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

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

Three hepatitis B virus carriers who were HB(e)Ag negative and having normal liver function developed fulminant hepatitis with evidence of HBV replication following intensive chemotherapy for non-Hodgkin's lymphoma. Each was continuously negative for HB(e)Ag. Analysis of the precore region of HBV isolated from each demonstrated that the HBV of each had a point mutation in the precore region that inhibited the synthesis and the release of hepatitis B(e) antigen. This observation suggests that all HB carriers receiving either immunosuppressive or cytotoxic therapy should be monitored closely even if standard assays suggest that viral replication is not present. Sudden enhanced replication of a HBV mutant as a result of such therapy can be a cause of either very severe hepatitis or occasionally fulminant hepatitis.
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PMID:Reactivation of precore mutant hepatitis B virus leading to fulminant hepatic failure following cytotoxic treatment. 149 51

Nodular regenerative hyperplasia (NRH) is a rare lesion of the liver associated with portal hypertension in more than half of patients. We present two cases demonstrating complications and diagnostic problems of NRH and review the pathogenesis, clinical, radiologic, and pathologic features of 240 cases in the literature. Patient 1 died from variceal bleeding as a complication of NRH. Patient 2 presented with ascites. Sonographic, computed-tomographic and magnetic resonance findings did not differ from liver cirrhosis. Three needle biopsies showed nonspecific reactive hepatitis. Wedge liver biopsy provided the correct diagnosis of NRH and a shunt operation was performed. Non-Hodgkin's lymphoma (centroblastic type) was diagnosed three years after NRH. At present there is no clinical or radiologic evidence of progression of NRH in this patient. The diagnosis of NRH cannot be made without histologic examination. Correct diagnosis is difficult in percutaneous needle biopsy. Therefore, laparoscopically guided liver biopsy or wedge biopsy is often necessary for diagnosis. NRH should be included in the differential diagnosis of portal hypertension. Portal diversion can be considered.
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PMID:Diagnostic problems in nodular regenerative hyperplasia (nodular transformation) of the liver. Review of the literature and report of two cases. 159 15

Giant-cell hepatitis is a frequent pattern of liver injury in the neonate, but it is rare after infancy. Such cases have been attributed to autoimmune disease, to non-A, non-B hepatitis and, most recently, to paramyxovirus infection. To better define the entity of postinfantile (syncytial) giant-cell hepatitis, we reviewed 24 biopsy specimens from 20 patients with this finding, either alone or in combination with other diagnoses. The number of multinucleated giant cells varied greatly from one specimen to another. Varying degrees of portal inflammation appeared in all but one of the patients, and all had hepatitislike acinar inflammation associated with hepatocellular injury. Fibrosis was a common finding, varying from mild periportal fibrosis to established cirrhosis (33%). The changes were interpreted as acute giant-cell hepatitis in 25%, as CAH in 42% and as active cirrhosis in the remainder. The patients ranged in age from 2 to 80 yr, with a mean of 35 yr and a male/female ratio of approximately 1:1. The signs and symptoms of liver disease were present for more than 1 mo in most patients. A positive antinuclear antibody titer was found in seven of the patients. Three patients had a direct Coombs reaction and anemia. Overall, evidence of autoimmune disease was found in 40% of the patients. One patient had non-Hodgkin's lymphoma involving the liver. Only one patient had a history of blood transfusion or risk factors for hepatitis C. No patient underwent serological study for paramyxovirus antibodies. Liver tissue from one patient was examined ultrastructurally, but no viral particles could be identified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postinfantile giant-cell transformation in hepatitis. 163 41

A case is described of an HIV+ man who was successfully treated for Hodgkin's lymphoma, but who later developed non-Hodgkin's lymphoma 3 years later when his immune system became suppressed. The patient was 22 years old when he presented with fever, asthenia, weight loss, and cervical lymphadenopathy. With Hodgkin's lymphoma he also had positive serology for HIV and hepatitis B. He was treated with alternate courses of MOPP and ABVD chemotherapy. In 1990 he again appeared with high fever, progressive cervical, axillary and inguinal lymphadenopathy, with hilar and mediastinal lymph node enlargement on x-ray. CD4 lymphocytes were 577/cubic mm, and the CD4/CD8 ratio was 0.57 (normal 1.8). His cervical lymph node biopsy was classified as non-B non-T large-cell anaplastic lymphoma which was EBV-positive. A Western Blot was positive for small amounts of p24 and p18 antigens. The man was treated with MACOP-B chemotherapy, with some results, but died of sepsis 6 weeks later. The relationships between Hodgkins and non-Hodgkin's lymphoma, the timing of the neoplasm in the course of HIV infection, and the possible re-activation of hepatitis virus were discussed.
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PMID:Non-Hodgkin's lymphoma after prolonged remission of Hodgkin's disease in an HIV-infected patient. 166 42

A pathogenetic relationship is postulated for the development of membranoproliferative glomerulonephritis type I in non-Hodgkin's lymphoma (B-cell lymphoma of low-grade malignancy) and myeloproliferative syndrome, which we have observed in eight patients. This hypothesis is supported by the fact that chronic lymphatic leukaemia and immunocytoma are often associated with immunodysregulative phenomena, and by the immunohistological and ultrastructural findings in the kidney, especially the frequent electron-microscopic finding of cryoglobulins, which results in the membranoproliferative type of immune-complex glomerulonephritis, an expression of a disturbance in immune balance. The pathogenetic mechanism may involve cryoglobulins themselves as immune complexes; it is also possible that monoclonal cryoglobulins combine with an antigen to form immune complexes or lead to in situ formation of immune complexes. In addition, other immune complexes, for example with endogenous tumour-associated antigens and exogenous antigens (e.g. hepatitis antigens), may be involved in the pathogenesis.
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PMID:[Membranoproliferative glomerulonephritis in non-Hodgkin's lymphoma nad myeloproliferative syndrome--a causal relationship?]. 172 39

Between March 1985 and December 1989, 86 patients underwent heart (80) or heart-lung (6) transplantation. Thirty-seven (43%) developed one or more significant gastrointestinal problems. Dyspepsia and gallbladder disease were common, but easily managed. Cytomegalovirus disease occurred in 25 patients (29%) and required aggressive investigation and early therapy with ganciclovir; all patients so treated responded satisfactorily. Features of acute peritonitis were seen in 6 patients and required exploratory laparotomy in 4. Non-Hodgkin's lymphoma of the stomach in one patient has regressed following a combination of reduction in immunosuppressive therapy and a course of chemotherapy. The development of hepatitis or severe liver dysfunction of unknown cause has been associated with significant morbidity and mortality. Since this study was undertaken, the incidence of gastrointestinal complications has been greatly reduced by modifications to our immunosuppressive and anti-infection prophylactic drug protocols. Nevertheless, such complications still occur and it is important that the gastroenterologist should understand the need for urgent and intensive investigation and therapy.
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PMID:The gastrointestinal management of patients undergoing heart transplantation. 175 34

Patients with the acquired immune deficiency syndrome (AIDS) frequently develop hepatic dysfunction. Although hepatic injury may indirectly result from malnutrition, hypotension, administered medications, sepsis, or other conditions, the hepatic injury is frequently due to opportunistic hepatic infection, directly related to AIDS. Infection with Mycobacterium avium intracellulare typically occurs in patients with advanced immunocompromise and with systemic symptoms due to widely disseminated infection. In contrast, hepatic tuberculosis often occurs with less advanced immunocompromise. Cytomegaloviral infection may produce a hepatitis. Cytomegaloviral and cryptosporidial infections have been implicated as causes of acalculous cholecystitis and of a secondary sclerosing cholangitis. About 10-20% of patients with AIDS have chronic hepatitis B infection. These patients tend to develop minimal hepatic inflammation and necrosis. The clinical findings in patients with hepatic cryptococcal infection are usually due to concomitant extrahepatic infection. Hepatic histoplasmosis usually develops as part of a widely disseminated infection with systemic symptoms. Hepatic involvement by Kaposi's sarcoma is rarely documented ante mortem because an unguided liver biopsy is an insensitive diagnostic procedure. Patients with non-Hodgkin's lymphoma of the liver typically have lymphadenopathy, hepatomegaly, and systemic symptoms. As a pragmatic approach, patients with liver dysfunction and HIV-related disease should have a sonographic or computerized tomographic examination of the liver. Patients with dilated bile ducts should undergo endoscopic retrograde cholangiopancreatography because opportunistic infection may produce biliary obstruction. Patients with a focal hepatic lesion should be considered for a guided liver biopsy. Patients with a significantly elevated serum alkaline phosphatase level should be considered for a percutaneous liver biopsy. When performed for these indications, liver biopsy will demonstrate a significant disease involving the liver in about 50% of patients with AIDS and in about 25% of patients who are HIV seropositive but who are not known to have AIDS. The clinical impact of a diagnostic biopsy is blunted by a lack of efficacious therapy for many opportunistic infections.
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PMID:Hepatobiliary manifestations of the acquired immune deficiency syndrome. 198 33

A 34-year-old patient was transplanted from an HLA-identical sister for high grade non-Hodgkin's lymphoma in first complete remission. One month post-transplant, he developed hepatitis and haemorrhagic cystitis. He died 2 months post-transplant from fulminant hepatic failure. Adenovirus type 5 was cultured from urine, and characteristic adenovirus inclusions were seen in the liver. Striking paracrystalline arrays of adenoviruses were seen in the liver on electron microscopy. Reactivation of adenovirus infection is increasingly recognized post-BMT, but this complication of type 5 infection is unusual, and we describe in detail this second reported case.
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PMID:Fulminant hepatic necrosis caused by adenovirus type 5 following bone marrow transplantation. 216 93

Fourteen patients with T-cell-derived leukemia and lymphoma underwent high-dose chemoradiotherapy and anti-T-cell monoclonal antibody-treated autologous bone marrow transplantation (ABMT). All patients were either in sensitive relapse or had adverse prognostic features, and five patients had a history of bone marrow involvement with disease. Patients received a median of 2 (1 to 3) prior chemotherapy regimens; 10 patients received local radiotherapy. After high-dose ablative therapy, greater than 500/mm3 granulocytes and greater than 20,000 untransfused platelets/mm3 were noted at a median of 23 (13 to 48) and 26 (15 to 43) days post-ABMT, respectively. Natural killer (NK) cells, T cells (predominantly T8+), and monocytes were noted within the first 1 to 2 months post-AMBT, as seen in other series. Disease-free survival was a median of 10.1 months, 5.9 months for patients with T acute lymphoblastic leukemia or lymphoblastic lymphoma and 25.6 months for patients with T non-Hodgkin's lymphoma (NHL). Toxicities were common and severe. Thirty-six percent of patients developed bacteremias early post-BMT. Late complications included a skin rash consistent with graft versus host disease; infections with Herpes zoster, hepatitis, and Pneumocystis carinii; and the development of Epstein-Barr virus associated lymphoproliferative syndrome. Our findings suggest that patients who have undergone T-depleted ABMT have a profound immunodeficiency not reflected in the phenotypic reconstitution of the T and NK cells. Characterization of the functional deficiency may facilitate the development of methods to reduce the long-term toxicity of AMBT in these patients.
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PMID:T-cell-depleted autologous bone marrow transplantation therapy: analysis of immune deficiency and late complications. 219 91


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