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

Four consecutive lymph node biopsies from one patient showed features typical of lymphocyte-pre-dominant Hodgkin's disease. When the patient developed lymphocytosis of the peripheral blood and a staging bone marrow biopsy was found to have nodular lymphoid infiltrates atypical for Hodgkin's disease, the fourth node biopsy was performed in order to perform immunologic marker studies. A monoclonal cell population was identified and the lymph nodes were interpreted as chronic lymphocytic leukemia mimicking lymphocyte-predominant Hodgkin's disease. The diagnostic usefulness of immunologic marker studies stressed.
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PMID:Differentiation of chronic lymphocytic leukemia from Hodgkin's disease using immunologic marker studies. 703 76

Clonal disorders of large granular lymphocytes (LGL) of either CD3- (NK cell) or CD 3+ (T-cell) phenotype have been described. B-cell malignancies such as hairy cell leukemia and non-Hodgkin's lymphoma have been observed in association with the T-cell type of LGL leukemia. Here we report the occurrence of LGL lymphocytosis in four patients with Hodgkin's disease. Immunophenotyping studies showed that these LGL were CD 3- in three patients and CD3+ in the other. LGL were polyclonally expanded in both patients in whom clonality could be assessed.
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PMID:Lymphocytosis of large granular lymphocytes in patients with Hodgkin's disease. 748 96

Several reports of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) and of coexisting or subsequent Hodgkin's disease (HD) have raised the question how these two disorders are related. The authors have identified eight new cases of B-cell low-grade lymphoproliferative disorders (LGLPD) and HD. Six of these cases were similar to those previously reported on by others in that the HD were mixed cellularity, nodular sclerosing, and lymphocyte depleted subtypes. The morphology in these cases was typical of HD, as was the immunohistochemical profile. However, the two remaining cases were notable in that the HD was of the nodular lymphocyte predominant type (NLPHD). To our knowledge, this association has not been well documented previously. In the two cases in this study, CLL and NLPHD were found simultaneously when each patient presented with lymphadenopathy and a lymphocytosis that was comprised of small monoclonal B lymphocytes coexpressing CD5. Lymph node biopsies in each case revealed typical NLPHD, with large, indistinct nodules containing scattered lymphocytic-histiocytic (L&H) cells. Focal, but distinct areas of CLL/SLL were also present. Immunostaining of the lymph node biopsy specimens showed the L&H cells to be CD20- and CD45 positive, and to lack CD15 or evidence of light chain restriction. In one of these patients, a NLPHD-associated large cell lymphoma developed 8 months later. The large cells were CD20- and CD45 positive, with lambda light chain restriction. In contrast, the original CLL cells in this patient expressed kappa light chains. This report indicates that LGLPD can be associated with all subtypes of HD, including the NLP type. The discordant light chain restriction between the CLL and the NLPHD-associated large cell lymphoma in one of these cases indicates that the CLL and HD were probably not derived from the same clone.
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PMID:Hodgkin's disease associated with chronic lymphocytic leukemia. Eight additional cases, including two of the nodular lymphocyte predominant type. 772 47

Gastrointestinal (GI) disease is frequent in all types of immunocompromised patients but occurs with greatest frequency in patients with acquired immunodeficiency syndrome (AIDS). Thus, much of this review deals with human immunodeficiency virus (HIV)-related GI diseases. Gastrointestinal diseases in other immunocompromised patients are compared with those in patients with AIDS. Conditions unique to transplant recipients, such as graft-versus-host disease (GVHD) and posttransplant lymphoproliferative disorders (PTLDs), are discussed separately. We have divided these GI diseases into four main categories: (1) HIV-related inflammatory conditions other than opportunistic infections (HIV-related enteropathy, proctocolitis, and CD8 lymphocytosis); (2) inflammatory conditions unrelated to HIV or opportunistic infections (neutropenic enterocolitis, regional enteritislike enteropathy, and GVHD); (3) opportunistic infections (illnesses caused by herpesvirus, cytomegalovirus, and miscellaneous other viruses; Mycobacterium, Candida, Histoplasma, Cryptococcus, Cryptosporidium, Microsporida, Isospora, Leishmania, Toxoplasma and Strongyloides organisms as well as Pneumocystitis carinii; and (4) neoplasias (Kaposi's sarcoma [KS], AIDS-related non-Hodgkin's lymphoma [NHL], HIV-related Hodgkin's disease [HD], PTLDs, and miscellaneous neoplasms). The prevalence, pathogenesis, clinical manifestations, gross pathological findings, and microscopic features of each disease entity are discussed.
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PMID:Gastrointestinal disease in the immunocompromised patient. 795 57

The structures of rearranged gamma-chain T-cell antigen receptor (TCR) genes were analyzed in 5 cases of T-cell acute lymphoblastic leukemia (T-ALL), in 15 cases of peripheral T-cell non-Hodgkin's lymphoma (T-NHL), in 1 case with large granular CD8 lymphocytosis, 1 case with CD8 lymphocytosis after autologous bone marrow transplantation for Hodgkin's disease, and in 2 cases with nonneoplastic diseases. Rearranged V-J TCR gamma-gene segments were amplified by the polymerase chain reaction (PCR). Because most of the biopsy tissue or bone marrow samples contained significant amounts of admixed nonmalignant T-cells, direct DNA sequencing of the PCR products yielded mixed sequence data because of coamplification of clonal together with polyclonal TCR gamma V-N-J junctions. Reliable data could only be obtained by cloning the V gamma-J gamma PCR products and sequencing several (4 to 10) randomly chosen clones. In the polyclonal samples, all PCR-derived clones differed in their specific V-N-J junctions, as expected. In the two T-cell lines and in most of the T-cell malignancies, monoclonal PCR products could be identified by the demonstration of clonally restricted V-N-J junctions. In most cases, this information yielded the desired clone-specific sequence and showed a background population of polyclonal TCR gamma cells in each specimen, except for those that were obtained from the T-ALL samples, the cell lines, or the NHL samples with high tumor cell fraction. The results obtained by PCR-directed sequencing were confirmed by temperature-gradient gel electrophoresis (TGGE) that showed distinct DNA bands only with the PCR products containing predominant (ie, monoclonal) TCR gamma V-N-J junctions. By combined sequence and TGGE analysis, it was found that PCR/TGGE is able to distinguish between monoclonal and polyclonal TCR gamma-PCR products. This finding prompted us to complete the analysis of the TCR gamma locus in the samples by PCR/TGGE using primer mixes which covered all possible V gamma and J gamma recombinations. Monoclonality was shown with all mixes by PCR/TGGE in 21 of 24 (87%) of the lymphoproliferations. In summary, the present study shows that the combination of amplifying TCR gamma V-N-J junctions by PCR with the identification of clonal PCR products by TGGE and DNA sequencing is a reliable method for the characterization of clonal TCR gamma sequences.
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PMID:Characterization of clone-specific rearrangement T-cell receptor gamma-chain genes in lymphomas and leukemias by the polymerase chain reaction and DNA sequencing. 802 83

Marrow regeneration is known to be associated with an increase in immature B cells, including CD10+ cells. A similar phenotype has been seen in some children with unusual cytopenias. This article describes 21 adult patients not recovering from chemotherapy, who had increased CD10+ cells in their marrows. These cells had the relatively uniform scatter properties of small lymphocytes by flow cytometry, and by multiparameter analysis were found to have a distinct phenotype in that they were CD19+, lacked surface immunoglobulin, and heterogeneity expressed CD20. In two of three patients tested, some but not all of these early B cells were TdT+. CD10+ cells accounted for 10-76% of total mononuclear cells. All 21 patients had some systemic illness. Thirteen patients had a diagnosis of lymphoma (three Hodgkin's, ten non-Hodgkin's); all ten of the latter were extranodal and seven of seven phenotyped cases were B-cell lymphomas. Seven patients had autoimmune disease (one also had lymphoma) and one had the acquired immunodeficiency syndrome with mycobacterial infection of the marrow. One patient with a history of a "viral illness" had a lymph node showing atypical lymphoid hyperplasia with progressive transformation of germinal centers. Examination of marrow core biopsies in these patients showed a proliferation of small lymphocytes ranging from a barely perceptible diffuse increase to numerous lymphoid aggregates. The extensive lymphocytosis seen in two marrows suggested a diagnosis of lymphoma on morphologic grounds alone, but neither these patients nor any others had B-cell clonal excess. The presence of this phenotype suggests nonspecific stimulation of marrow B-cell precursors associated with systemic B-cell activation in either an immunologic or neoplastic disorder. Presence of this unusual phenotype does not imply involvement of marrow by B-cell neoplasia.
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PMID:Marrow B-cell precursors are increased in lymphomas or systemic diseases associated with B-cell dysfunction. 834 38

A febrile illness with atypical peripheral blood lymphocytosis (polyclonal CD8+ suppressor/cytotoxic phenotype), complement activation and IgA/G class hypergammaglobulinaemia was found in a 76-year old male with clinical stage III follicular non-Hodgkin lymphoma (NHL). There was serological evidence of active cytomegalovirus (CMV) as well as reactivated chronic Epstein-Barr virus (EBV) infection. Spontaneous regression of NHL appeared, the signs of viral infection improved but hypergammaglobulinaemia persisted. In patients with malignant lymphoma, clinical signs and abnormalities of peripheral blood lymphocytes and serum immunoglobulins should not automatically be considered a consequence of the lymphoma.
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PMID:[A man with spontaneous regression of non-Hodgkin lymphoma, hypergammaglobulinemia and infection caused by 2 herpesviruses; causality or coincidence?]. 838 9

An immunohistochemical study was performed on 132 routinely processed trephine biopsies of the bone marrow (40 reactive lymphocytosis, 80 B-cell lymphomas, 7 T-cell lymphomas, 5 Hodgkin's diseases), using 4 monoclonal antibodies, DBB.42, DNA.7, DBA.44, DND.53, which are directed against B-lymphocyte associated antigens, not destroyed by fixation. DBB.42, DNA.7 and DBA.44 are formalin and Bouin resistant. They do not stain myeloid, erythroblastic, histiomonocytic and endothelial cells, and are particularly suitable for bone marrow biopsies. DBB.42 and DNA.7 in association, identify all B-cell lymphomas and no T-cell lymphoma. DBB.42 recognizes respectively 65/65 and 13/15 low and high grade malignancy B-cell lymphomas, and DNA.7, 54/65 and 15/15. In our hands, these 2 antibodies are more reliable than L26 and MB2 on bone marrow biopsies. DBA.44 identifies 15/15 hairy-cell leukemias, and interestingly stains only 10% of other B-cell lymphomas, and no T-cell lymphoma. DND.53 is less specific, but reveals Reed-Sternberg cells. Combined immunostaining with anti T-lymphocyte antibody CD3, let us appreciate the contribution and the limits of immunohistochemistry in the diagnosis of bone marrow lymphoproliferative diseases, especially for interstitial and nodular lymphoid infiltrates of undetermined significance. These results point out the value of these 4 monoclonal antibodies in routinely processed bone marrow biopsies, particularly of DBB.42 and DBA.44.
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PMID:[Immunophenotyping of B lymphoma in bone marrow biopsies. Contribution of 4 monoclonal antibodies used on paraffin-embedded tissues:DDB.42,DNA.7,DNA.44 and DND.53]. 839 39

Low-grade malignant non-Hodgkin lymphoma [NHL] and chronic lymphocytic leukemia [CLL] as its special form are slowly progressing malignancies which may present with lymphadenopathy, splenomegaly or, more rarely, hepatomegaly. The diagnosis is made by bone marrow or lymph node histology, while laboratory tests are relatively unspecific and may only hint towards the diagnosis. In contrast to high-grade malignant lymphoma, low-grade malignant NHL is often associated with the appearance of malignant lymphoma cells in peripheral blood. These malignant lymphocytes may be differentiated microscopically from normal lymphocytes, so that the diagnosis of NHL may be suspected not only because of clinical symptoms or lymphocytosis, which may present late in the natural history of the disease, but also on morphological grounds. Three types of low-grade malignant NHL cells may be recognized in peripheral blood: A mature appearing lymphocytic type with only slight alterations of the nucleus, a lymphoplasmocytic type, and a lymphocytic type with prominent alterations of the nucleus. The appearance of smudge cells and a monotony in lymphocyte morphology may serve as further diagnostic aids. Once the diagnosis has been suspected on morphological grounds, it may be verified in the case of B-cell lymphomas by flow cytometry. The clonality of T-cell lymphoproliferative disorders in addition has to be proven by demonstrating a clonal rearrangement of the T-cell receptor in Southern blots. An early diagnosis of low-grade malignant NHL may not only provide new insights into the natural history of monoclonal cytopathies but may also be of importance in the clinical management of patients.
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PMID:[Value of the blood picture and flow cytometry immunotyping in the early diagnosis of low-grade lymphoma]. 862 61

We describe post-splenectomy lymphocytosis (PSL) in 23 patients, a majority (20/23) of whom have undergone splenectomy as a staging procedure for Hodgkin's disease. The absolute lymphocyte count ranged from 4.0 to 8.7 x 10(9)/l. The lymphocytosis was noted 4-242 (median 70) months after splenectomy and persisted almost unchanged in most patients on prolonged follow up (median 50 months). Immunophenotyping of the lymphocytes revealed no monoclonal B cell population.
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PMID:Post-splenectomy lymphocytosis. 869 29


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