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

Two cases of what is apparently Epstein-Barr virus (EBV)-associated atypical lymphoproliferation which clinically suggested malignant lymphoma are discussed. Immunohistology revealed polyclonal T- and B-cell proliferation resembling progressive infectious mononucleosis. Giant cell formation and marked plasmacytosis was suggestive of Hodgkin's disease. EBV serology was initially not diagnostic, but during the course of the disease, elevated titers against early antigens and EBV-associated nuclear antigen suggested virus replication. EBV DNA was demonstrated in lymphoid cells of both cases by in situ hybridization. One case progressed to overt monoclonal B-cell malignant lymphoma. Atypical polyclonal lymphoproliferation in persistent active EBV infection may thus be considered a prelymphomatous condition.
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PMID:Persistent active Epstein-Barr virus infection and atypical lymphoproliferation. Report of two cases. 282 51

From this review of the natural history of EBV infection in humans, it is clear that the virus has evolved to a symbiotic state with humans. Once individuals are infected, EBV establishes a permanent infection that is maintained at a low level by replication of the virus in the oropharyngeal region with subsequent seeding of circulating B-lymphocytes. Individuals with normal immune systems are able to control the pronounced proliferative potential of EBV-infected cells and thus prevent the emergence of lymphoproliferations. Disease states result when the immune system is altered by other infections, developmental conditions, immunosuppressive agents, or debilitating circumstances such as cancer or starvation. In some cases, localized lymphoproliferations resembling large-cell non-Hodgkin's lymphomas can result that are monoclonal by immunoglobulin gene rearrangement studies. Remarkably, many of the localized masses will regress if the immunosuppressive agents or condition can be ameliorated in these individuals. In patients with hereditary immune deficiencies, these localized masses can progress to a fatal disease without further cytogenetic events. Burkitt's lymphoma, which is associated with EBV infection, appears to result when EBV-driven lymphoproliferations undergo cytogenetic translocations involving predominantly chromosome 8. Most of the conditions that are associated with EBV can be diagnosed by accurate application of EBV-serology, examination of peripheral blood films, a careful history and physical examination, and, in some cases, more sophisticated techniques such as the establishment of lymphoblastoid cell lines, EBNA staining, DNA probes, and pedigree analysis.
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PMID:Epstein-Barr virus--associated lymphoproliferative lesions. 283 36

Hepatic fibrin-ring granulomas were the main histological finding in the liver of a 38-year-old man with Epstein-Barr virus primary infection. The patient presented with fever, hepatomegaly, icterus, abnormal liver tests, autoimmune hemolytic anemia, and mononucleosis syndrome. There was neither enanthema nor lymphadenopathy or splenomegaly. Serologic tests disclosed an Epstein-Barr primary infection profile: anti-viral capsid antigen IgM antibodies and anti-early antigen antibodies were present, whereas anti-Epstein-Barr nuclear antigen antibodies were absent. There was no evidence for Q fever, Hodgkin's disease, or allopurinol-induced hepatitis, which are recognized causes of hepatic fibrin-ring granulomas. It is suggested that Epstein-Barr virus infection might be an additional cause of these peculiar hepatic granulomas.
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PMID:Epstein-Barr virus infection and hepatic fibrin-ring granulomas. 283 98

This case report describes a case of chronic Epstein-Barr virus infection resulting in lymphadenopathy morphologically indistinguishable from Hodgkin's disease. Morphologic, immunologic, and virologic studies could be performed on three consecutive lymph nodes. For the first time in the literature, Epstein-Barr Nuclear Antigen (EBNA) could be demonstrated in the nuclei of Sternberg-Reed cells.
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PMID:Lymphadenopathy morphologically consistent with Hodgkin's disease associated with Epstein-Barr virus infection. 299 59

Antibody titers to Epstein-Barr virus (EBV)-associated early antigens (EA) and the viral capsid antigen (VCA) were determined by ELISA on 263 sera obtained from healthy donors, patients with Hodgkin's disease (HD), non-Hodgkin lymphomas (NHL), infectious mononucleosis (IM), Burkitt's lymphoma (BL), and nasopharyngeal carcinoma (NPC). As expected, most lymphoma patients showed markedly elevated anti-VCA IgG and anti-EA IgG antibody titers. Only one patient in the NHL group (n = 56) consisting of patients with lymphomas other than chronic lymphocytic leukemia (CLL) and hairy-cell leukemia (HCL), and 3 patients with HCL (n = 19) had high antibody titers of the IgA class to VCA and EA. Seventeen out of 48 patients (36%) with CLL had high IgA anti-VCA titers and 10 of these sera (21%) also contained IgA anti-EA. The geometric mean titer (GMT) of IgA anti-VCA was 2,510, the GMT of IgA anti-EA was 780. These antibody titers were about 10 times lower than the corresponding GMT of the NPC patients investigated in this study. The elevated IgG and IgA antibody titers to VCA and EA in CLL and HCL patients seem to reflect an immunodeficiency secondary to the malignant disease leading to reactivation of latent EBV infection. The possibility that at least some of these B-cell lymphomas are associated with EBV cannot be excluded.
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PMID:Increased incidence of IgA antibodies to the Epstein-Barr virus-associated viral capsid antigen and early antigens in patients with chronic lymphocytic leukemia. 301 85

Hodgkin's disease was found in five members of the same generation in a large Swiss family. At presentation, the patients were between 20 and 30 years old. The histological diagnosis was confirmed in three patients. In one woman the differential diagnosis of histiocytic non-Hodgkin's lymphoma was considered. The patient history did not provide any conclusive evidence for environmental factors shared by all patients. Three siblings had grown up in the same household. They had never been in contact with the other pair of affected sisters. No clustering of cases in time occurred, as individual cases were diagnosed at least two years apart. Antibodies against Epstein-Barr viral capsid antigen were found in four patients (IgG: 1:10 to 1:160). There was no single HLA-haplotype common to all patients. However, two affected sisters were HLA-identical (paternal haplotype: Aw24(9), Bw62(15), DRw6; and maternal haplotype: A2, B7, DR2). Their brother with Hodgkin's disease was homozygous for A-, B- and DR-antigens. He shared all these antigens with his two affected sisters (A2, Bw62(15), DR2). A genetic predisposition in combination with environmental factors, in particular subclinical Epstein-Barr virus infection, may have been responsible for the development of Hodgkin's disease in this family.
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PMID:[Hodgkin's disease in a Swiss family]. 358 32

Male patients with the X-linked lymphoproliferative syndrome (XLP) have an inherited immune deficiency to Epstein-Barr virus (EBV) infection that results in fatal infectious mononucleosis (IM), acquired hypogammaglobulinemia- or agammaglobulinemia, virus-associated hemophagocytic syndrome, and non-Hodgkin's malignant lymphoma (ML). A clinicopathologic analysis of 17 patients with XLP who developed ML was performed. The median age of the patients at the time of diagnosis was 4.0 years (range, 2-19 years). The median overall survival was 12 months (range, 1-216 months). Eight patients had maternally related male relatives with ML. Other phenotypes of XLP were documented in male relatives of the remaining nine patients. Common presenting symptoms were fever, nausea, vomiting, and abdominal pain. Nine patients had "B" symptoms. All ML occurred at extranodal sites. The intestines, most commonly ileocecal, were involved in 76.5% of the cases. Thirteen patients had localized disease (Stages I and II) and four patients had advanced disease (Stages III and IV). A diffuse histologic pattern of growth was observed in all cases. The distribution of histologic subtypes included small noncleaved (41.2%), large noncleaved (17.6%), immunoblastic (17.6%), small cleaved or mixed cell (11.8%), and unclassifiable (5.9%) ML. Surgical resection, radiation therapy, and chemotherapy resulted in disease-free survivals of up to 192 months in eight patients (median 114 months; range, 12-192 months). Eight of 17 patients (47%) are still alive. A median survival of only 6.0 months (range, 1-12 months) was observed in the nine patients who died. No residual ML was found at autopsy. The small noncleaved subtype had an adverse prognosis (seven of nine deaths versus one of eight survivors; P less than 0.05). Bacterial infection was the major cause of death (seven of nine patients). Characteristics that distinguish ML in XLP from other ML include a maternal family history of XLP, early age of onset, acquired hypogammaglobulinemia, post-EBV infection, and ileocecal involvement.
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PMID:Malignant lymphoma in the X-linked lymphoproliferative syndrome. 381 12

Hodgkin's disease displays an intriguing variation in incidence with age. For adult disease, there is striking bimodality in incidence with peaks in young adulthood and in older adulthood. On epidemiologic grounds, there appear to be three different diseases: childhood (0-14 years), young adult (15-34 years), and older adult Hodgkin's disease (55+ years). There are marked geographic variations in Hodgkin's disease incidence, but the variations are different for the three age groups. There are also interesting associations between Hodgkin's disease and markers of social class. For the young adult disease, the higher the socioeconomic status of a person, the greater the Hodgkin's disease risk. Additionally, Hodgkin's disease patients appear to have had fewer of the childhood infectious diseases or to have had these diseases at older ages than controls. These factors suggest an analogy between young adult Hodgkin's disease and Epstein-Barr virus, poliomyelitis, and tuberculosis infections. Thus, the descriptive epidemiology of Hodgkin's disease suggests an infectious disease process underlying its etiology in young adulthood and perhaps in childhood. There is a curious relationship between Hodgkin's disease and Epstein-Barr virus infection. Persons with Epstein-Barr virus infection have an increased risk of developing Hodgkin's disease, and the Epstein-Barr virus infection precedes the development of Hodgkin's disease. The virus has never been isolated from or identified in Hodgkin's disease tissue. The mechanisms underlying this association are unknown and may provide important clues to the etiology of Hodgkin's disease and other lymphomas. It is likely that there is no direct person-to-person spread of Hodgkin's disease. This is suggested by several negative studies of linkages between cases, time-space clustering, and aggregation of exposures at schools. Studies have shown that neither physicians nor nurses, groups with greater likelihood of encountering Hodgkin's disease patients than the general public, have an increased risk. There appears to be familial aggregation of Hodgkin's disease. Siblings of young adult cases are at increased risk, whereas siblings of older adult cases have no increase in risk. Among sibling pairs with Hodgkin's disease, there is a marked excess of like-sex pairs. Like-sex siblings have almost twice the risk of discordant-sex siblings, suggesting an interaction between environmental and genetic factors. Thus, it would be of interest to known the risk to spouses of cases who share environments but who do not share genes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiology of Hodgkin's disease. 609 22

We report a case of Hodgkin's disease associated with Epstein-Barr virus (EBV) infection in a 75-year-old male. The patient was given a 5-day course of acyclovir to which he responded well, with partial resolution of the lymphoma and return to well-being. A biopsy from the lymphoma after acyclovir treatment showed a change in the histological picture with a reduction in the number of giant cells. Relationships between EBV infection and Hodgkin's lymphoma are discussed.
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PMID:Diagnosis of Hodgkin's disease hampered by an Epstein-Barr virus infection treated with acyclovir. 609 61

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


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