions. Numerous nonhepatic manifestations in HCV infection have been previously reported. For some (eg, cryoglobulinemia), the association is well established. For others, such as sialadenitis and lichen planus, the association is probable (but not completely documented) and, for the remainder, the associations are weak. Extrahepatic manifestations may result from immunological mechanisms as well as virus invasion and replication in the affected extrahepatic tissues and organs. Thyroid abnormalities, primarily Hashimoto's disease, and isolated increases of anti-thyroid antibodies (ATPO) appear to be more frequent in chronic hepatitis C than B or D, with high ATPO titers clustering mainly among females. Interferon-alpha (IFN-alpha) therapy is associated with development of thyroid dysfunction in 5.5-12.9% of patients, usually exposing preexisting subclinical thyroid abnormalities. Mixed cryoglobulinemia (MC) is commonly found (36-45%) in patients with chronic HCV infection; however, only in a minority of cases does it become clinically manifested as systemic vasculitis with purpura, neuropathy, or Raynaud's phenomenon. In a number of patients, MC may terminate in non-Hodgkin's B-cell lymphoma. Treatment of these lymphoproliferative disorders with IFN-alpha is advocated. Idiopathic thrombocytopenia is now recognized more frequently in association with chronic HCV infection and is usually aggravated by IFN-alpha therapy. Patients with porphyria cutanea tarda (PCT) have demonstrated serological markers of HCV infection in 62-82% of cases. The usefulness of IFN-alpha in PCT remains to be demonstrated. Lichen planus has also been found in association with chronic HCV infection, particularly when severe or affecting the oral cavity. Other nonhepatic manifestations have also been reported in HCV infection such as diabetes, corneal ulceration, uveitis, and sialadenitis. These manifestations deserve further study and documentation. Finally, markers of autoimmunity occur with high frequency in chronic HCV infection; however, combination with the classical syndrome of autoimmune hepatitis is rare. In the presence of various autoantibodies, the clinical features of chronic hepatitis C do not appear to be modified and, contrary to general perception, IFN-alpha therapy within randomized controlled trials should not be withheld since the response rate to IFN-alpha does not appear to differ in the presence or absence of low titers of these markers.
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PMID:Nonhepatic manifestations and combined diseases in HCV infection. 901 79

Fifty one patients with acute lymphoblastic leukaemia (ALL) and non-Hodgkins lymphoma (NHL) undergoing chemotherapy were studied prospectively to determine the incidence, aetiology and natural course of hepatitis. Of 51 patients (31 NHL and 20 ALL), 22 developed hepatitis. Hepatitis B (IgM anti HBc positive) was the cause in 11 patients (50%), hepatitis C in 4 patients, and septicaemia and cytotoxic drugs in 3 patients each. Malignant infiltration of the liver was the cause in the remaining 1 patient. Hepatitis was predominantly (75%) anicteric. Mean duration of hepatitis was 21 days. Of 51 patients, 21 acquired hepatitis B and/or C virus infection. They had received 6.4 (+/- 3.4) units of packed red cells and 5.3 (+/- 11) units of platelet concentrate as compared to 3.4 (+/- 4.8) units of red cells and 5.3 (+/- 12.1) units of platelet concentrate received by those who did not acquire virus infection (P < 0.05 for packed red cells). Only transient stoppage of chemotherapy was necessary following development of hepatitis and most of the patients who developed hepatitis could complete their chemotherapy schedule. None of the patients who developed viral B or C infection cleared the infection. We conclude that there was a high incidence of hepatitis B and C infection amongst patients with lymphoproliferative disorders with an increased carrier rate. Transfusion was a major risk factor for such infections.
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PMID:A prospective study on the incidence of hepatitis B & C infections amongst patients with lymphoproliferative disorders. 954 Feb 81


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