alpha-thalassemia

a-thalassemia

Updated: 07/12/2024

© Jun Wang, MD, PhD

 

General features

  • Anemia associated with reduced Hb, hemolysis and ineffective erythropoiesis
  • Reduced HbA, and presence of HbH and/or Hb Bart
  • DNA analysis of gene copy numbers required for diagnosis

Pathogenesis

  • Deletions of one or more a globin gene
  • Reduced or absent synthesis of a-globin
  • Unpaired b chains and g chains (in infants) more soluble and form fairly stable tetramers

Classification

o   Deletion of one a gene

o   Minimal reduction in a globin synthesis

o   Usually asymptomatic

o   May have slight microcytosis

o   Diagnosed by genetic test

  • a thalassemia trait

o   Deletion of two a genes

o   Usually not associated with anemia

o   High RBC count with low MCV and MCH

  • HbH disease

o   Deletion of 3 a genes

o   HbH (over 30%), composed of 4 b chains

  • Hb Bart fetal hydrops

o   AKA hydrops fetalis

o   Deletion of 4 a genes

o   Usually died in utero

o   Greater than 30%  Hb Bart (aka Bart’s Hb, Hb Bart’s), composed of 4 g chains

o   HbH may present, but no HbA or HbF

a thalassemia trait

  • Deletion of two genes
  • Cis

o   Both genes from the same chromosome

o   SEA, THAI, FIL type deletion

o   More common in Southeast Asians

o   Offspring at higher risk for HbH disease or hydrops fetalis

  • Trans

o   Deletion involving both chromosomes

  • Usually NO anemia
  • High RBC count with low MCV and MCH
  • Normal Hb electrophoresis
  • DNA analysis needed to confirm diagnosis

HbH disease

  • Deletion of 3 a genes
  • Formation of HbH

o   4 b chains

o   ≥ 30% needed for diagnosis

o   High oxygen affinity for oxygen

o   Tissue hypoxia disproportionate to absolute level of Hb

o   Oxidation resulting in formation of intracellular inclusions promoting red cell sequestration and phagocytosis

o   Detected by hemoglobin electrophoresis or HPLC

  • Poikilocytosis: microcytes, target cells, schistocytes, tear drop cells
  • No iron overload
  • No extramedullary hematopoiesis

Hb Bart fetal hydrops

  • Deletion of 4 a genes
  • Formation of Hb Bart

o   Tetramers of g globin

o   ≥ 30% for diagnosis

o   Very high affinity for oxygen and does not dissociate

o   Severe tissue hypoxia

o   Detected by hemoglobin electrophoresis or HPLC

o   May have HbH (up to 30% of total hemoglobin)

  • Death in utero unless intrauterine blood transfusions
  • Embryonic hemoglobins (Gower I, Portland, no alpha globins) in first trimester
  • Hb Bart formed later in pregnancy, causing severe tissue hypoxia
  • Tissue anoxia may lead to fetal death
  • If fetal transfusions given and infant born alive, lifelong supportive transfusions necessary unless bone marrow/stem cell transplant

Hb electrophoresis findings

  • Carrier state: Normal
  • Trait: mild decrease (~10-15%) of HbA, no abnormal Hb
  • HbH

o   Combination of HbA, HbH, and Hb Bart

o   HbH ≥ 30% for diagnosis

  • Hydrops fetalis:

o   Hb Bart (≥30%) and HbH

o   NO HbA or HbF

Management

  • Mild forms:  NO specific treatment, iron supplementation
  • HbH

o   Supplementation of folic acid

o   Lifelong transfusion likely for severe anemia

  • Hb Bart

o   Managed at specialized perinatal centers

o   In utero transfusions (IUTs) and allogeneic hematopoietic stem cell transplantation (HSCT) if family consented

 

Back to anemia

Back to contents

 

Comments

Popular posts from this blog

Contents

Anemia

Lymphoid neoplasms