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) |
A–A– | Homozygous, A– variant, affected | 0 (0.0) |
G6PD: glucose-6-phosphate dehydrogenase.
Note: We analysed dried blood spots from infants aged 0–24 months.