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Table 3 Differentiation between TDT and NTDT

From: Identification and key management of non-transfusion-dependent thalassaemia patients: not a rare but potentially under-recognised condition

  TDT more likely NTDT more likely
Clinical
Presentation (years) <2 >2
Hb levels (g/dL) 6-7 8-10
Liver/spleen enlargement Severe Moderate to severe
Growth retardation/pubertal failure* +++/++++ Negative to ++
Clinical anaemia affecting daily living Yes No
Bone deformity/thalassaemic facie Yes Negative to mild
Haematologic
Nucleated RBC (mm3) Numerous Negative to few
Reticulocytosis ≥10% of RBC <10% RBC
Molecular
Type of globin defects Severe Mild/silent
Co-inheritance of ameliorating genetic modifiers No Yes
Co-inheritance of deteriorating genetic modifiers Yes No
  1. Modified from Thalassaemia International Federation Guideline (2008'second edition).
  2. *Growth retardation; ++, P < 25P, +++, <10P and ++++ = <3P;
  3. Ameliorating genetic modifiers represent genetic factors that can reduce globin imbalance such as β-thalassaemia and/or quantitative trait loci that increase †-globin expression in β-thalassaemia intermedia or HbE/β-thalassaemia, β-thalassaemia gene in HbH disease.
  4. Deteriorating genetic modifiers include genetic polymorphisms that can further advance disease severity directly and indirectly such as multiple alpha globin gene rearrangements, genetic haemochromatosis, vitamin D receptor, UGT1A1, α-Hb stabilizing protein polymorphism etc.