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Aplastic Anemia and Other Bone Marrow Failure Syndromes

  • Nasrollah T. Shahidi

Table of contents

  1. Front Matter
    Pages i-xvii
  2. Mehdi Tavassoli
    Pages 1-24
  3. Blanche P. Alter
    Pages 38-50
  4. Arleen D. Auerbach
    Pages 51-62
  5. F. Roy MacKintosh, Jean C. Schulman, Esmail D. Zanjani
    Pages 63-81
  6. Kristine Doney, Kenneth Kopecky, Rainer Storb, C. Dean Buckner, Jack Singer, Claudio Anasetti et al.
    Pages 104-114
  7. N. T. Shahidi, W. Wang, S. Shurin, J. Finlay, P. Sondel, P. Dinndorf
    Pages 155-165
  8. Emmanuel N. Dessypris
    Pages 179-198
  9. Grover C. Bagby Jr.
    Pages 199-223
  10. David G. Nathan
    Pages 224-229
  11. Back Matter
    Pages 231-236

About this book

Introduction

During the past decade, there have been numerous direct and indirect scientific contributions to both the etiology and therapy of aplastic anemia and related bone marrow failure syndromes. Clinical observations, such as autologous bone marrow recovery after conditioning with immunosup­ pressive agents for bone marrow transplantation; failure to achieve en­ graftment in some identical twins without prior immunosuppressive ther­ apy; and hematologic response to immunosuppressive agents, have led to the concept of immune-mediated etiology of acquired aplastic anemia. Such a concept was further strengthened by laboratory findings, implicat­ ing the role of activated cytotoxic T lymphocytes and abnormal produc­ tion of inhibitory lymphokines. The immunologic mechanisms may also apply to the idiosyncratic bone marrow aplasias associated with drugs, toxic chemicals, and viruses. These agents may alter normal cellular recog­ nition sites by interacting with cellular components and result in loss of self tolerance. Immunologic mechanisms have long been advocated in many other organ failures, and the hemopoietic organ is no exception. It is of interest that parallel clinical and laboratory investigations in juvenile diabetes mellitus type I and in rodent models of this disease have yielded results compatible with the same pathogenic mechanisms. The infiltration of pancreatic islets by activated T lymphocytes, functional and morphological alterations of islet cells upon incubation with lymphokines such as gamma interferon and tumor necrosis factor, and clinical response to cyclosporine are a few examples.

Keywords

Viruses anemia bone marrow cell classification cytogenetics genetics hematopoiesis immunosuppression interferon lymphocytes necrosis thymus transplantation tumor

Editors and affiliations

  • Nasrollah T. Shahidi
    • 1
  1. 1.Department of PediatricsUniversity of Wisconsin-MadisonMadisonUSA

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