Immune Pancytopenia

Daneshbod-Skibba, Ghodsi; Shahidi, Nasrollah T.; Becker, G. A.; Martin, Jean‐Charles

doi:10.1111/j.1365-2141.1979.tb03714.x

Cited by 10 publications

(4 citation statements)

References 25 publications

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“…Recent observation indicated that lymphocytes, especially T lymphocytes, may play a role in the pathogenesis of aplastic anemia (5,6,(24)(25)(26). Furthermore, Bagby and Gabourel (27) reported the T lymphocyte-mediated suppression of granulopoiesis in rheumatic disorders, and Abdou et a1 (28) reported the suppressor cell-mediated neutropenia in Felty's syndrome.…”

Section: Discussionmentioning

confidence: 99%

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Granulopoiesis in systemic lupus erythematosus

Yamasaki

Niho

Yanase

1983

Arthritis & Rheumatism

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The pathogenesis of granulopoietic failure in systemic lupus erythematosus (SLE) was studied. In 16 Japanese women with SLE, a decreased number of granulocyte/monocyte progenitor cells (CFU‐C) in the bone marrow was demonstrated, and the number of CFU‐C correlated significantly with the peripheral blood granulocyte/monocyte count. The peripheral and bone marrow T lymphocytes suppressed the colony formation of autologous or allogeneic bone marrow CFU‐C. These findings suggest that the decreased marrow CFU‐C may be due to suppression by T lymphocytes, an event that may play an important role in the pathogenesis of granulopoietic failure in SLE.

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Section: Discussionmentioning

confidence: 99%

“…Patients 3, 12, Arthritis and Rheumatism, Vol. 26 and 16 had previously received corticosteroid therapy for a short time, and patients 7,8, 11, and 14 had previously been treated with nonsteroidal antiinflammatory drugs for a short time. Only patient 8 had been given a blood transfusion.…”

Section: Methodsmentioning

confidence: 99%

Granulopoiesis in systemic lupus erythematosus

Yamasaki

Niho

Yanase

1983

Arthritis & Rheumatism

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“…This proposal was based upon favorable effects of immunosuppressive therapy in vivo, and upon improved in vitro colony formation of CFU-c, CFU-e and BFU-e after removal of T lympho cytes and/or monocyte-macrophages [1,2,4,6,17]. Removal of T lymphocytes from our patient's bone marrow caused an increase particularly of the BFU-e com partment.…”

Section: Discussionmentioning

confidence: 99%

“…T-cell-mediated suppression of hemato poietic progenitor cells has been suggested as a likely mechanism of aplastic anemia [1,2,4,6]. This proposal was based upon favorable effects of immunosuppressive therapy in vivo, and upon improved in vitro colony formation of CFU-c, CFU-e and BFU-e after removal of T lympho cytes and/or monocyte-macrophages [1,2,4,6,17].…”

Section: Discussionmentioning

confidence: 99%

A Case of Acquired Pure Red Cell Anemia Studied by Cloning of Erythroid Progenitor Cells in vitro

Konwalinka¹,

Huber²,

Tomaschek³

et al. 1983

Acta Haematol

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A 70 year-old woman developed typical clinical symptoms of pure red cell anemia (PRCA) following a history of rheumatoid arthritis (RA). The patient’s bone marrow erythropoietic progenitors cells were cloned in a micro agar culture system several times over a period of 11 months, revealing a diminished frequency of bone marrow erythroblasts paralleled by a markedly reduced number of CFU-e and BFU-e in vitro. No inhibitory activity in the patient’s IgG fraction could be detected either by preincubation with IgG and/or rabbit complement, or in the continuous presence of IgG. Depletion of T lymphocytes from the patient’s bone marrow cells led to an improved in vitro erythroid proliferation. Cytostatic therapy with cyclophosphamide clinically induced a marked increase in the bone marrow erythroblast and reticulocyte number, correlated in vitro by normalization of CFU-e levels and increase in the number of BFU-e. Nevertheless, BFU-e values never attained normal levels, which could be attributed to a reduced stem cell pool resulting from previous therapy with cyclophosphamide and/or antirheumatic drugs. Two independent factors, a reduced pool of committed stem cells as well as an autoimmune cell-mediated suppression, may both contribute to the pathomechanism of the disease in this patient.

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CFU‐gm assay, cytochemical and electron microscopic studies in agar in patients with preleukemic syndrome and aplastic anemia

Konwalinka

Peschel

Schmalzl

et al. 1985

The International Journal of Cell Cloning

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Thirty-seven patients with chronic cytopenia were studied using a CFU-gm assay in agar. Cell proliferation was evaluated on days 2, 3, 5, 7, and 10 of incubation. Growth patterns were different in cultures of hematologically healthy persons versus patients with preleukemic syndrome (PL) and aplastic anemia (AA). Three types of PL syndrome and two types of AA (C1 and C2) were distinguished. Bone marrow dysfunction was evaluated further using cytochemistry and electron microscopy to morphologically study cell proliferation in vitro. Cytochemical staining performed in agar demonstrated well-defined maturation defects in myelopoietic precursor cells from the bone marrow of PL patients. Electron microscopic findings of Auer-body-like inclusions in "statu nascendi" in the vacuoles of preleukemic cells supported our results. PL patient groups at high risk for development of overt leukemia and patients with grave prognosis in AA were distinguished. Our results are relevant for the clinical diagnosis and prognosis of patients with cytopenia.

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Immune Pancytopenia

Cited by 10 publications

References 25 publications

Granulopoiesis in systemic lupus erythematosus

Granulopoiesis in systemic lupus erythematosus

A Case of Acquired Pure Red Cell Anemia Studied by Cloning of Erythroid Progenitor Cells in vitro

CFU‐gm assay, cytochemical and electron microscopic studies in agar in patients with preleukemic syndrome and aplastic anemia

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