Interferon therapy for agnogenic myeloid metaplasia complicated by immune hemolytic anemia.

Abstract

A 69-year-old man with agnogenic myeloid metaplasia was treated with interferon-alpha 2 as part of a Phase II clinical trial. The patient responded to this treatment with a definite improvement in bone marrow histology, demonstrating increased numbers of hematopoietic colonies and partial resorption of the myelofibrosis. Chromosomal analysis on 20 cells suggested the re-emergence of normal hematopoietic progenitor cells: whereas previously, all metaphase spreads demonstrated a deletion in chromosome 20, the patient was now chimeric, with two of 20 cells exhibiting a normal karyotype. Nevertheless, the patient's anemia progressed during interferon therapy, with the development of an immunologically mediated hemolytic disorder. This hemolytic process developed after prolonged treatment with interferon, accelerated during therapy, and resolved following splenectomy and withdrawal of the drug. Initially, screening tests failed to detect the presence of the autoantibody. Similar immunologic processes may have been overlooked in other patients treated with interferon, especially if tests for autoantibodies were obtained early in their course of treatment. This case suggests a therapeutic role for interferon-alpha 2 in the management of the myeloproliferative diseases. It is presented, too, to underscore the immunomodulatory potential of the biologic response modifiers and their capacity to induce immunologic disorders.