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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper, we emphasize the uses of serum banks in cancer research. These include not only case/control studies but also prospective seroepidemiological studies in which the development of a serological marker, such as a viral antibody or viral antigen, can be correlated with the subsequent development of cancer in either an active surveillance program or the use of cancer registries or hospital records. Several different methods of application of the cohort technique are illustrated by studies of hepatitis B antigen and hepatocellular carcinoma and of Epstein-Barr virus in relation to African Burkitt's lymphoma, Hodgkin's lymphoma, and non-Hodgkin's lymphoma. Collections of sera done for one purpose can often be utilized for another purpose, if properly stored and documented. Two examples are tests for human T-cell leukemia virus, type 1, antibody from sera done for a health survey in Barbados approximately 8 years earlier and the use of data determined for a prospective study of the incidence of Epstein-Barr virus infection and infectious mononucleosis in West Point Cadets for psychological factors affecting the development of clinical illness among those infected. Archival materials, such as frozen tissues and paraffin sections, may also now be utilized for identifying genomes of potential oncogenic viruses by the polymerase chain reaction.
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PMID:The past is prologue: use of serum banks in cancer research. 139 73

The association of malignancies, such as non-Hodgkin's lymphoma and Kaposi's sarcoma, with human immunodeficiency virus infection has been recognized since the beginning of the epidemic. However, an increasing number of tumors not diagnostic of acquired immunodeficiency syndrome has been described in this setting. Taking into consideration that survival of patients with human immunodeficiency virus infection is increasing because of improvement of supportive care and better control of human immunodeficiency virus and related opportunistic infections, oncogenic viruses such as human papillomavirus, hepatitis B virus, Epstein-Barr virus, in a setting of prolonged immunosuppression could increase the risk of a variety of malignant tumors.
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PMID:Human immunodeficiency virus as a risk factor in miscellaneous cancers. 145 6

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

The long-term clinical course of patients with primary Type II essential mixed cryoglobulinaemia is unclear as many reports fail to separate this group from patients with Type III disease. We have reviewed 13 patients with Type II essential mixed cryoglobulinaemia who presented to the Hammersmith Hospital between 1976 and 1990. All patients had a cryoglobulin level greater than 0.1 mg/ml (range 0.27-6.50 mg/ml), and characterization of the cryoglobulin in all cases revealed the presence of a monoclonal IgM kappa component with rheumatoid factor activity together with polyclonal IgG. All patients had evidence of activation of the classical pathway of complement with greatly reduced levels of C4, while C3 levels were moderately reduced in three patients. All patients had skin disease and joint symptoms were reported by nine patients, with erosive arthritis in one. Eight patients had peripheral sensorimotor neuropathy. Renal disease was observed in 10 patients, manifesting as raised creatinine level, proteinuria or haematuria. Renal tissue was examined in eight patients: in six the appearances were those of a mesangiocapillary glomerulonephritis Type I while in the other two patients there was a mesangioproliferative glomerulonephritis, in one diffuse and in the other focal and segmental. Glomerular capillary 'hyaline thrombi' were found in six biopsies, extracapillary proliferation was found in three and evidence of vasculitis was found in all eight. Liver biopsy showed macronodular cirrhosis in one patient, while a second with recurrent episodes of jaundice showed only chronic inflammatory changes. No patient was positive for hepatitis B surface antigen; however one patient had low titre anti-hepatitis B surface antibody. Normochromic normocytic anaemia was present in nine patients. Bone marrow examination was carried out in 13 patients at presentation to our unit: 10 showed no evidence of a lymphoproliferative disorder, while three suggested the presence of a non-Hodgkin's lymphoma (some years after original presentation in all three). Unusual clinical features included one patient with retinal vasculitis and one patient with severe pulmonary haemorrhage.
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PMID:Type II essential mixed cryoglobulinaemia: presentation, treatment and outcome in 13 patients. 162 Aug 12

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

This review first considered some general problems in establishing causal links between a virus and a human cancer and offered some guidelines in the pursuit of this objective. Second, it reviewed the current causal associations for several candidate oncogenic viruses in relation to the tumors with which they are associated. These include Epstein-Barr virus in relation to Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease, and non-Hodgkin's lymphoma; hepatitis B and C viruses in relation to hepatocellular carcinoma; human T-cell leukemia/lymphoma virus type 1 and atypical leukemia/lymphoma; and human papilloma viruses in relation to cervical carcinoma. For some, the causal relationship is strong: hepatitis B virus with hepatocellular carcinoma, and human T-cell leukemia/lymphoma virus with adult T-cell leukemia/lymphoma. For one, the causal relationship is moderate: Epstein-Barr virus with African Burkitt's lymphoma. For others it is incomplete or inconclusive: Epstein-Barr virus with Hodgkin's disease and non-Hodgkin's lymphoma, and hepatitis C virus with hepatocellular carcinoma. Current techniques do not permit an answer for some: human papilloma virus with cervical carcinoma.
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PMID:Viruses and cancer. Causal associations. 166 91

A total of 92 patients with previously untreated intermediate- or high-grade non-Hodgkin's lymphoma attending the University Department of Medicine, Queen Mary Hospital, Hong Kong, were treated with the m-BACOD chemotherapy regimen (methotrexate, bleomycin, doxorubicin, cyclophosphamide, vincristine and dexamethasone). Additional involved-field radiotherapy was given to 32 (35%) patients. Myelosuppression was the major toxicity, and 5 (5%) treatment-related deaths occurred due to pneumonia, bleomycin sensitivity, doxorubicin cardiotoxicity and reactivation of hepatitis B infection. The overall complete response (CR) rate was 65/92 (71%) and the relapse rate was 22/65 (34%). The disease-free survival of the 65 CR patients at 2 years was 52% and the overall survival of all 92 patients at 3 years was 56%. The CR rate of stage I and II patients was significantly better than that of those with stage III and IV disease (87% vs 59%; P = 0.01), and the CR rate of stage III patients was superior to that of those with stage IV disease (86% vs 50%; P = 0.05). The overall survival of stage III and IV patients was significantly worse than that of subjects with stage I and II disease (31% vs 73%; P = 0.02). Multivariate analysis revealed that the independent prognostic variables significantly determining the CR rate and survival included the clinical stage and the serum lactate dehydrogenase level. From this study, the results of treatment with the m-BACOD regimen in patients with advance disease appeared to be similar to those obtained using the conventional CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone).
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PMID:m-BACOD chemotherapy for intermediate- and high-grade non-Hodgkin's lymphoma. 171 34

Four Chinese patients with non-Hodgkin's lymphoma and asymptomatic chronic hepatitis B infection developed fulminant hepatitis three to four weeks after two to five courses of chemotherapy. One was initially positive for hepatitis B e antigen and three were positive for antibody to HBeAg. They had normal initial serum aminotransferase levels. In all four patients, the hepatic illness appeared to be caused by reactivation of hepatitis B virus replication as evidenced by the appearance of HBV DNA in serum at the onset of hepatitis, seroreversion from anti-HBe to HBeAg positivity, and the absence of other incriminating drugs or viral markers. All died within three weeks after the onset of jaundice. Serum HBV DNA level dropped to undetectable level as the hepatitis progressed. We postulate that potent cytotoxic therapy reactivated HBV replication and permitted widespread infection of hepatocytes. Upon withdrawal of chemotherapy, the immunologic rebound resulted in rapid destruction of infected hepatocytes and massive liver necrosis. Several methods for the prevention of such hepatic reactivation are discussed.
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PMID:Fatal reactivation of chronic hepatitis B virus infection following withdrawal of chemotherapy in lymphoma patients. 262 23

This report describes a case of primary non-Hodgkin's lymphoma occurring in the liver of an 11-year-old boy. Preoperative imaging established a large mass confined to the right lobe of the liver; complete removal was effected by right hepatic lobectomy. At presentation, there was serological evidence of active hepatitis B infection, which was confirmed histologically in the nonneoplastic portion of resected liver. The right lobe of liver was virtually replaced by a multinodular tumor mass that histologically resembled small-cell lymphoma. No evidence of either a B- or T-cell lineage could be established by immunophenotyping. However, immunohistochemical staining for panleukocyte markers demonstrated membrane staining. Gene rearrangement studies were not available. The patient remains well with no evidence of disease 2 1/2 years after surgery.
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PMID:Undifferentiated primary hepatic non-Hodgkin's lymphoma in childhood. 297 Aug 9

Fifty children with malignant diseases were vaccinated against hepatitis B. Twenty-nine children suffered from leukaemia or non-Hodgkin's lymphoma; 14 of these were on intensive chemotherapy (group I) and 15 were without intensive therapy (group II). The other 21 children had various forms of solid tumours, 14 of them were on intensive therapy (group III) and 7 were without intensive therapy (group IV). To evaluate the immune response, we determined antibody titres over a period of more than 14 weeks after the first vaccination. As 22 out of 50 patients had received passive immunisation together with either the first or the first and second vaccination, antibody titres at the 14th and 18th week (i.e. more than 10 weeks after passive immunisation) were used to evaluate the vaccination results. An antibody titre of greater than or equal to 10 mIU/ml was considered to be a positive response. All patients of group IV, but only 4 out of 14 in group III, 4 out of 15 in group II, and 0 out of 14 in group I produced antibody titres higher than 50 mIU/ml. In contrast to the full response in group IV, two-thirds of all other patients had no immune response (less than 10 mIU/ml). Based on our experience we recommend vaccinating patients suffering from solid tumours and receiving no intensive therapy (group IV) against hepatitis B and protecting all the other children with malignant diseases by passive immunisation, if necessary.
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PMID:Hepatitis B vaccination and immune response in children with malignant diseases. 404 27


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