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)

A case report of a 28-year-old mother of two children with FUO is presented. Physical examination revealed an anemic and febrile woman, who lost 10 kg of weight during the past 3 months. Furthermore, two lymphatic nodes with diameters below 1 cm were detected at the neck and inguinal region. A search for origin of fever including evaluation of foci, malignancies and laboratory investigations was primarily unsuccessful. At day 7 after admission a pericardial murmur could be heard. Echocardiography revealed a pericardial effusion, which increased up to 4 cm during the following days, leading to hemodynamic impairment and asystole. Immediate CR was successful, pericardial effusion was aspirated. Looking for etiology of fever the presence of IgM-antibodies against toxoplasma gondii by an ELISA test was possible. Therefore, toxoplasmosis was diagnosed and a treatment-regimen comprising pyrimethamin and sulfadiazin was initiated. Because of the threat to life and very high titers of C-reactive protein, antibiotic therapy (imipenem) was given additionally. An immunologic impairment was excluded by normal ratio of CD4:CD8 of lymphocytes, normal HIV-test and a nonsuspicious Jamshidi-biopsy of the bone marrow. However, in week 9 after admission lymphatic node-tumors suddenly appeared at the neck and pulmonary hilus. After diagnostic exstirpation a malignant non-Hodgkin-lymphoma (T-cell-type) was diagnosed. It is concluded that in obscure pericardial effusion toxoplasmosis should be considered and that this manifestation may be a precursor of malignant non-Hodgkin-lymphoma.
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PMID:[Toxoplasmosis peri-myocarditis as initial manifestation of highly malignant non-Hodgkin's lymphoma]. 817 47

Acquired pure red cell aplasia (PRCA) has been associated with various lymphoproliferative conditions but its occurrence with Hodgkin's disease is rare. We report a case of PRCA occurring immediately following the completion of induction chemotherapy in a patient with Stage IIIB nodular sclerosing Hodgkin's disease. In vitro erythroid colony studies documented evidence for T cell mediated suppression of erythropoiesis and lack of a serum inhibitor. Addition of cyclosporin to the in vitro cultures stimulated erythroid colony growth. Following in vivo treatment with cyclosporin peripheral blood CD4/CD8 ratios returned to normal. However, serum erythropoietin levels were inappropriately low. Subsequent treatment with erythropoietin induced a reticulocytosis and transfusion independence. Since discontinuing the erythropoietin, the patient has been able to maintain a hemoglobin of 100 g/L. This case illustrates that red cell aplasia occurring in the setting of Hodgkin's disease may be due to T cell mediated suppression of erythropoiesis. A response to cyclosporin may be masked by inappropriately low erythropoietin levels.
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PMID:Pure red cell aplasia after chemotherapy for Hodgkin's lymphoma: in vitro evidence for T cell mediated suppression of erythropoiesis and response to sequential cyclosporin and erythropoietin. 818 75

Expression of CD4 or CD8 on the cell surface is an important guide for discriminating the immunologic functions of T-cells. However, a minor T-cell subset lacking both CD4 and CD8 molecules but bearing the usual form of T-cell receptor (TCR)-alpha beta (CD4-CD8-TCR-alpha beta+ T-cells) has recently been found not only in mice but also in humans, and the clinical relevance of this newly defined subpopulation to human diseases is now of considerable interest. The authors present a patient in whom CD4-CD8-TCR-alpha beta+ T-cells showed monoclonal proliferation in the peripheral blood for more than 3 years, then disappeared spontaneously, followed by subsequent development of Hodgkin's disease. The pathologic roles of double-negative T-cell proliferation in this case are discussed from the viewpoint of premalignancy in lymphoproliferative diseases.
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PMID:Monoclonal proliferation of double-negative (CD4-CD8-) T-cells bearing T-cell receptor-alpha beta followed by subsequent development of Hodgkin's disease. 819 23

We measured the soluble (s) receptors CD23, CD8, CD4, interleukin-2 receptor (IL-2R, CD25), and transferrin receptor (TfR, CD71), in normal serum and in patients with chronic lymphocytic leukemia (CLL) and evaluated them in relation to clinical and biological parameters of the disease, as well as serum immunoglobulin E (IgE). Compared to 31 normal individuals, 42 CLL patients had increased levels of sCD23 (98.4 +/- 127.7 versus 0.9 +/- 0.3 U/ml, p < 0.001), sIL-2R (6080 +/- 7030 versus 1420 +/- 640 pg/ml, p < 0.001), sTfR (12,100 +/- 11,250 versus 5000 +/- 1050 ng/ml, p < 0.001), and sCD8 (510 +/- 191 versus 234 +/- 89 U/ml, p < 0.001), but normal sCD4 levels. Mean sCD23 levels remained normal in patients with non-Hodgkin's lymphoma (other than small lymphocytic), Hodgkin's disease, hairy cell leukemia, acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), chronic myelogenous leukemia (CML), multiple myeloma, or solid tumors. Advancing Rai clinical stage was associated with a progressive elevation of sCD23 (p < 0.001), while sCD8 (p < 0.05), sIL-2R (p < 0.001), and sTfR (p < 0.005) were highest in stage 2 patients. Discriminant analysis confirmed the value of soluble receptor determinations in the clinical evaluation of CLL patients. sCD23 correlated with sIL-2R (p < 0.001) and sTfR (p < 0.05) but not with sCD4 or sCD8, and displayed an inverse relationship with serum IgE (NS) and total gamma-globulin (p < 0.05). sIL-2R correlated with sCD23 (p < 0.001), sTfR (p < 0.001), sCD4 (p < 0.01), and sCD8 (p < 0.01). The lymphocyte count correlated with serum lactate dehydrogenase (LDH) (p < 0.05), sCD23 (p < 0.001) and sIL-2R (p < 0.01) but not sTfR, sCD8, or sCD4. Chemotherapy produced consistent reductions of sCD23 levels in two responding patients. We conclude that: (i) sCD23 is considerably elevated in CLL, correlates with the tumor mass and clinical stage, and could be helpful in monitoring these patients; and (ii) sIL-2R, sCD8, and sTfR levels are less specifically increased and could be influenced by other factors such as immune activation and erythropoiesis.
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PMID:Soluble CD23 and other receptors (CD4, CD8, CD25, CD71) in serum of patients with chronic lymphocytic leukemia. 825 2

A 53-year-old Japanese male noticed pigmented lesions on his right upper gingiva and hard palate in February of 1986. Histological examination revealed in situ malignant melanoma. Chemotherapy, beta-interferon, and oral BCG were given. However, tumors subsequently developed in the nasal cavity in March of 1989. The patient died in April of 1990 after developing Garcin's syndrome and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Autopsy revealed aggressively infiltrating, whitish tumor masses invading the hard palate, the nasal cavity, the paranasal sinuses, the base of the skull, cranial nerves I-X, and the pituitary body, as well as severe necrosis of the soft palate. However, there was no evidence of malignant melanoma. Instead, these oval tumor cells had atypical nuclei and scanty cytoplasm. They contained no melanin granules, were negative for S-100 protein, and were also negative for various melanoma-associated antigens. They were positive for CD2, CD3, and CD8 by avidin-biotin-peroxidase complex immunohistochemistry. It was concluded that the patient had CD8+ non-Hodgkin's malignant lymphoma (diffuse, large cell type) of the nasopharyngeal region, which was preceded by in situ malignant melanoma of the palate.
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PMID:A case of CD8+ T cell lymphoma occurring during treatment for in situ malignant melanoma of the palate. 834 26

The recombination activating gene, RAG-1, which is supposed to encode a molecule regulating V(D)J recombination, has been isolated. In the current study, the distribution of RAG-1 expression in human neoplastic hematopoietic cells was compared with the phenotypic and genotypic status of differentiation. Thirty-one hematopoietic cell lines (16 B-lineage, 9 T-lineage, 2 Hodgkin's disease, and 4 nonlymphoid cell lines) were investigated for the expression of human RAG-1 using the reverse-transcriptase polymerase chain reaction (RT-PCR). RAG-1 was not expressed in nonlymphoid, Hodgkin's disease, or mature-stage lymphoid cell lines, but was present in some acute lymphoblastic leukemia (ALL)/lymphoblastic lymphoma (LBL) cell lines. The investigation was extended to 45 cases of fresh ALL/LBL cells. The patterns of RAG-1 expression found in the cell lines and fresh ALL/LBL cells were similar. In B-lineage cells, the product of RAG-1 RT-PCR was detected in CD19+ CD10- CD20- CD5- stage (stage II, Nadler's classification) and was at the highest level in CD19+ CD10+ CD20- CD5- stage (stage III), but was absent or limited in CD19+ CD10+ CD20-+ CD5- (stage IV) or CD19+ CD10+ (or CD10-) CD5+. In stage II, monoclonal gene rearrangements of only the immunoglobulin heavy chain (IgH) were found, whereas monoclonal gene rearrangements of both IgH and T-cell receptor (TCR)-beta chain were frequently noted in stages III and IV. The expression of CD20 or CD5 antigen apparently correlated with the decline of RAG-1 expression. In T-lineage cells, RAG-1 was highly expressed in CD3- CD4+ CD8+/CD3+ CD4+ CD8+ thymic stages, but was negative or only weakly expressed in the CD3- CD4- CD8- prothymic or early thymic stage, in which the TCR-beta gene was often germline, or the CD3+ CD4+ CD8- mature thymic stage. The relative levels of RAG-1 mRNA give an additional delineating frame to the schemes of lymphoid differentiation based on phenotypic and genotypic status. RAG-1 is exhibited by cells of the thymic stage capable of synthesizing TCR or expressing it on the cell surface. The weak or absent expression of RAG-1 in the prothymic or early thymic stage suggests that the contribution of RAG-1 to the gene rearrangement may differ quantitatively between TCR-delta/TCR-gamma and TCR-beta.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Human recombination activating gene-1 in leukemia/lymphoma cells: expression depends on stage of lymphoid differentiation defined by phenotype and genotype. 839 73

We describe an unusual case of Sezary syndrome which transformed into a large T-cell non Hodgkin's lymphoma (immunoblastic) in a black man of Caribbean descent with negative HTLV-I serology and no evidence of HTLV-I infection by DNA analysis using sensitive techniques. The disease presented as a small-cell Sezary syndrome and transformed in an inguinal lymph node one year from diagnosis. Immunological markers in the small and large cells showed a mature T-cell phenotype CD4+, CD8- with expression of T-cell activation markers and a high proliferative rate. Ultrastructural analysis confirmed small Sezary cells with serpentine nucleus in the peripheral blood and immunoblasts in the lymph node. Cytogenetics demonstrated complex clonal chromosome abnormalities with involvement of 7q35, the locus for the beta chain of the T-cell receptor (TCR). Southern-blot analysis showed the same rearrangement of the TCR beta, gamma, delta chain genes in lymph node and peripheral blood cells. Antibodies to HTLV-I were not detected in the serum by ELISA and particle agglutination (PA) nor HTLV-I specific sequences were demonstrated by nested polymerase chain reaction with primers to the envelope proteins, LTR and tax/rex of HTLV-I in both tissues, blood and lymph node. The disease had an aggressive course and was refractory to therapy; the patient died of progressive disease 28 months from presentation. Two unusual features characterised this patient's illness: immunoblastic transformation of a Sezary syndrome in a patient of Afro-Caribbean origin without evidence of HTLV-I DNA sequences and negative HTLV-I serology and the atypical lymph node histology resembling ATLL.
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PMID:Immunoblastic transformation of a Sezary syndrome in a black Caribbean patient without evidence of HTLV-I. 852 63

Reed-Sternberg (RS) and Hodgkin's (H) cells are considered to be the neoplastic cells in Hodgkin's disease. Although most data suggest a lymphoid origin, the nature of these cells still remains the subject of considerable controversy. Recently, monoclonal antibodies became available, directed against granzyme B, a serine protease specifically expressed by activated cytotoxic T cells (CTLs) and natural killer (NK) cells. Using two granzyme B-specific antibodies directed against different epitopes, we studied the expression of granzyme B in a well characterized group of Epstein-Barr virus (EBV)-positive and EBV-negative cases of Hodgkin's disease. Granzyme B expression was found in part of the H-RS cells in 11 out of 61 tested cases (18%, 9 of 46 cases of nodular sclerosing and 1 of 12 mixed cellularity Hodgkin's disease). In none of these cases did H-RS cells express B-cell markers, whereas in four cases, expression of either the T-cell marker CD3 or CD8 was found in a small minority of H-RS cells. The percentage of granzyme B-positive H-RS cells ranged from < 10% to > 50%. Granzyme B-positive H-RS cells were present in 6 of 26 EBV-positive cases and in 5 of 35 EBV-negative cases, indicating no relationship with the presence of EBV. Moreover, no significant differences were found regarding either stage at presentation or clinical outcome. We conclude that in a restricted number of cases of Hodgkin's disease, the H-RS cells express granzyme B, and therefore might be considered the neoplastic equivalent of either activated CTLs or NK cells.
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PMID:Granzyme B expression in Reed-Sternberg cells of Hodgkin's disease. 854 10

We report a patient from an endemic area of adult T-cell leukemia/lymphoma (ATLL), who developed lymphoma with features characteristic of Hodgkin's disease (HD). Large atypical Reed-Sternberg/Hodgkin's cells (RS/H cells) had a CD3-CD15+CD20-CD30+CD45RO- immunophenotype. Epstein-Barr virus (EBV) latent membrane protein and EBV-encoded small RNA were detected in the RS/H cells. The patient received C-MOPP/ABVD chemotherapy for the HD resulting in a partial response. However, relapse occurred and he died of disease progression associated with serious bacterial infection. Although serial lymph node biopsies revealed consistent presence of the EBV-positive RS/H cells, the background small lymphocytes showed progressive increase in pleomorphism and nuclear irregularity. The lymphocytes had the T-cell phenotype, CD3+CD4+CD7-CD8-. Southern blot analysis using DNA probes for the human T-cell lymphotrophic virus-I (HTLV-I) and the T-cell receptor beta-chain gene demonstrated expansion of the HTLV-I infected monoclonal T-cells with the disease progression. We concluded that the patient synchronously presented two independent lymphoproliferative disorders; EBV-associated HD and ATLL resulting from HTLV-I infection.
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PMID:Synchronous presentation of Epstein-Barr virus-associated Hodgkin's disease and adult T-cell leukemia/lymphoma (ATLL) in a patient from an endemic area of ATLL. 854 10

We analyzed the stimulating capacities of malignant B cells from non-Hodgkin's lymphomas (NHL) to induce an allogeneic response in primary mixed lymphocyte reaction (MLR). T cells purified from a single healthy donor (KS) were used to compare the responses induced by either malignant or hyperplastic cells. Malignant B cells induced strong proliferation of KS cells independently of their level of expression of adhesion molecules. The KS cells after MLR were predominantly CD3+, CD25+, HLA-DR+, Ki67+ and CD45RO+ T cells, and the CD4/CD8 ratio was heterogeneous (from 0.8 to 2.7). To investigate the role of co-stimulatory molecules CD80 and CD86 for the stimulatory capacities of B cells, the expression of both molecules was analyzed before and during the MLR. Most fresh malignant B cells were negative for CD80 and CD86, whereas co-cultured B cells expressed high levels of both molecules. This expression was crucial for T cell proliferation, since monoclonal antibodies directed against CD80 and CD86 completely abrogated the MLR. We also report that KS responding cells at the end of co-culture were able to lyse fresh B cells used as stimulator cells to different extents (from 10 to 51%), and the level of lysis was enhanced after PMA activation of the target cells. Inhibition experiments using CD8 and CD4 mAb showed that effector cells were mainly CD8+. This report is the first to describe the accessory function of human malignant B cells from NHL and their sensitivity to lysis mediated by CD8+ T cells, and suggests new strategies for the development of antitumor immunity in NHL.
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PMID:Malignant B lymphocytes from non-Hodgkin's lymphoma induce allogeneic proliferative and cytotoxic T cell responses in primary mixed lymphocyte cultures: an important role of co-stimulatory molecules CD80 (B7-1) and CD86 (B7-2) in stimulation by tumor cells. 856 20


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