Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Pathophysiology of acquired aplastic anemia
- Part II Epidemiology and clinical features of acquired aplastic anemia
- Part III Treatment of acquired aplastic anemia
- 9 Supportive treatment of patients with severe aplastic anemia
- 10 Immunosuppressive treatment of aplastic anemia
- 11 Role of cytokines in the treatment of aplastic anemia
- 12 HLA-identical sibling bone marrow transplantation to treat severe aplastic anemia
- 13 Alternative donor bone marrow transplantation for severe acquired aplastic anemia
- 14 Treatment of children with acquired aplastic anemia
- 15 Long-term follow-up of patients with aplastic anemia: clonal malignant and nonmalignant complications
- 16 Guidelines for treating aplastic anemia
- Part IV Fanconi's anemia
- Index
9 - Supportive treatment of patients with severe aplastic anemia
from Part III - Treatment of acquired aplastic anemia
Published online by Cambridge University Press: 18 August 2009
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Pathophysiology of acquired aplastic anemia
- Part II Epidemiology and clinical features of acquired aplastic anemia
- Part III Treatment of acquired aplastic anemia
- 9 Supportive treatment of patients with severe aplastic anemia
- 10 Immunosuppressive treatment of aplastic anemia
- 11 Role of cytokines in the treatment of aplastic anemia
- 12 HLA-identical sibling bone marrow transplantation to treat severe aplastic anemia
- 13 Alternative donor bone marrow transplantation for severe acquired aplastic anemia
- 14 Treatment of children with acquired aplastic anemia
- 15 Long-term follow-up of patients with aplastic anemia: clonal malignant and nonmalignant complications
- 16 Guidelines for treating aplastic anemia
- Part IV Fanconi's anemia
- Index
Summary
Introduction
The survival of patients with severe aplastic anemia (SAA) has improved greatly over the last few decades. Several factors have contributed to this improvement, including better immunosuppressive therapy, better results following allogeneic bone marrow transplantation (BMT), and improved supportive therapies. The major causes of mortality in patients with SAA are infections, bleedings, and graft-versus-host disease (GVHD) in patients who have undergone allogeneic BMT. This chapter covers transfusion therapy and the management of infection.
Prevention and treatment of infections
Risk of infections
The risk of infection in patients with SAA is determined by several factors. The most important factor is the number of leukocytes during the different phases of the disease. In a study including 150 patients, the absolute neutrophil count (ANC) and the absolute monocyte count at diagnosis were correlated to the development of febrile episodes (Weinberger et al., 1992). In another small series of patients the monocyte count and total leukocyte count were associated with the risk of infection (Keidan et al., 1986). T-cell defects must also be considered as a risk factor for infection in patients who receive immunosuppressive therapy with antilymphocyte/antithymocyte globulin (ALG/ATG) combined with cyclosporin. In one randomized study the risk of infectious complications was higher in patients receiving ATG combined with prednisone than in patients treated with cyclosporin alone. Recently it was suggested in a pilot study that the addition of granulocyte colony-stimulating factor (G-CSF) to ATG and cyclosporin can reduce the risk of severe infectious complications (Bacigalupo et al., 1995).
- Type
- Chapter
- Information
- Aplastic AnemiaPathophysiology and Treatment, pp. 137 - 153Publisher: Cambridge University PressPrint publication year: 1999