Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with human immunodeficiency virus type 1 (HIV-1) primarily involves a subgroup of T-lymphocytic cells, but other cell types are also invaded by the virus, including cell lines within the haematopoietic system. Together with infectious, inflammatory and neoplasic processes, invasion of haematopoietic tissue explains the haematological alterations which are seen during the course of infection with HIV-1. Anaemia develops in the large proportion of patients. Thrombocytopenia frequently occurs during the course of the disease, but may be seen in some patients already at the time of diagnosis, where the condition may be misdiagnosed as "idiopathic" thrombocytopenic purpura. Neutropenia is seen in all disease stages, but is most severe in patients with advanced disease. Bone marrow changes include varying degrees of dysplasia in one or more cell lines, which in some patients may mimic a myelodysplastic syndrome. The number of plasma cells is always increased. In many patients the bone marrow stroma exhibits an increased amount of reticular fibres. HIV-1 infection is associated with an increased risk of non-Hodgkin malignant lymphoma. Acute myelogenous leukaemia and myelomatosis have been described in patients with advanced disease. Treatment of the above mentioned haematological abnormalities aims primarily at reducing replication of HIV-1, thereby diminishing suppression of haematopoiesis by the virus infection, and at controlling the opportunistic infections during the course of the disease. Specific antiviral therapy (AZT) is most successful in correcting thrombocytopenia. The possibility of bone marrow suppression mediated by a toxic drug effect should always be considered in this patient group.
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PMID:[Hematological changes associated with human immunodeficiency virus (HIV-1) infection]. 831 70

Infection with HIV is associated with an increased risk of systemic and primary central nervous system non-Hodgkin's lymphoma. Patients with systemic non-Hodgkin's lymphoma usually present with high- or intermediate-grade histology and extranodal dissemination. Although the prognosis for such patients is poor, some patients clearly benefit from combination chemotherapy, and several new treatment approaches appear promising. Primary central nervous system lymphoma usually occurs in patients with more profound immunosuppression and is associated with a dismal prognosis. Selected patients with good performance status may benefit from therapy, particularly if opportunistic infections have been few and nondebilitating. Finally, Hodgkin's disease has been reported in patients with HIV infection, particularly in patients with a history of intravenous drug use, and it is more likely to present with advanced-stage disease and unfavorable histology.
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PMID:Treatment of AIDS-related lymphomas. 854 90

While uncommon, many musculoskeletal disorders may be seen in association with the acquired immune deficiency syndrome (AIDS). Infections such as osteomyelitis, bacterial myositis and septic arthritis, neoplasms such as non-Hodgkin lymphoma and Kaposi sarcoma, and myopathies and polymyositis have been reported in this patient population. Computed tomography and magnetic resonance imaging frequently detect unanticipated musculoskeletal disease in a patient with AIDS, and may further help to distinguish infections from neoplastic disorders.
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PMID:CT/MRI of musculoskeletal complications of AIDS. 854 41

Hodgkin's disease represents a phenotypically and genotypically heterogeneous lymphoma of CD30-positive tumour cells. Infection of the putative tumour cell population with Epstein-Barr virus (EBV) represents the most common genetic abnormality detectable in HD, yet the role of EBV in the pathogenesis of HD is only poorly understood. In virus-associated HD cases, monoclonal EBV genomes are detectable in all Hodgkin and Reed-Sternberg (HRS) cells, indicating that EBV infection takes place before expansion of the HRS cell population and, by implication, supporting the concept of a monoclonal origin of HRS cells. EBV infection does not define a distinct subgroup of HD but is detectable in different histotypes and in HRS cells expressing lymphocyte differentiation antigens of different cell lineages. Through the EBV-encoded protein, LMP1, the virus may superimpose an activated phenotype on genotypically immature lymphocytes. EBV-induced modulation of the cytokine expression pattern of HRS cells may contribute to the local inhibition of EBV-specific immunity observed in EBV-positive cases.
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PMID:The role of Epstein-Barr virus in the pathogenesis of Hodgkin's disease. 883 3

Hodgkin's disease (HD) represents a phenotypically and genotypically heterogeneous lymphoma of CD30-positive tumour cells. Infection of the tumour cells with Epstein-Barr virus (EBV) is found in significant proportions of cases with geographical variation and represents the most common genetic abnormality detectable in HD. If present, EBV is found in all tumour cells with an usually monoclonal composition of episomes, indicating that EBV infection occurs prior to clonal expansion of the tumour cells. Largely by the EBV-encoded protein LMP1, the virus may influence the expression of differentiation antigens and apoptosis. EBV-induced modulation of cytokine expression results in the activation of autocrine and paracrine regulatory loops and may contribute to the local inhibition of EBV-specific immunity observed in EBV-positive HD.
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PMID:Epstein-Barr virus in Hodgkin's disease. 894 2

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

AIDS-related small noncleaved cell lymphoma (AIDS-SNCCL) includes Burkitt's lymphoma (BL) and high-grade B-cell Burkitt-like lymphoma (BLL). Due to the marked polymorphism of AIDS-related non-Hodgkin's lymphomas (AIDS-NHL), the morphologic distinction between these two types of lymphomas is frequently controversial, although it may bear clinical relevance. Although the molecular features of AIDS-BL have been clarified to a certain extent, the genetic peculiarities of AIDS-BLL have not been investigated in detail. In this study we have compared morphologic and genetic features of AIDS-BL and AIDS-BLL in a blind coded fashion. Molecular studies were focused on the genetic lesions known to be implicated in AIDS-NHL, including alterations of c-MYC, BCL-6, p53, deletions of 6q, as well as infection by EBV and HHV-8. Alterations of c-MYC occurred in 10/10 AIDS-BL, whereas they were restricted to 2/10 AIDS-BLL (P < 0.01). Mutations of p53 were present in 5/10 AIDS-BL, whereas they were consistently absent among AIDS-BLL (n = 10; P < 0.05). Infection by EBV occurred in 30% of both AIDS-BL and AIDS-BLL. Rearrangements of BCL-6, deletions of 6q and infection by HHV-8 scored consistently negative in both AIDS-BL and AIDS-BLL. Based on the genetic lesions tested, the molecular profile of AIDS-BLL appears to be closer to that of AIDS-related diffuse large cell lymphoma (AIDS-DLCL) than to that of AIDS-BL. In contrast to AIDS-BLL however, AIDS-DLCL carried rearrangements of BCL-6 in a fraction of cases (2/9). This study, the largest of its kind reported so far, suggests that AIDS-BL and AIDS-BLL have a different molecular pathogenesis and that characterization of genetic lesions may help to distinguish between these two lymphomas.
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PMID:Genetic heterogeneity of AIDS-related small non-cleaved cell lymphoma. 933 31

Spinal cord compression is an infrequent event in patients with non-Hodgkin's lymphomas (NHL) and early diagnosis and therapy are required. The main clinical and histologic characteristics as well as the response to therapy in 10 NHL patients with spinal cord compression diagnosed at a single center in a 7-year period are referred. The main initial clinical manifestations were pain in dorsal or lumbar regions (5 cases) and paraparesia or paraplegia (5 patients). Infection by human immunodeficiency virus (HIV) was present in four cases. In 8 patients spinal cord compression was the initial manifestation of NHL. Pathologic diagnosis showed intermediate or high-grade lymphoma in 8 out of 10 cases and immunologic phenotype was B-cell in all cases. Laminectomy followed by radiation therapy and chemotherapy was performed in 4 cases, radiotherapy and chemotherapy in two, isolated chemotherapy in 3 and radiation therapy was administered to the remaining case. Complete response was observed in 4 cases and 6 cases were resistant to treatment. No patient with HIV infection responded to treatment. Six patients had died, median survival time for the whole series being 4 months, and the actuarial probability of survival was 40% at the first year.
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PMID:[Spinal cord compression in non-Hodgkin's lymphoma. A study of 10 patients]. 937 20

Infection of rhesus monkeys with SIV leads to AIDS-like symptoms. Similar to human AIDS patients, some monkeys develop B cell non-Hodgkin lymphoma (NHL). We determined transcription of cytokine genes regulating the activation of B and T cells, which play a role in intratumoral immune surveillance. Therefore, we compared the transcription of the cytokine genes encoding IL-2, IL-4, IL-6, IL-10, IFN-gamma, TNF-alpha, and TGF-beta1, and the Epstein-Barr virus-encoded BCRF 1 gene, in cells from five monkey and two human tumor specimens. The immune-suppressive IL-10 and TGF-beta1 genes were predominantly transcribed in all tumor specimens analyzed. Cytokine gene transcription patterns appeared to be similar in human and animal tumor cells. The transcription patterns corresponded to their histological classification as diffuse large-cell lymphoma according to the REAL classification and as immunoblastic or centroblastic tumors according to the Kiel classification. The determination of cytokine gene transcription pattern in the NHL may improve our understanding of pathogenesis and immune surveillance in this heterogeneous group of tumors. Our data show that SIV-associated NHLs of rhesus monkeys are comparable to human HIV-1-associated EBV-positive non-Hodgkin lymphoma.
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PMID:Cytokine gene transcription in simian immunodeficiency virus and human immunodeficiency virus-associated non-Hodgkin lymphomas. 943 Feb 51

Infection has long been suspected as a possible factor in the aetiology of leukaemia and lymphoma. If seasonal variation in the onset of disease could be shown in any of the diagnostic subgroups of leukaemia or lymphoma, this would provide supportive evidence of an aetiology linked to exposure to infection. All cases in the Manchester Children's Tumour Registry (aged 0-14 years at diagnosis) with acute lymphoblastic leukaemia (ALL), acute non-lymphocytic leukaemia (ANLL), Hodgkin's disease (HD) or non-Hodgkin lymphoma (NHL) between 1 January 1954 and 31 December 1996 were included in an analysis of seasonal variation in the month of first symptom and the month of diagnosis. Cases of common acute lymphoblastic leukaemia (c-ALL) diagnosed from 1979 onwards were also analysed separately. The groups considered for analysis were: all cases of ALL (n = 1070), ALL diagnosed between 18 and 95 months of age (n = 730), ALL diagnosed over 95 months of age (n = 266), c-ALL (n = 309), ANLL (n = 244), all infant acute leukaemias (ALL and ANLL under 18 months; n = 107), HD (n = 166) and NHL (n = 189). Using the Edwards method, both c-ALL and HD demonstrated significant seasonal variation (P = 0.037 and 0.001 respectively) in date of first symptom, with peaks occurring in November and December respectively. Using this method, no indication of seasonal variation was found in the other diagnostic groups for date of first symptom or in any of the diagnostic groups for date of diagnosis. For comparison with a previous study, a further analysis based on date of diagnosis for all ALL cases, using summer-winter ratios, showed a significant summer excess. These results provide supportive evidence for an infectious aetiology for c-ALL and HD, and possibly for all ALL, which warrants further investigation.
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PMID:Seasonal variations in the onset of childhood leukaemia and lymphoma. 966 61


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