Figure 3.
Biological parameters with HU therapy. (A) MCV during HU therapy as a function of the number of α genes. In the absence of α thalassemia, (4 α genes), median (Q1-Q3) MCV during HU treatment was 100 (93-106.9) fL, and it was significantly lower (P < .001) in α-thalassemia patients with 1 deleted gene (88.1 [84.9-96.0] fL) or 2 deleted genes (74.7 [70.7-82.3] fL). (B) Platelets during HU therapy as a function of the number of α genes. Platelet counts were significantly lower in HU-treated patients with α thalassemia. Median (Q1-Q3) platelet count was 217 × 109/L (172-372) in patients with 2 deleted genes, 284 × 109/L (217-378) in those with 1 deleted gene, and 350 × 109/L (274-408) in those without α thalassemia. (C) Delta HbF on HU was significantly higher (P = .026) in BEN/BEN than in CAR/CAR patients. (D) HbF during HU treatment in the 3 major homozygous β haplotypes. Median (Q1-Q3) HbF with HU therapy was significantly higher in BEN/BEN patients (21.1% [13.7-27.6%] than in SEN/SEN patients (20.9% [11.6-24.8%]) (P = .016) and CAR/CAR patients (16.7% [11.4-20.1%] (P = .005). (E) Hb levels with HU treatment in the 3 major homozygous β haplotypes. Median (Q1-Q3) Hb levels during HU therapy were significantly higher in BEN/BEN patients (9.4 [8.1-10.1] g/dL) than in SEN/SEN patients (8.7 [7.8-9.8] g/dL) (P = .017) and CAR/CAR patients (8.4 [7.8-9.2] g/dL) (P = .007).

Biological parameters with HU therapy. (A) MCV during HU therapy as a function of the number of α genes. In the absence of α thalassemia, (4 α genes), median (Q1-Q3) MCV during HU treatment was 100 (93-106.9) fL, and it was significantly lower (P < .001) in α-thalassemia patients with 1 deleted gene (88.1 [84.9-96.0] fL) or 2 deleted genes (74.7 [70.7-82.3] fL). (B) Platelets during HU therapy as a function of the number of α genes. Platelet counts were significantly lower in HU-treated patients with α thalassemia. Median (Q1-Q3) platelet count was 217 × 109/L (172-372) in patients with 2 deleted genes, 284 × 109/L (217-378) in those with 1 deleted gene, and 350 × 109/L (274-408) in those without α thalassemia. (C) Delta HbF on HU was significantly higher (P = .026) in BEN/BEN than in CAR/CAR patients. (D) HbF during HU treatment in the 3 major homozygous β haplotypes. Median (Q1-Q3) HbF with HU therapy was significantly higher in BEN/BEN patients (21.1% [13.7-27.6%] than in SEN/SEN patients (20.9% [11.6-24.8%]) (P = .016) and CAR/CAR patients (16.7% [11.4-20.1%] (P = .005). (E) Hb levels with HU treatment in the 3 major homozygous β haplotypes. Median (Q1-Q3) Hb levels during HU therapy were significantly higher in BEN/BEN patients (9.4 [8.1-10.1] g/dL) than in SEN/SEN patients (8.7 [7.8-9.8] g/dL) (P = .017) and CAR/CAR patients (8.4 [7.8-9.2] g/dL) (P = .007).

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