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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper we review our experience with HIV-related thrombocytopenic purpura (TP) in 24 patients seen from October, 1985 through April, 1988: the median follow-up was 16 months (range 3-32). All patients belonged to risk groups for AIDS and intravenous drug abusers represented 83% of the entire cohort. The male/female ratio was 4, and most of the patients were Walter Reed stage 3. The mean value of platelets at diagnosis was 33 x 10(9)/liter (range 6-120), and half of the patients had severe thrombocytopenia with hemorrhagic symptoms. Anemia and/or neutropenia were concomitant with TP in 21% and 17% of cases; four cases had pancytopenia. Marrow pictures showed megakaryocytic hyperplasia in 68% of cases; myelodysplasia or hypoplasia were observed in 14% and 18% of patients, respectively; lymphoid aggregates were present in two cases. Antiplatelet antibodies and circulating immune complexes were detected in 40% and 50% of cases, and the mean T4/T8 ratio was 0.9 (range 0.4-1.8). Half of the patients did not require specific therapy due to lack of bleeding; however no spontaneous reversions to normal platelet values occurred. The response to steroids and to immunoglobulins (either high-dose or anti-D) was good but temporary, and required maintenance therapy. The 2-year actuarial risk of evolution into overt AIDS was 30%, with a crude rate of 4 cases over 365 person-months at risk. The events which determined AIDS were opportunistic infections in two cases, Kaposi's sarcoma and malignant lymphoma in the other two. A comparison with the features of idiopathic TP is made and hypotheses regarding the pathogenetic mechanisms are discussed.
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PMID:HIV-related thrombocytopenic purpura: a study of 24 cases. 249 84

Physical characteristics of bone marrow cells of normal donors were comparatively studied with those of children with immune neutropenia. As a result of the bone marrow cell separation in the density gradient according to their sedimentation rate, fractions enriched with cells of one histogenetic series (lymphoid, erythroid and granulocytic) were obtained. Electrophoretic mobility of immature granulocytes in normal donors differed from that in children with immune neutropenia.
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PMID:[Two-dimensional size-charge distribution of bone marrow cells in children with chronic immune neutropenia]. 258 63

In a series of 320 patients with lymphoid neoplasms treated with polychemotherapy, three patients with non-Hodgkin's lymphoma and one with myeloma were diagnosed as having neutropenic enterocolitis (NEC). All patients were adult, all had received multiple chemotherapeutic drugs and, during neutropenia, they had clinically presented with fever and abdominal pain, generally in the right lower quadrant. The diagnosis was clinical in all cases, and the imaging techniques provided only the suspicion of retro-cecal abscess in one of them. Two patients were operated on because of the development of features of peritoneal involvement, another because of septic shock and another because of retro-cecal abscess. Surgery and pathological study confirmed the diagnosis. The fundamental findings were ileocecal wall edema, mucosa ulceration, local necrosis, hemorrhage and thrombosis, and clusters of bacterial colonies without evidence of granulocytic or tumoral infiltration. NEC can develop with varying types of morphological involvement resulting in a highly variable clinical severity spectrum ranging from nonspecific abdominal symptoms to acute abdomen. Thus, diagnosis is very difficult and is only possible with a high suspicion index. It should rely on clinical data, which are unique, to assess the evolution and to indicate medical or surgical therapy. These therapeutic modalities should be individualized in each patient. All physicians treating neutropenic patients should be familiar with this condition and consider it in the differential diagnosis of abdominal pain.
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PMID:[Neutropenic enterocolitis during treatment of lymphoproliferative neoplasms]. 261 46

Colony-stimulating factors (CSFs) have entered the clinical arena. Several investigators have explored, in first clinical phase I studies, different routes of administration to define the optimum biological dose, maximum tolerated dose, toxicity, and pharmacokinetics of these reagents. It has been demonstrated that recombinant human (rh) granulocyte-macrophage CSF (GM-CSF) and granulocyte CSF (G-CSF) can be safely administered over a broad dose range to increase number of circulating granulocytes in man. More recently, GM-CSF and G-CSF have been involved in phase Ib/II studies to assess the granulopoietic responses of patients with granulocytopenia due to various underlying disease states including myelodysplastic syndrome, aplastic anemia, cyclic neutropenia, Kostmann's syndrome, and the acquired immuno-deficiency syndrome. Both factors were also investigated with respect to their potential to prevent chemotherapy induced granulocytopenia or to accelerate recovery from that condition. The short-term effects of rh GM-CSF after autologous bone marrow transplantation for various solid tumors and lymphoid malignancies were assessed as well. In this article we will focus on recent results that have emerged from in vivo studies utilizing CSFs.
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PMID:Polypeptides controlling hematopoietic blood cell development and activation. II. Clinical results. 265 Jul 57

Adult wild-trapped opossums were infected with Leishmania donovani (Khartoum strain, WR 378) and evaluated as an animal model of visceral leishmaniasis. All infected opossums died within 32 days. Loss of body fat, hepatomegaly, and petechiae of skin and abdominal musculature were seen at necropsy. Microscopically, numerous amastigote-laden macrophages were seen in histologic sections of liver, spleen, and lymph nodes; fewer parasite-laden macrophages were in the bronchial-associated lymphoid tissues and renal glomeruli. Hematological findings included thrombocytopenia (terminal), neutropenia, and lymphopenia. Blood lymphocyte blastogenesis in response to concanavalin A and phytohemagglutinin was decreased markedly at day 24 post-infection (PI). Serum antibodies (1:40 dilution) to promastigotes of L. donovani were detected in five of eight infected opossums tested on days 10 and 24 PI. Total bilirubin concentrations and alanine aminotransferase and aspartate aminotransferase activities were increased after day 25 PI. Activated partial thromboplastin times and one-stage prothrombin times were prolonged before death. Concurrently, factors V, VIII, and XII activities were decreased.
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PMID:Experimental visceral leishmaniasis in the opossum. 276 21

The authors studied 35 marrow biopsies from 32 patients with rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, polymyositis, and psoriatic arthritis. Reasons for biopsy included cytopenia, fever of unknown origin, and malignancy. Cellularity was abnormal in 71%. Plasma cells were increased in 60% and associated with lymphoid aggregates. Immunoperoxidase stains showed polyclonal perivascular plasma cells and increased T-cells forming lymphoid aggregates. Two patients had granulomas without documented infection. Anemic patients had findings consistent with anemia of chronic disease, erythroid aplasia, hemolysis, and iron deficiency. Iron stores were variable. Platelet and granulocyte precursors were variably altered and did not predictably correlate with the presence, absence, or cause of thrombocytopenia and neutropenia. Myelodysplastic syndromes were present in two patients with rheumatoid arthritis. Osteomalacia and osteoporosis were seen, resulting from renal failure and steroids. Marrow findings are unpredictable and reflect the diverse causes of cytopenias in patients with connective tissue disorders.
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PMID:Bone marrow findings in connective tissue disease. 281 17

Sixty cats with hematologic abnormalities indicative of non-lymphoid hematopoietic neoplasia were classified into two groups, myelodysplastic syndromes (MDS) and acute myelogenous leukemias (AML), using criteria developed for human patients with similar diseases. Cats with myeloblast counts in bone marrow of less than 30% were classed as MDS and cats with myeloblast counts of 30% or greater were classed as AML. The clinical, laboratory, and postmortem findings in each group were described and compared. Clinical signs of disease were similar in both groups, the most common being inappetance, lethargy, and weakness. Non-regenerative anemia, macrocytosis, neutropenia, and thrombocytopenia were frequent hemogram abnormalities in both groups. Diagnostically useful differences in physical and peripheral blood findings were a higher prevalence of splenomegaly and/or hepatomegaly, thrombocytopenia, and severe anemia in the AML group. Circulating myeloblasts were found only in cats in the AML group. Outcome of disease was similar in both groups; 85% of the cats in each group died or were euthanatized within one week of diagnosis. In cats that were necropsied, extramedullary leukemic infiltrates were found in all cats in the AML group and in none of the cats in the MDS group.
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PMID:Non-lymphoid hematopoietic neoplasia in cats: a retrospective study of 60 cases. 282 80

gamma-Glutamyltranspeptidase (GGT) activity (per mg protein) in blood lymphoid cells of 27 children with acute lymphoblastic leukemia (ALL) (1.05 +/- 0.15) was significantly below that of controls (2.25 +/- 0.30), became normalized during chemotherapy-induced remission (2.47 +/- 0.26), and was low again (1.59 +/- 0.62) in relapsed subjects. Individual variations in the GGT activity of the blood lymphoid cell fraction (per mg protein) bore a significant inverse correlation to the number of white blood cells (WBC) as well as of blasts per ml blood. Blasts had minimal GGT activity; however, partial GGT deficiency was also exhibited by the microscopically normal circulatory lymphocytes of several patients prior to treatment and in relapsed subjects whose blood was still devoid of blasts. Significantly diminished GGT activity (per mg protein) was found in the blood granulocytes of ALL subjects. This deficit, restored during remission and present again at relapse, varied in magnitude but showed no statistically significant correlation to the different patients' degree of neutropenia. In about one-third of the newly diagnosed or relapsed pre-B ALL children, the circulatory granulocytes' GGT activity was only 10-20% of normal. The results suggest that 1) the presence or absence of this sign of functional maldifferentiation in granulocytes is a factor in the heterogeneity of disease manifestation among subjects with apparently the same type of ALL and that 2) measurement of GGT in the circulatory granulocytes, as well lymphocytes, may be useful for monitoring the efficacy of chemotherapy.
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PMID:Diminished lymphocyte and granulocyte gamma-glutamyltranspeptidase activity in acute lymphocytic leukemia and response to chemotherapy. 288 7

Morphologically distinct lymphoid cells with homogeneous, condensed chromatin and scant cytoplasm can be observed in large numbers in the bone marrow of children with a variety of hematologic and nonhematologic disorders. In some patients, these cells may account for greater than 50% of the bone marrow cells, creating a picture that can be confused with acute lymphoblastic leukemia (ALL) or metastatic tumor. Although originally called hematogones (HGs), a variety of other names have been proposed for these unique cells. The clinical significance of expanded HGs has not been resolved, and the biologic features of these cells are incompletely described. In this study, we correlate the clinical, morphologic, cytochemical, flow cytometric, molecular, and cytogenetic properties of bone marrow samples from 12 children with substantial numbers of HGs (range 8% to 55% of bone marrow cells). Diagnoses in these patients included anemia, four; neutropenia, one; anemia and neutropenia, one; idiopathic thrombocytopenic purpura, two; retinoblastoma, two; Ewing's sarcoma, one; and germ cell tumor, one. Flow cytometric analyses of bone marrow cells demonstrated a spectrum extending from early B-cell precursors (CD10+, CD19+, TdT+, HLA-Dr+) to mature surface immunoglobulin-bearing B cells in these patients, corroborating our morphologic impression of HGs, intermediate forms, and mature lymphocytes. DNA content was normal, and no clonal abnormality was identified by either cytogenetic or immunoglobulin and T-cell receptor (TCR) gene rearrangement studies. Follow-up ranged from 3 months to 3 years. None of the patients has developed acute leukemia or bone marrow involvement by solid tumor. The possible role of HGs in immune recovery and hematopoiesis is presented.
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PMID:Hematogones: a multiparameter analysis of bone marrow precursor cells. 291 89

The association of neutropenia with an indolent chronic T-suppressor cell lymphoproliferative disorder (LPD) has been well documented. The morphologic features and course suggest that this is a benign disorder. The authors studied a 58-year-old man with a chronic T-cell LPD, splenomegaly, and neutropenia. Chromosomal analysis revealed multiple abnormalities which progressively increased in number as the marrow lymphocytosis became more prominent. Subsequently he developed small bowel infiltration. A splenectomy resulted in only brief improvement in the neutropenia. Immunopathologic examination of the spleen was consistent with a well-differentiated lymphocytic lymphoma of a mature peripheral T-cell type without subset specific markers. Granulocyte-monocyte colony (CFU-GM) formation from the patient's marrow was normal and not augmented by T-cell depletion. Neither the patient's splenic T-cells nor serum suppressed granulopoiesis. In contrast to previous T-LPD with neutropenia whose malignant nature has been questioned, the clinical, cytogenetic, and pathologic features and course in this case indicate a malignant lymphoid process which was effectively treated with chemotherapy. Although the histologic pattern of red pulp involvement simulated hairy cell leukemia, that diagnosis was excluded by this patient's clinical, morphologic, and cytochemical features.
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PMID:A unique malignant T-cell lymphoproliferative disorder with neutropenia simulating hairy cell leukemia. 293 14


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