A trial of immunotherapy in aplastic anemia and pure red cell aplasia

Young, Neal S.; Klein, Harvey G.; Griffith, Patricia; Nienhuis, Arthur W.

doi:10.1002/jca.2920010206

Cited by 17 publications

(2 citation statements)

References 22 publications

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“…2, 4, 8, 13) and in three this was without effect, although one (no. 2) did not respond to a second course of therapy but achieved an incomplete response following lymphocytapheresis [23] and plasma exchange [24]. A sixth patient (no.…”

Section: Nonresponding Patientsmentioning

confidence: 96%

Treatment of aplastic anaemia with antilymphocyte globulin and high‐dose methylprednisolone

1991

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Twenty-three consecutive adults with bone marrow aplasia who, apart from one individual, lacked a sibling suitable for allogeneic transplantation, received five daily infusions of 50 mg/kg of antilymphocyte globulin (ALG) concurrently with high-dose (500 mg) methylprednisolone (HDMP), followed by oral prednisone at a dose of 30 mg until day 30. One patient died early so that response could not be determined, but data are available and included in the toxicity as well as survival analysis. Haematological response occurred in 13 of the remaining 22 (59%). This followed a single course of treatment in 12, with complete response achieved in five of this group and a second course required in one. At a median follow-up of 20 months (range 5-60), there have been five relapses and 13 patients are alive, including 12 responders who have Karnofsky ratings between 90% and 100%. Of the other nine individuals, only two are alive, with 1 at 12 months still requiring active support and the second, after failing further courses of treatment, at 41 months having a partial response to lymphocytapheresis and plasma exchange. Failure to respond was a significant adverse predictor for survival (P = 0.022). This study involved two distinct batches of ALG, with response occurring in 1/7 (14%) patients treated with the first lot, but in 12/15 (80%) of those individuals who were treated with the second (P = 0.007). Only a pretreatment mean cell volume (MCV) greater than 100 fL predicted for response (P = 0.0088). Confirmation is hereby provided for the efficacy of ALG used in combination with HDMP for treatment of aplastic anaemia, with further support for the observation that not all batches of this product are comparable in bringing about haematologic response in these individuals.

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Section: Nonresponding Patientsmentioning

confidence: 96%

Treatment of aplastic anaemia with antilymphocyte globulin and high‐dose methylprednisolone

1991

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“…Aplastic anemia (AA) is the stereotypical bone marrow failure (BMF) syndrome, featuring characteristic marrow hypocellularity and peripheral blood pancytopenia. 1 A significant role of immune dysfunction in AA pathology is inferred from many clinic observations of hematologic recovery following immunosuppressive therapy (IST), 2 , 3 , 4 , 5 as well as from animal models of AA in which infusion of allogeneic lymphocytes incites massive T-cell expansion and leads to marrow destruction. 6 , 7 , 8 , 9 …”

Section: Introductionmentioning

confidence: 99%

Granulocytic myeloid-derived suppressor cells to prevent and treat murine immune-mediated bone marrow failure

et al. 2023

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Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells which originate in the bone marrow (BM) and have immunoregulatory functions. MDSCs have been implicated in the pathogenesis of several autoimmune diseases but have not been investigated in immune aplastic anemia (AA). We examined the roles of granulocytic-MDSCs (G-MDSCs) in murine models of human AA and bone marrow failure (BMF). As both prophylaxis and therapy, BM-derived G-MDSCs improved pancytopenia and BM cellularity and suppressed BM T cell infiltration in major histocompatibility complex (MHC)-matched C.B10 BMF mice. These effects were not obtained in MHC-mismatched CByB6F1 AA model, likely due to MHC disparity between G-MDSCs and donor T cells. Single cell RNA sequencing demonstrated that G-MDSCs downregulated cell cycle related genes in BM infiltrated T cells, consistent with suppression of T cell proliferation by G-MDSCs through reactive oxygen species pathway. Clearance of G-MDSCs in MHC-mismatched CByB6F1 model using anti-Ly6G antibody facilitated T cell-mediated BM destruction, suggesting an intrinsic immunosuppressive property of G-MDSCs. However, the same anti-Ly6G antibody mildly mitigated marrow failure due to expansion of an intermediate Ly6G population in the BM of MHC-matched C.B10 AA model. Our results demonstrate that G-MDSC eradication and therapeutic efficacy are immune context-dependent.

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Guidelines on the use of therapeutic apheresis in clinical practice—Evidence‐based approach from the apheresis applications committee of the American society for apheresis

Szczepiórkowski

Winters

Bandarenko

et al. 2007

J of Clinical Apheresis

450

519

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The American Society for Apheresis (ASFA) Apheresis Applications Committee is charged with a review and categorization of indications for therapeutic apheresis. This elaborate process had been undertaken every 7 years resulting in three prior publications in 1986, 1993, and 2000 of "The ASFA Special Issues." This article is the integral part of the Fourth ASFA Special Issue. The Fourth ASFA Special Issue is significantly modified in comparison to the previous editions. A new concept of a fact sheet has been introduced. The fact sheet succinctly summarizes the evidence for the use of therapeutic apheresis. A detailed description of the fact sheet is provided. The article consists of 53 fact sheets devoted to each disease entity currently categorized by the ASFA. Categories I, II, and III are defined as previously in the Third Special Issue. However, a few new therapeutic apheresis modalities, not yet approved in the United States or are currently in clinical trials, have been assigned category P (pending) by the ASFA Clinical Categories Subcommittee. The diseases assigned to category IV are discussed in a separate article in this issue.

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A trial of immunotherapy in aplastic anemia and pure red cell aplasia

Cited by 17 publications

References 22 publications

Treatment of aplastic anaemia with antilymphocyte globulin and high‐dose methylprednisolone

Treatment of aplastic anaemia with antilymphocyte globulin and high‐dose methylprednisolone

Granulocytic myeloid-derived suppressor cells to prevent and treat murine immune-mediated bone marrow failure

Guidelines on the use of therapeutic apheresis in clinical practice—Evidence‐based approach from the apheresis applications committee of the American society for apheresis

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