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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of 600 cases of lymphadenopathy in which an initial histological diagnosis of Hodgkin's disease was reviewed in a reference laboratory this interpretation was confirmed in 317 cases (53%). In the 283 other cases the diagnosis of Hodgkin's disease was considered to be mistaken. The condition most frequently confused with Hodgkin's disease was chronic non-specific lymphadenitis. Reticulum cell sarcoma, metastatic tumours, infectious mononucleosis, dermatopathic lymphadenopathy, toxoplasmosis, and early sarcoidosis were also notably frequent among the conditions mistaken for Hodgkin's disease.
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PMID:Survey of the eventual diagnosis in 600 cases referred for a second histological opinion after an initial biopsy diagnosis of Hodgkin's disease. 488 Apr 13

The Epstein-Barr virus (EBV) has been consistently found to be associated with Hodgkin's disease (HD) in two ways: cases generally have elevated titer distributions of antibodies against the viral capsid antigen, and the occurrence of HD among persons with a history of EBV infectious mononucleosis is two or three times higher than expected. We evaluated this association by measuring the prevalence and level of antibodies against EBV and related viruses among 304 cases of HD interviewed in a population-based study in comparison to 285 of their siblings. The most significant finding was that antibody titers to the viral capsid antigen of EBV were elevated (greater than or equal to 1:320) in 39% of the cases and in only 14% of the sibling-controls; the relative risk adjusted for age and sex was 4.1. The geometric mean titer was three-fold higher among cases (175.6 vs. 58.1) Subjects who reported a history of IM had a higher distribution of titers than those who did not. Cases also had elevated titers against the early antigen of EBV - the D Component being most prominent. A significantly higher proportion of cases has elevated titers against CMV, relative risk = 3.4, but the prevalence of CMV antibody was relatively low and not consistently higher among cases. The findings support the hypothesis that EBV may play a role in the pathogenesis of HD among persons with elevated titers. The findings neither confirm nor deny a possible role of CMV.
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PMID:A population-based case-control study of EBV and other viral antibodies among persons with Hodgkin's disease and their siblings. 608 1

The epidemiologic similarities between Hodgkin's disease in the young and paralytic poliomyelitis suggest that Hodgkin's disease may be a rare consequence of a common infection, with the probability of oncogenesis increasing with age at the time of infection. In a study of 225 cases and 447 controls 15 to 39 years of age, we investigated the association of Hodgkin's disease with factors in childhood that influence age of exposure to infectious agents. Risk among persons with five or more siblings was nearly half that among those with one or none; risk was also reduced among persons of late birth order. Subjects who had lived in multiple-family homes had half the risk of those in single-family housing. Cases had fewer playmates and better-educated mothers than did controls, and cases had twice the rate of infectious mononucleosis. Risk is therefore associated with a set of factors that tend to decrease or delay early exposure to infections, and this association might be explained by a viral origin of the disease, with age at infection as a major modifier of risk.
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PMID:Childhood social environment and Hodgkin's disease. 625 29

Epstein-Barr virus (EBV) infection in a family resulted in a fatal disseminated heterophil negative infectious mononucleosis syndrome in a nine-year-old girl. This was followed closely by a similar disease process in her six-year-old brother which evolved over a one-year period into Stage IIIB Hodgkin's disease. Finally, three years after the index EBV case in the daughter, the mother was diagnosed with a non-Burkitt's-type undifferentiated lymphoma that proved rapidly fatal. The EBV involvement in the sister and brother was well documented serologically and virologically. The pathologic diagnosis was established and confirmed by more than one pathologist. There was no obvious evidence for either a specific or general immune defect in any of the family members tested. The progression of the six-year-old boy's EBV infection from a benign, yet disseminated disease process into a histopathologically confirmed case of Hodgkin's disease offers a strong suggestion that this virus was not behaving solely as a passenger. Especially relevant is the fact that the boy never fully recovered from his EBV infection and essentially became persistently infected with the virus as evidenced by his EBV-EA serology and virology results.
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PMID:Epstein-Barr virus, fatal infectious mononucleosis, and Hodgkin's disease in siblings. 629 4

In order to investigate the relationship between antibodies to RANA and other Epstein-Barr virus induced antigens, we have tested 50 sera from subjects without rheumatoid arthritis and with various EBV serology patterns for aRANA, aEA, aVCA, aEBNA. Patients were either suffering from Burkitt's lymphoma, infectious mononucleosis, nasopharyngeal carcinoma, Hodgkin's disease or immunodeficiencies, or were healthy controls. RANA was detected by indirect immunofluorescence on G1 synchronized Raji cells. The correlation was very strong between aEBNA and aRANA (r = 0.86) without any correlation between aRANA and aVCA. These data not only strongly support the opinion that aRANA is frequently found in non-rheumatoid diseases but cast doubt on the distinction between RANA and EBNA.
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PMID:Epstein-Barr virus and rheumatoid arthritis: are rheumatoid arthritis associated nuclear antigen and Epstein-Barr virus nuclear antigen different? 630 67

In order to study the relationship between anti-RANA antibodies (aRANA) and the antibodies capable of recognising other Epstein-Barr induced antigens, we examined the sera of 51 patients without rheumatoid arthritis for anti-RANA, anti-EA, anti-VCA, and anti-EBNA antibodies. These subjects were cases of Burkitt's lymphoma, infectious mononucleosis, naso-pharyngeal carcinoma, immune disorders, Hodgkin's disease and normal controls. A blind study was conducted in two separate laboratories. Anti-RANA was detected by indirect immunofluorescence on RAJI cells synchronised in phase G1. There was a very strict correlation between anti-RANA and anti-EBNA with no correlation between anti-RANA and anti-EA or anti-VCA. In another experiment, 15 coded sera from patients with classical rheumatoid arthritis were tested following adsorption of the rheumatoid factor. One serum was found to be devoid of both anti-RANA and anti-EBNA. These results demonstrate that anti-RANA is widely distributed outside of rheumatoid arthritis and they question the distinction between EBNA and RANA, as the antibody titres directed against these antigens are regularly linked together.
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PMID:[Strict correlation between anti-RANA antibodies and anti-EBNA antibodies apart from rheumatoid arthritis. Assessment of the diagnostic value of anti-RANA antibody]. 630 24

Peripheral blood lymphocytes (short-term cultures) and permanent lymphoid cell lines (long-term cultures) of patients with Hodgkin disease (5), lymphoma (1), plasma cell leukemia (1), angioimmunoblastic lymphadenopathy (1), and infectious mononucleosis (3) were investigated for C-band variants and nucleolus organizer region (NOR)-activities by C-banding and silver-staining, and compared to those of healthy adults (5) and newborn children (3). Heterochromatin polymorphisms were found in malignant diseases (33%) as well as in controls (29%). In the lymphoma patients, heterochromatin of class 3 (Patil and Lubs 1977) was seen more frequently than in the controls (83%:57%). No marker C-band variants could be detected in any of the lymphatic diseases. There was no difference in the heterochromatin polymorphism between short-term cultures (predominantly T-cells) and long-term cultures (B-cells), and there was little but inconsistant difference in the NOR-activities. Silver-staining showed differences between healthy adults (8.8 AgNORs; SD:0.5) and newborn children (6.9; SD:0.4). In the lymphoma patients we found 8.3 (SD:0.7) AgNORs. Thus, using silver staining there was no detectable increase in the number of active NORs in cells of patients with malignant diseases as an expression of increased nucleolus activation in malignancies. The remarkably low NOR-activity in infectious mononucleosis (6.7; SD:1.0) may reflect an influence of acute virus infection (Epstein-Barr virus) on NOR-activity.
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PMID:Heterochromatin and nucleolus organizer regions in cells of patients with malignant and premalignant lymphatic diseases. 649 6

Preparations obtained by the chloroform-methanol extraction procedure from spleen tissues of patients with Hodgkin's disease, lymphomas, and leukemias, as well as from peripheral blood buffy coat of infectious mononucleosis (IM) patients were studied for the presence of 2 Paul-Bunnell (P-B) antigens; BS antigen shared by bovine red blood cells (BRBC) and sheep red blood cells (SRBC) and another, B antigen characteristic for BRBC. Both BS and B antigens were demonstrated by means of agglutination inhibition tests in over 40% of these extracts. None of the extracts from spleens, tonsils, and buffy coat of apparently normal human beings contained these antigens. P-B antigens of lymphoma-leukemia extracts were further purified by DEAE-Sephadex column chromatography. The purified fractions of some of these spleen extracts formed a precipitation line with IM sera, which merged into a reaction of identity with the lines formed by P-B antigens of BRBC. In studying various pathologic sera, B antigen was detected in sera of 28% of lymphoma-leukemia patients, 15% of patients with carcinomas of internal organs, and 3% of patients with systemic lupus erythematosus. On the other hand, BS antigen was found in only 3% of lymphoma-leukemia sera. These results confirmed our previous observations and indicated that both BS and B antigens are expressed as neoantigens on the patient's spleen cells as a result of pathologic processes in lymphoreticular malignancies.
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PMID:Studies on Paul-Bunnell (P-B) antigen-antibody system. II. P-B antigens in extracts of lymphoma-leukemia spleens and pathologic sera. 697 12

The reactive cell population in Hodgkin's disease consists of predominantly CD4+ helper T cells and lacks CD8+ cytotoxic T cells and natural killer cells. This lack of a CD8+ response is surprising in view of the expression of the latent Epstein-Barr viral protein LMP by Reed-Sternberg cells in many cases of Hodgkin's disease, Deficient HLA class I expression would be one possible mechanism to avoid a CD8+ cytotoxic immune response. To test this possibility we studied the expression of HLA class I and II determinants on Reed-Sternberg cells in tissue sections and cell suspensions of Hodgkin's disease. Frozen tissue sections of 40 cases and cytocentrifuge preparations from cell suspensions of 10 lymph nodes involved by Hodgkin's disease were studied with monoclonal antibodies reactive with HLA determinants. As a control frozen tissue sections of two cases of infectious mononucleosis were studied. Careful examination of the tissue sections and subsequently of cytospins of cell suspensions showed that the Reed-Sternberg cells frequently lacked HLA class I but showed strong staining for HLA class II. Absence of HLA class I expression on Reed-Sternberg cells and their variants provides an explanation for the lack of a CD8+ cytotoxic immune response against antigens expressed on Reed-Sternberg cells.
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PMID:Absence of HLA class I expression by Reed-Sternberg cells. 751 95

Recent nucleic acid hybridization studies have implied that Reed-Sternberg/Hodgkin (RS/H) cells are infected with Epstein-Barr virus (EBV) before malignant transformation, and hence, that Hodgkin's disease could develop as a consequence of malignant transformation of an EBV-infected cell. This study is a detailed immunohistochemical and in situ hybridization characterization of the various lymphoid cells in nine cases of infectious mononucleosis (IM), the acute manifestation of EBV infection. The RS/H-like cells of IM were similar in most respects to their morphologically identical counterparts in Hodgkin's disease; they expressed the EBV-encoded protein LMP1, EBV EBER1 transcripts, and CD30 and rarely, if ever, expressed CD45/LCA or T cell markers. Dissimilarities were limited to CD15 negativity and the absence of a collarette of T cells around the RS/H-like cells of IM compared with their Hodgkin's counterparts. Expression of the immortalizing bcl-2 oncoprotein was variable in the RS/H-like cells of IM, as has been demonstrated in the RS/H cells of Hodgkin's disease by other investigators. An apoptosis assay suggested that many apoptotic cells in IM were EBV-infected T cells, in keeping with the previous in vitro observation that IM-derived T cells succumb to apoptosis. Additionally, the apoptosis assay suggested that RS/H-like cells of IM can succumb to programmed cell death, reminiscent of the mummified RS/H cells seen in Hodgkin's disease. The accumulation of evidence suggests that RS/H-like cells of IM are more similar to true RS/H cells than previously recognized.
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PMID:New characterization of infectious mononucleosis and a phenotypic comparison with Hodgkin's disease. 753 53


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