Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunotherapy with interleukin-2 (IL-2) and lymphokine-activated killer (LAK) cells generated from autologous lymphocytes has produced significant tumor regressions in patients with advanced cancer. In the current study, we reviewed the hematologic effects associated with this therapy in our initial 42 patients. Eighty-eight percent of the treated patients developed anemia that required greater than or equal to 4 units of red cell transfusions, and 43% received at least 8 units. Only a blood loss of 2 to 3 units could be attributed to repeated phlebotomy, cytophereses, and hemodilution. IL-2 administration also resulted in thrombocytopenia as well as lymphopenia and eosinophilia. Forty-three percent of patients developed platelet counts of less than or equal to 50,000/microL, and 36% of the total group required platelet transfusions. Mild neutropenia and a rebound lymphocytosis followed discontinuation of IL-2 treatment. To explore the possible mechanisms for these hematologic effects, standard hematopoietic colony assays were conducted on serial blood samples from five patients. IL-2 produced a significant decline in circulating erythroid (BFU-E) and granulocytic/macrophage (CFU-C) progenitors, which rebounded after the discontinuation of IL-2 therapy. Infusion of IL-2 also resulted in measurable serum levels of gamma-interferon. Some of the hematologic effects of immunotherapy with LAK cells and IL-2 may be the result of IL-2-mediated suppression of hematopoiesis.
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PMID:Hematologic effects of immunotherapy with lymphokine-activated killer cells and recombinant interleukin-2 in cancer patients. 349 2

A characteristic of the trichothecene mycotoxin, anguidine, is its extreme toxicity to organs with populations of rapidly dividing cells. In preparation for evaluation of compounds that may protect against anguidine toxicity, we measured the LD50 of anguidine administered by gastric gavage (ig) or intraperitoneal injection (ip) and studied the dose- and time-dependent effects of anguidine on lymphohematopoietic organs, intestine, and testis, and measured hematocrit and peripheral blood leukocyte counts in male CD-1 mice. The ig LD50 at 96 hr was 15.5 mg/kg; after ip administration the LD50 at 96 hr was 20.0 mg/kg. Characteristic changes caused by sublethal doses of anguidine were cell depletion and necrosis in lymphohematopoietic organs, multifocal necrosis of intestinal epithelium, and diffuse necrosis of germinal epithelium followed by progressive tubule degeneration in the testes. There was leukocytosis due to both lymphocytosis and neutrophilia in the first few hours following anguidine exposure, followed by lymphopenia, neutropenia, and anemia by 3 days. After lethal doses, the intestinal necrosis was transmural, and there was extensive necrosis of lymphohematopoietic organs. There was rapid recovery after sublethal anguidine exposure of all anguidine-sensitive organs except for testis where decreased weights and abnormal spermatogenesis persisted for the 2-week observation period. Our results suggest that intestinal necrosis is an important cause of death following anguidine exposure. Atrophy of seminiferous tubules may have some value as an indicator of prior anguidine exposure, but the testicular changes are not unique to this compound.
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PMID:Toxicity of anguidine in mice. 373 67

Absolute lymphocytosis after nonsurgical trauma was investigated in three patient groups at an acute-care tertiary referral hospital. The first group, with mild-to-moderate trauma, consisted of 64 patients who survived knife wounds to the chest and abdomen. Thirteen of the 64 patients had admission lymphocyte counts greater than 5.0 X 10(9)/L (mean +/- SD: 6.0 X 10(9) +/- 2.4 X 10(9]. Within 24 hours, all 13 showed a significant drop in lymphocyte count to 1.9 X 10(9) +/- 0.9 X 10(9)/L. The second group, with severe trauma, consisted of 11 patients admitted to the intensive care unit. Admission lymphocyte values averaged 5.9 X 10(9) +/- 0.6 X 10(9)/L and decreased to 1.54 X 10(9) +/- 0.3 X 10(9)/L within six hours. The relative importance of trauma as a cause of lymphocytosis was established by reviewing all hospitalized patients with lymphocyte counts greater than 5.0 X 10(9)/L between August 1983 and October 1985. The survey indicates that trauma and hemorrhage account for 16% of all cases of lymphocytosis, and that trauma, together with other acute stresses, constitutes the most common cause of lymphocytosis studied. The authors conclude that trauma is frequently associated with a lymphocytosis that usually changes to a lymphopenia within hours of injury.
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PMID:Absolute lymphocytosis associated with nonsurgical trauma. 376 60

1. In mice rendered lymphocytopenic by X-irradiation or hydrocortisone acetate, pertussis vaccine evoked both lymphocytosis and polymorphonuclear leukocytosis. 2. When mice with lymphocytosis induced by pertussis vaccine were X-irradiated, prompt and extensive destruction of circulating as well as tissue small lymphocytes occurred. The devitalized circulating cells were cleared from the blood primarily by the Kupffer's cells of the hepatic sinusoids. 3. Hydrocortisone acetate administered to mice with lymphocytosis did not cause acute lymphopenia nor was there any evidence of destruction of circulating small lymphocytes. However, destruction of these cells within lymphoid tissues was apparent. These observations suggested that adrenal cortical hormones are not "lymphocytolytic" with respect to circulating lymphocytes.
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PMID:The effect of hydrocortisone and x-irradiation on the lymphocytosis induced by Bordetella pertussis. 428 58

When neonatally thymectomized CBA mice were implanted at 9 to 12 days of age with Millipore diffusion chambers (pore size, 0.1 micro) containing either syngeneic or allogeneic neonatal thymus, they were subsequently found to have the capacity to reject skin homografts and to form antibodies to sheep erythrocytes. In spite of displaying restored immune reactivity, thymectomized mice bearing thymus-filled diffusion chambers still had a lymphopenia and diminished numbers of small lymphocytes in their spleens, lymph nodes and Peyer's patches. Comparison of the lymphoid organs of these mice with those of the thymectomized control mice did not reveal any appreciable difference in the numbers of primary follicles or small lymphocytes. It is postulated that the thymus humoral factor induced immunological competence in lymphoid cells which had left the thymus prior to neonatal thymectomy. The paucity of circulating and tissue small lymphocytes in thymectomized animals, the immune reactivity of which was restored by thymus tissue in diffusion chambers, argues against the theory that the thymus humoral factor has a lymphocytosis-stimulating effect. There was no restoration of immune reactivity in those neonatally thymectomized mice which had been implanted with diffusion chambers containing neonatal or adult spleens, or adult lymph nodes. Thus, the competence-inducing factor is elaborated by the thymus but not by the spleen or lymph nodes. Allogeneic (C57Bl) neonatal thymus tissue, enclosed within diffusion chambers, had the capacity to restore the immune reactivity of totally thymectomized CBA mice, not only to skin homografts of a totally unrelated strain (Ak), but also to grafts isogeneic with the donor of the allogeneic thymus. Therefore, there is no strain barrier to the action of thymus humoral factor. To explain the apparent lack of full participation of thymus lymphocytes in immune reactions it is postulated that thymus lymphocytes are functionally immature in situ, and that they leave the thymus before attaining immunological competence. In the periphery, they undergo further maturation under the influence of the competence-inducing factor produced by the thymus.
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PMID:The effects of thymus and other lymphoid organs enclosed in millipore diffusion chambers on neonatally thymectomized mice. 532 Apr 32

Staphylococcal enterotoxin A (SEA) administration to monkeys produced an initial lymphocytic leukopenia lasting approximately 24 h. Lymphocytes isolated from blood circulation (PBL) during this stage had normal or decreased [3H]thymidine incorporating activity. After 48 h, however, a significant increase (five- to sixfold) in [3H]thymidine incorporating activity into PBL was apparent. The peak of incorporating activity (seven- to eightfold) was reached 3 to 4 days after SEA administration, followed by a gradual decline, reaching the baseline after 2 weeks. The increased levels of [3H] thymidine incorporation in PBL were concomitant with the conversion of lymphopenia into lymphocytosis, accompanied by the release of many immature cells into the circulation. Lymphocytes isolated 24 h after SEA administration in vivo did not respond to the mitogenic action of SEA in vitro. Lymphocytes isolated at later stages after SEA challenge were fully activated by toxin. From a series of studies, it was concluded that SEA administered to monkeys caused, during the initial 24 h, the removal of a great proportion of lymphocytes from the circulation, followed by the release of new immature cells with augmented DNA synthesis activity. The lymphocytic leukocytosis state declined gradually and reached normal levels between 3 and 4 weeks after the SEA challenge. The biological implications of the hematological changes occurring after SEA challenge in vivo are discussed.
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PMID:In vivo effect of staphylococcal enterotoxin A on peripheral blood lymphocytes. 671 41

Nephritis was induced in 300, 18-day-old male Arbor Acre broiler chicks by feeding diets high (42.28%) in protein, high (3.27%) in calcium, containing urea (5%), or deficient in vitamin A. Various hematological parameters were studied at weekly intervals. Normocytic-normochromic anemia, characterized by a decrease in total erythrocyte counts, hemoglobin, packed cell volume, and an increase in erythrocyte sedimentation rate, was evident in the birds kept on diets high in protein, high in calcium, or deficient in vitamin A. Increased total erythrocytes, hemoglobin packed cell volume, and erythrocyte sedimentation rate was observed in birds fed urea. Differential leucocyte counts revealed lymphopenia, heterophilia and monocytosis in birds kept on diets high in protein, containing urea, or deficient in vitamin A. However, lymphocytosis, heteropenia , and monocytosis were recorded in birds fed the high calcium diet.
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PMID:Hematological changes in nephritis in poultry induced by diets high in protein, high in calcium, containing urea, or deficient in vitamin A. 672 70

The absolute count for a particular type of blood cell is the total white blood cell count multiplied by the differential percentage for that cell type. Neutrophilia is caused by increased marrow proliferation, redistribution among body neutrophil pools, stress and corticosteroids. Neutropenia is caused by decreased marrow proliferation, ineffective marrow production, reduced neutrophil survival and redistribution of neutrophils. Lymphocytosis is caused by chronic infections and allergic reactions, while lymphopenia is caused by increased lymphocyte destruction, neoplasia and lymphocyte loss. Monocytosis is associated with stress, infections, hematologic disorders, GI disease, necrosis and hemolysis. Eosinophilia is caused by allergic reactions, parasitism, skin diseases, neoplasia and adrenocortical insufficiency.
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PMID:Interpreting absolute WBC counts. 673 20

The participation of leukocytes in regeneration was studied by determining changes in circulating leukocyte counts following putative immunological manipulations. Splenectomy failed to produce leukopenia during regeneration, although a 24-35% reduction in leukocytes occurred in otherwise intact newts. Bovine serum albumin and anti-lymphocyte serum produced initial lympho- and granulocytopenias, but blood counts soon returned to more normal levels. Lymphocytosis followed treatment with cobra venom factor, but marked lymphopenia occurred shortly thereafter. Regeneration occurred in all cases. These data failed to establish a clear correlation between the nature of quantitative changes in circulating leukocyte levels following these treatments and regenerative capacity.
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PMID:Blood cells and their role in regeneration. II. Effects of putative immunological manipulations on circulating blood cell counts during regeneration. 684 Mar 86

We investigated the effects of carrageenans (CAR) on mouse hematopoiesis, one of the many biologic systems affected by these galactan polysaccharides. Mice were injected intravenously with potassium CAR (K+-CAR) or iota CAR (I-CAR) and studied for 7 or 14 days, respectively, thereafter. Treatment with either compound induces anemia, granulocytosis, and early profound thrombocytopenia. Treatment with I-CAR results in an early lymphocytosis, and both compounds induce lymphopenia by 18 h after treatment. Treatment with either CAR compound is associated with an early moderate reduction in the number of nucleated cells and granulocyte/macrophage colony forming cells (CFUGM) per femur. Both compounds induce splenomegaly, and I-CAR treated mice develop hypoplasia of the thymus by 18 h after treatment. The splenomegaly is associated with intense splenic hematopoiesis and an increase in the number of spleen histiocytes; many of the latter are engorged with metachromatically staining material, most likely CAR. There is a sustained increase in the numbers of spleen CFUGM after treatment with either compound; in the case of I-CAR this may be due to proliferation of CFUGM in this organ, perhaps effected by the increased levels of plasma colony stimulating activity. Although it has been suggested that I-CAR is relatively nontoxic, and, therefore, potentially useful for in vivo studies, our observations indicate that it has profound effects on hematopoiesis which must be considered when planning and interpreting in vivo studies using this compound.
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PMID:Effects of carrageenan on the mouse hematopoietic system. 697 Jan 38


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