Serum Inhibitor in Systemic Lupus Erythematosus Associated With Aplastic Anemia

Brooks, Barbara A.; Broxmeyer, Hal E.; Bryan, Christopher; Leech, Stephen H.

doi:10.1001/archinte.1984.00350190172030

Cited by 37 publications

(21 citation statements)

References 21 publications

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“…These mechanisms include the destruction of peripheral blood cells by circulating autoantibodies [I], the dysreguiation of haematopoietic progenitor cell growth mediated by T lymphocytes and/or monocytes through direct contact and/or abnormal cylokine networks 112-15], and the suppression of progenitor cell growth by humoral inhibitors [2][3][4][5][6].…”

Section: Discussionmentioning

confidence: 99%

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Suppression of haematopoiesis by IgG autoantibodies from patients with systemic lupus erythematosus (SLE)

Liu

Ozaki

Matsuzaki

et al. 1995

Clinical and Experimental Immunology

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SUMMARYThe inhibiting activity of serum on haematopoiesis has been described in patienis with SLE. To explore further the features of serum inhibitor, we first examined the suppression of granulocytic and erythroid colony formation in vitro by serum from palients with SLE using methylcellulose culture. The potent inhibiting activity was demonstrated in six of 20 patients. All of these six patienis were associated with leukocytopenia and/or anaemia. Five of 10 sera from patients with active SLE suppressed the colony formation of both burst-forming units of erythrocyte (BFU-E) and colony-forming units of granulocyte/niaerophage (CFU GM). and one serum suppressed BFU-E only, IgG fraction isolated from sera with inhibiting activity suppressed colony formation without complement involvement. The elimination of monocytes and lymphocytes from target mononuelear cells did not affect Ihe suppression by the IgG fractions. The suppressive effect was completely eliminated after incubation ofthe IgG fractions with progenitor-enriched mononuclear cells. Flow cytometric analysis showed these igG bound to CD34' haematopoietic progenitor cells, but not to CD33^ cells. These data suggest that (i) the inhibitor of colony formation in serum was observed in IgG fraction; (ii) its suppressive efTect on colony formation was mediated by neither monocytes and lymphocytes nor complements; and (iii) IgG fraction could bind to primitive haematopoietie progenitor cells and suppress the growth of these cells. Thus. IgG autoantibodies to primitive haematopoietic progenitor eells are demonstrated to be present in the sera ofa significant proportion of active SLE patients with anaemia and leukocytopenia and to suppress the progenitor cell growth.

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Section: Discussionmentioning

confidence: 99%

“…The destruction ofperipheral blood cells by circulating autoantibodies is considered to play a major role in this pathogenesis. Recently, it has been reported that the proliferation of haematopoietic progenitor cells Is suppressed by serum inhibitor [2][3][4][5][6]. Fitchen etal.…”

Section: Introductionmentioning

confidence: 99%

Suppression of haematopoiesis by IgG autoantibodies from patients with systemic lupus erythematosus (SLE)

Liu

Ozaki

Matsuzaki

et al. 1995

Clinical and Experimental Immunology

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“…Brooks et al [7] reported a case of SLE-associated aplastic anaemia in which an IgG complement-dependent antibody was obtained from the patient's diseasephase serum but not from remission-phase serum and this suppressed in-vitro growth of granulocyte-macrophage progenitor cells from the bone marrow of normal donors. Bailey et al [8] were also able to demonstrate the presence of an IgG antibody, although noncomplement-dependent, that suppressed proliferation in vitro of bone marrow from normal donors as well as bone marrow obtained from the patient during the recovery phase.…”

Section: ]mentioning

confidence: 99%

“…However, Burkhardt [6] showed significant alterations in bone marrow biopsies in 21 SLE patients. Occasional reports have suggested that bone marrow alterations, such as aplastic anaemia [7][8][9][10][11][12][13] and myelofibrosis [14][15][16][17], may be part of the SLE disease spectrum. In order to evaluate the role of bone marrow in haematological alterations in SLE, we have studied the bone marrow aspirates and trephine biopsies of 21 patients.…”

Section: Introductionmentioning

confidence: 99%

Bone marrow findings in systemic lupus erythematosus patients with peripheral cytopenias

et al. 1998

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We studied 21 bone marrow specimens from 21 patients with systemic lupus erythematosus (SLE) and peripheral cytopenias: anaemia (Hb < 10 g/dl), and/or leucopenia (white blood cell count < 4 x 10(9)/l), and/or thrombocytopenia (platelets < 150 x 10(9)/l). None of the patients had used immunosuppressive drugs in the 2 months before the study, and 11 (52.4%) had never used these drugs. The global and specific series cellularity, degree of fibrosis and necrosis were evaluated by bone marrow trephine; morphological abnormalities and iron stores were evaluated by cytological smears. The most important abnormalities viewed in bone marrow biopsies were: global hypocellularity (47.6%), increased reticulin proliferation (76.2%) with myelofibrosis in one patient, and necrosis (19.0%). The marrow aspirates were difficult to obtain in four patients, who showed an increased reticulin proliferation on histological analysis. Plasmocytosis was present in 26.7% of cases and in one there was a serum monoclonal component (IgG kappa). Iron stores were normal or increased in 26.7% of specimens and decreased or absent in 73.3%. The most frequent peripheral abnormality was leucopenia in 90.4% (19/21) and granulocytic hypoplasia was observed in 47.3% (9/19) of these patients. We conclude that the bone marrow may be a target organ in SLE with cytopenias.

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“…A coincidence of autoimmune-mediated disorders and SAA is extremely rare and the few published reports have included eosinophilic fasciitis [24], lupus erythematosus [25], chronic thyroiditis and Sjogren's syndrome [26], A coincidence of MS and aplastic anemia, however, has not yet been reported. Many studies have documented altered T-cell functions in both diseases which may enhance IFNy and TNF-a production by mononuclear cells.…”

Section: Discussionmentioning

confidence: 99%

Coincidence of Severe Aplastic Anaemia with Multiple Sclerosis or Thyroid Disorders

Hinterberger-Fischer¹,

Kier²,

Forstinger³

et al. 1994

Acta Haematol

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Five patients with severe aplastic anaemia (SAA) who, simultaneously (n = 3) or consecutively (n = 2), presented with multiple sclerosis (MS) (n = 2) or immune hyperthyroidism (IHT) (n = 2) or subacute thyroiditis (n = 1) are described. Two female patients with MS developed SAA after a small dose of azathioprine. Another patient simultaneously presented with IHT and SAA. SAA and MS responded to cyclosporine while IHT required ¹³¹I. Relapsing SAA in 1 patient with MS was treated with antithymocyte globulin (ATG) which induced acute exacerbation of MS. Despite the low total dose of ATG (31.5 mg/kg), complete remission of SAA was obtained. Two other patients developed thyroid disorders, 42 and 106 months after successful immunosuppression with ATG/high-dose methylprednisolone. IHT and subacute thyroiditis were successfully treated with ¹³¹I or prednisolone, respectively, without recurrence of SAA in both cases. These are the first documented cases of SAA evolving in the course of MS while the coincidence with IHT was already described. Since enhanced expression of interferon-γ plays a crucial role in SAA as well as in MS and in IHT, similar pathogenetic principles may apply for these seemingly unrelated disorders.

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Serum Inhibitor in Systemic Lupus Erythematosus Associated With Aplastic Anemia

Cited by 37 publications

References 21 publications

Suppression of haematopoiesis by IgG autoantibodies from patients with systemic lupus erythematosus (SLE)

Suppression of haematopoiesis by IgG autoantibodies from patients with systemic lupus erythematosus (SLE)

Bone marrow findings in systemic lupus erythematosus patients with peripheral cytopenias

Coincidence of Severe Aplastic Anaemia with Multiple Sclerosis or Thyroid Disorders

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