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. 2020 Sep 28;98(12):859–868. doi: 10.2471/BLT.20.253583

Table 4. Prevalence of α-thalassaemia and G6PD deficiency observed in infants, north-western United Republic of Tanzania, February 2017–May 2018.

Genotype Clinical effect No. (%)
α-thalassaemia (n = 143)
5 copies, αα/ααα 1-gene duplication, unaffected 0 (0.0)
4 copies, αα/αα 0-gene deletion, unaffected 61 (42.7)
3 copies, αα/–α3.7 1-gene deletion, α-thalassaemia minima 61 (42.7)
2 copies, –α3.7/–α3.7 2-gene deletion, α-thalassaemia trait 21 (14.7)
G6PD deficiency (n = 143)
Males (n = 73)
  B Wild type, unaffected 52 (71.2)
  A+ A+ variant, unaffected 7 (9.6)
  A A variant, affected 14 (19.2)
Females (n = 70)
  BB Homozygous, wild type, unaffected 33 (47.1)
  BA+ Heterozygous, wild type/A+ variant, unaffected 16 (22.9)
  A+A+ Homozygous, A+ variant, unaffected 3 (4.3)
  BA Heterozygous, wild type/A variant, carrier 15 (21.4)
  A+A Heterozygous, A+ variant/A variant, carrier 3 (4.3)
  AA Homozygous, A variant, affected 0 (0.0)

G6PD: glucose-6-phosphate dehydrogenase.

Note: We analysed dried blood spots from infants aged 0–24 months.