Alpha-thalassemia phenotype induced by the new IVS-II-2 (T --> A) splice donor site mutation on the alpha2-globin gene

Hemoglobin. 2006;30(1):3-7. doi: 10.1080/03630260500453784.

Abstract

We present a family of North European extraction referred for a refractory non iron depleted microcytic anemia. The proband, a 36 year-old male, presented with chronic borderline anemia and microcytic hypochromic parameters. No abnormal hemoglobin (Hb) fractions were observed on high performance liquid chromatography (HPLC) or on alkaline electrophoresis. Gap-polymerase chain reaction (gap-PCR) excluded the seven common alpha-thalassemia (thal) deletion defects. However, the beta/alpha-globin chain synthesis ratio measured in vitro was unbalanced, indicating a reduced expression of the alpha-globin genes. Direct sequencing of the alpha-globin genes revealed heterozygosity for a T --> A transversion at the IVS-II-2 position of the alpha2 gene. This is the first IVS-II splice donor site mutation described on the alpha2-globin gene.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Alleles
  • Alternative Splicing*
  • Anemia, Hypochromic / blood
  • Anemia, Hypochromic / genetics*
  • Chronic Disease
  • DNA Mutational Analysis
  • Family Health
  • Gene Deletion*
  • Globins / genetics*
  • Hemoglobins / genetics*
  • Humans
  • Male
  • Pedigree
  • Phenotype
  • Point Mutation*
  • Protein Subunits / genetics
  • alpha-Thalassemia / blood
  • alpha-Thalassemia / genetics*

Substances

  • Hemoglobins
  • Protein Subunits
  • Globins