Familial sideroblastic anemia with emergence of monosomy 5 and myelodysplastic syndrome

Med Pediatr Oncol. 1996 Jan;26(1):54-6. doi: 10.1002/(SICI)1096-911X(199601)26:1<54::AID-MPO7>3.0.CO;2-U.

Abstract

The case history of two sisters with pyridoxine-refractory familial sideroblastic anemia (FSA) is presented in which one developed a myelodysplastic syndrome (MDS) with monosomy for chromosome 5. Bone marrow examination of both patients at diagnosis showed erythroid hyperplasia with more than 50% ring sideroblasts. Karyotypic analysis initially showed a normal 46, XX karyotype in both of the children. Therapeutic trials with pyridoxine, prednisone, and erythropoietin were unsuccessful. The first patient required regular transfusions and developed a significant hemosiderosis. At the age of 9 years, 7.5 years after the diagnosis of FSA, refractory anemia with excess of blasts (RAEB) was diagnosed. Bone marrow cytogenetic analysis revealed a clone with monosomy for chromosome 5. Her sister's illness was detected at the age of 12 years. She has a more benign course of disease, remains largely transfusion independent and until now shows no signs of myelodysplasia. To our knowledge this is the first observation of a transition of FSA to MDS accompanied by the appearance of a chromosomal abnormality. FSA might be another type of bone marrow failure syndrome, therefore close follow-up of these patients may be necessary.

Publication types

  • Case Reports

MeSH terms

  • Anemia, Refractory, with Excess of Blasts / complications
  • Anemia, Sideroblastic / complications*
  • Anemia, Sideroblastic / drug therapy
  • Anemia, Sideroblastic / genetics*
  • Child
  • Chromosomes, Human, Pair 5*
  • Female
  • Humans
  • Infant
  • Karyotyping
  • Monosomy
  • Myelodysplastic Syndromes / complications*
  • Myelodysplastic Syndromes / drug therapy
  • Myelodysplastic Syndromes / genetics*
  • Pyridoxine / therapeutic use

Substances

  • Pyridoxine