Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used the membrane fluorescence and the rosette formation test to study the lymphocyte populations in 25 patients with untreated chronic lymphocytic leukemia (CLL). The results show a significant increase, absolute and percent of S-Ig bearing cells, whereas the E and EA rosette forming cells are decreased in per cent, increased in absolute. The number of lymphocytes with the receptor for the Fc fragment of IgG, is unchanged. The lymphocytosis causes mainly a significant decrease in percentage of E rosette forming cells. A big splenomegaly and a bad clinical stage, according to Rai et al. classification, are responsible for a decrease of E, EA, EAC rosette forming cells; unchanged the percentage of S-Ig bearing cells. Such a modification of the surface receptor pattern is present not only in those CLL more advanced in clinical stage and with hyperleucocitosis and/or splenomegaly, but also in those forms with worse clinical feature and prognosis. Our work confirms that CLL is mainly a B proliferative disease; we observed only one case due to T cell proliferation. Four cases were impossible to classify immunologically: one had no cells bearing the markers, three had a subnormal surface receptor pattern.
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PMID:[Lymphocyte typing in chronic lymphoid leukemia]. 30 12

Lymphocyte subpopulations in thirty-nine patients with the tropical splenomegaly syndrome (TSS) were studied using the E-rosette, EAC rosette and direct immunofluorescent staining techniques. In the peripheral blood a decrease in the percentage of T-lymphocytes was found which was accompanied by an increase in the percentage and number of B-lymphocytes. These abnormalities reverted towards normal on treatment. Splenic aspirates contained an increased proportion of T-lymphocytes. The relative T-cell lymphoenia in TSS is probably due to specific trapping or non-specific sequestration of lymphocytes in the liver and splen. B-cell lymphocytosis is probably due to persistent antigenic or mitogenic stimulation by malaria.
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PMID:T- and B-lymphocyte subpopulations in the tropical splenomegaly syndrome (TSS). 30 10

A 68-yr-old male with chronic lymphocytic leukemia (CLL) presented with splenomegaly and skin infiltration but no lymphadenopathy. The peripheral blood WBC cound was 300 x 10(9)/liter, with 95% small mature-appearing lymphocytes that were E-rosette positive and EAC-rosette negative. Further characterization of the patient's cells was performed using antisera with known lymphoid sub-population specificity. Anti-p23,30, which reacts with normal circulating B cells but not with T cells or thymocytes, was unreactive with the patient's cells. Anti-311, which reacts with both thymocytes and circulating T cells, was reactive with the patient's cells. Anti-Bk, which reacts only with thymocytes and not with circulating T-cells, failed to react with the patient's cells. The enzyme terminal deoxynucleotidyl transferase, present in thymocytes but absent for circulating T-cells, was also absent from the patient's lymphoid cells. Multimarker analysis therefore showed a mature T-lymphocyte phenotype on this patient's leukemia cells. Further functional analysis will probably show that such cells represent clonal expansion of a mature T-cell subpopulation, analogous to the B-cell clonality of common-variant CLL.
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PMID:Multimarker analysis of T-cell chronic lymphocytic leukemia. 34 7

A case of acute lymphoblastic leukemia with a giant splenomegaly in an 8-year-old boy was investigated by immunological, cytochemical and electronmicroscopical techniques. Bone marrow and peripheral blood were largely replaced by large blast cells with a nonconvoluted nucleus. Cytochemically, most of the blast cells showed strong focal acid phosphatase activity. In the surface marker studies, these blast cells formed EAC rosettes but not E rosettes, while they showed positive reactivity with anti-T lymphocyte serum but not with anti-B lymphocyte serum. This membrane phenotype E-, C3R+, T+, B- suggested that leukemic blast cells in this patient presumably originated from precursor T cells.
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PMID:Precursor T cell leukemia--immunological, cytochemical and morphological studies. 697 49