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

78 children with acute lymphoblastic leukemia or non-Hodgkin-lymphoma were treated at the Children's Hospital of the University of Heidelberg from December 1971 to April 1979. Following cytostatic treatment and irradiation of the skull 11 children developed CNS-symptoms (mainly seizures and paresis) which were caused by intracerebral hemorrhage, infectious or degenerative CNS-diseases. Cranial axial tomography (CAT) was helpful in finding the cause of the CNS-complication. We recommend routine CAT in the beginning and during the course of treatment of leukemia to document CNS-changes as early as possible and to prevent further damage by alterations of therapy.
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PMID:[ZNS complications in children with acute lymphatic leukemia. Computer tomographic studies]. 29 67

Acute nonlymphocytic leukaemia developed in seven patients treated for Hodgkin's disease. All had received intensive radiotherapy and chemotherapy. One patient had clinical evidence of active Hodgkin's disease at the time of diagnosis of acute leukaemia, and of four other patients who had a post mortem examination another showed evidence of Hodgkin's disease. The median time from the first presentation with Hodgkin's disease to the development of acute leukaemia was 7.7 years. Chromosomal abnormalities were found in four patients. A preleukaemic phase was present in three patients. Survival following diagnosis of acute leukaemia was short (median four weeks) and only one patient achieved a complete remission. Although published data suggests that radiation exposure is an important aetiologic factor in the induction of acute leukaemia in patients with Hodgkin's disease, it appears likely that additional chemotherapy may have a significant potentiating effect.
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PMID:Hodgkin's disease terminating in acute leukaemia: report of seven cases. 29 79

Two children who presented initially with a lymphoid malignancy were noted to develop recurrences with myeloid features late in the course of their disease. In both cases, evidence of lymphoid differentiation was present in the myelogenous cells that were Ph1 chromosome negative. The first patient had acute myelogenous leukemia and developed a recurrence with morphologic features of acute myelogenous leukemia. Terminal transferase was present in the myelogenous blasts. The second patient initially had a diffuse lymphoblastic non-Hodgkin lymphoma. During the course of her illness she developed a myeloproliferative disorder characterized by basophilic meningitis, splenomegaly, and hypereosinophilia. Lymphocyte T-cell (E-rosette) markers were present on the eosinophils. These observations lend further support to the hypothesis of varying lymphoid and myeloid differentiation in certain cases of leukemia.
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PMID:Myelogenous leukemia evolving during the course of lymphoid malignancy in children. 29 24

Despite the incomparability in the reporting of leukemia and lymphoma incidence among populations and the relative rarity of these diseases, real differences in rates are discernible from available data. In general, the incidence of each of the leukemias and lymphomas is lower in Japan than in other Pacific rim populations whose rates are known. Particularly striking is the low incidence of CLL in Japan. Among Japanese in Hawaii, rates of some of these cancers (lymphosarcoma, CML) approach those of whites, whereas rates of other cancers (Hodgkin's disease, multiple myeloma, ALL, CLL, and AML) more closely resemble those of native Japanese. The number of Chinese living in countries served by population-based cancer reporting systems is too small for any firm conclusions to be made about leukemia and lymphoma incidence in this group. The incidence of these diseases in certain other nonwhite Pacific rim residents (i.e., Mexican Americans, blacks, and Maoris) is, by and large, similar to that of whites.
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PMID:Geographical variation in the incidence of the leukemias and lymphomas. 29 90

In a groups of 254 patients treated for Hodgkin's disease with a follow up period of minimum 2 years, 3 cases of acute non lymphoid leukaemia (ANLL) were observed: erythroleukaemia, myelomonocytic and myeloblastic leukaemia, respectively. The crude incidence of leukaemia in all patients was 0.0128 and patient year risk was estimated to be 0.003652. All 3 patients had received radiation therapy and chemotherapy. In all cases of haemopoietic dysplasia preceded ANLL. Bone marrow chromosome investigations showed an abnormal karyotype in all patients: chromosomal changes were present in 100% of cells and revealed a non-random distribution, the most frequent involvement being clustered to chromosomes nos 11, 17 and 21. Hypodiploidy was prevalent and multiple structural rearrangements, such as markers, rings and minutes, were present in a high percentage of cells. Other changes involved chromosomes nos 5, 7 and 14. Our results are compared with other previously reported cases and possible pathogenetic implications are discussed.
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PMID:Acute non lymphoid leukaemia following Hodgkin's disease. Clinical, biological and cytogenetic aspects of 3 cases. 29 50

It is well known that there are many independent and inter-related clinical and pathologic factors which influence the prognosis of patients with benign and malignant conditions. Lymphocyte level is an index of cell-mediated immunity which is important in host defense against cancer. But it is surprising that a simple test such as peripheral lymphocyte count could be correlated with clinical stages and survival results in patients with Hodgkin's disease, non-Hodgkin's lymphoma and non-lymphomatous solid tumors. Regarding the latter, lymphocyte count had prognostic values in patients with cancer of the bone, Ewing's sarcoma; breast; colon; kidney, neuroblastoma; uterine cervix, and other sites. In general, higher lymphocyte counts before therapy correlated with longer survival. Using newer immunologic techniques, T and B lymphocytes can be identified and the different subtypes of leukemia, immunodeficiency and lymphoproliferative diseases have been studied intensively. Chronic lymphocytic leukemia represents a proliferation of B cells, while the Sezary syndrome represents that of T lymphocytes. There is a qualitative and quantitative disturbance of Blymphocytes in patients with multiple myeloma. In Hodgkin's disease, there is hyperactivity of the B cells and functional defect of the T cells. Finally, the nodular non-Hodgkin's lymphoma resulted from neoplastic transformation of the B lymphocytes. In several nonmalignant autoimmune conditions, abnormality of T-cell or B-cell counts has been reported. For example, T cells were reported to be decreased in patients with ulcerative or granulomatous colitis and in patients with rheumatoid arthritis, However, it needs to be pointed out that, in 1973, Farid and associates (44) reported a significant increase in T and a proportionate reduction of B rosette in 17 patients with untreated Grave's disease and 16 with Hashimoto's thyroiditis as compared with 24 normal and eight goiter controls. In 1975, six publications later, they (143) had to announce a retraction because further studies by them and by other investigators could not repeat the earlier results. Despite variations and lack of standardization of the test systems, some consistent deviations of T-lymphocyte and B-lymphocyte counts have been reported. T lymphocytes were quantitatively decreased in patients with carcinoma of the brain, breast, head and neck, liver, lung and urologic organs and with malignant melanoma. In general, there is a marked decrease of T cells with increasing stage of disease and a return of T cells to normal level after successful therapy. Cellular immunity is depressed, often lasting for years after localized radiation therapy, whether or not the thymus is included in the treatment field...
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PMID:Peripheral lymphocyte count and suppopulations of T and B lymphocytes in benign and malignant diseases. 30 Jan 79

Four patients with chronic lymphatic leukaemia, M. Hodgkin and metastatic breast carcinoma developed particularly severe generalised herpes zoster, with complications of herpes zoster pneumonia, signs of encephalitis and phrenic nerve paresis. Virus specific complement-fixing antibodies increased regularly or delayed, without strict correlation to the clinical course. However, in all these cases there was a relative or absolute deficiency of T-lymphocytes in the peripheral blood, as a result of the underlying illness and of treatment with cytostatic agents. Because of the vital role of cell-mediated immunity in the control of the varicella-zoster virus (VZV), the observed T-cell deficiency seems to be an important pre-condition for the development of severe generalised herpes zoster.
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PMID:[Severe generalized courses of zoster due to cellular immunologic defects. Importance of an absolute or relative T-cell deficiency]. 30 13

A patient who developed an immunoblastic leukemia of T-cell type two and one half years after initial diagnosis of mixed cellularity Hodgkin's disease, stage IIIB, is described. The patient's course was characterized by an initial 15-months remission following radiation therapy. A relapse of Hodgkin's disease was treated with intensive chemotherapy. Thirteen months later the patient entered a rapid terminal course with multiple organ infiltrates and a leukemic peripheral blood. The leukemic phase was characterized by a 55,000 WGC with 48% immunoblasts, greater than 90% of which marked as T-cells. Although acute myelogenous leukemia, acute lymphocytic leukemia, lymphosarcoma cell leukemia and other tumors have been described in Hodgkin's disease after intensive therapy, this is the first report of the unusual association of a T-cell immunoblastic leukemia with Hodgkin's disease.
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PMID:Hodgkin's disease terminating in a T-cell immunoblastic leukemia. 30 39

Human lymphocytes from peripheral blood, bone marrow spleen and lymph nodes were cultured. Continuous phytoheamagglutinin (PHA) stimulation was used, first during a 24 h liquid preincubation, then during a 5 day culture in methylcellulose. In normal donors a rapid colony formation took place, with a mean of 124+/-82 colonies per 1 times 10(5) preincubated lymphocytes. Cells from such colonies were studied by cytology, scanning electron microscopy and rosette formation techniques; arguments favour the hypothesis that these could be T lymphocytes. Neither granulocytes nor macrophages could be grown, and no lymphoid colony formation occurred without PHA stimulation. The same technique was applied to patients with various lymphoproliferative disorders. Significant colony suppression was observed in nearly every case of chronic lymphatic leukaemia; the number of colonies was reduced in some patients with acute lymphatic leukaemia, lymphosarcoma, dysglobulinaemia and Hodgkin's disease. This lymphoid culture method should be applied to a larger number of patients to determine whether it has a classification value and/or prognostic significance. When colonies were grown in pathological states, rosette formation was identical to that of normal donors; colony formation could be due to persisting normal lymphocytes.
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PMID:T-lymphocyte colonies in the lymphoproliferative disorders. 30 52

Cytochemical identification of T lymphocytes on the basis of alpha-naphthyl acetate esterase (NAE) activity was compared with immunologic markers for cell suspensions and/or cryostat sections of 113 specimens. Nonneoplastic tissues (peripheral blood, lymph nodes, spleens, tonsils, thymus, and pleural fluid) and specimens from various lymphoproliferative disorders, including acute and chronic lymphocytic leukemia, lymphosarcoma cell leukemia, hairy cell leukemia, non-Hodgkin's lymphomas of B-and T-cell types, and Hodgkin's disease, were evaluated. T (E-rosetting) cells demonstrated several patterns of NAE reactivity: 1) a strong globular reaction product, the most specific pattern for T-cell identification, 2) granular cytoplasmic staining, or 3) no reactivity. B lymphocytes revealed a granular pattern of NAE staining, were devoid of enzyme, or, in rare instances, exhibited strong NAE activity. Percentages of lymphoid cells with strong (globular) NAE activity closely paralleled T-cell (E-rosette) values in the majority of cases, with the best correlations observed for peripheral blood studies. However, discordant results were noted for some neoplastic and nonneoplastic tissues, including cases of T-cell lymphoma or leukemia. Markedly discrepant results were noted for thymic lymphocytes, most of which revealed E-rosette formation and weak or absent NAE activity. Lymph nodes involved by Hodgkin's disease demonstrated a heterogeneous pattern of staining in E-rosetting cells and in Reed-Sternberg variants. Cryostat section studies of reactive lymph nodes and nodular lymphomas demonstrated strong NAE staining in lymphoid cells of T-cell (interfollicular, internodular) areas, with little or no positivity in follicles or nodules (B-cell areas). NAE staining patterns further suggested that T cells comprise part of the follicular cuff and possibly represent a minor population of some neoplastic nodules. Although NAE determinations do not represent a consistently reliable alternative to immunologic methods for T-cell identification, this easily applicable cytochemical marker is complementary to other techniques in assessing neoplastic or nonneoplastic tissues, particularly cryostat sections. (Am J Pathol 97:17--42, 1979).
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PMID:alpha-Naphthyl acetate esterase activity--a cytochemical marker for T lymphocytees. Correlation with immunologic studies of normal tissues, lymphocytic leukemias, non-Hodgkin's lymphomas, Hodgkin's disease, and other lymphoproliferative disorders. 31 66


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