![Figure 2. Biological parameters at baseline. Impact of G6PD deficiency and the number of α genes and β haplotypes (boxplots showing the median and interquartile range for each biological parameter). (A) Hb at baseline as a function of the presence or absence of G6PD deficiency in the 3 major homozygous β haplotypes. Median (quartile 1 [Q1] to Q3) hemoglobin was significantly lower in CAR/CAR patients with G6PD deficiency (7.3 [6.6-7.8] g/dL) than in CAR/CAR patients with normal G6PD activity (7.9 [7.2-8.5] g/dL; P = .005), whereas no such difference was observed in BEN/BEN and SEN/SEN patients. (B) MCV at baseline as a function of the number of present α genes. In the absence of α thalassemia (4 α genes), median (Q1-Q3) MCV was 82.8 (77.8-88.0) fL, whereas MCV was significantly lower in patients with α thalassemia (76.8 [73.0-81.3] fL in patients with 1 deleted gene and 67.5 [63.1-70.2] fL in those with 2 deleted genes). (C) HbF at baseline as a function of the major homozygous β haplotypes. Median (Q1-Q3) HbF was significantly lower in CAR/CAR patients (8.8% [4.8-14.0%]) than in BEN/BEN patients (12.8% [7.9-20.0%]; P < .001) and SEN/SEN patients (15.1% [10.0-23.5%]; P < .001), whereas the difference between BEN/BEN and SEN/SEN was not significant (P = .058). (D) Hb at baseline as a function of α-thalassemia presence or absence in the 3 major homozygous β haplotypes. The impact of α thalassemia on Hb was higher in CAR/CAR patients. Median (Q1-Q3) hemoglobin was 7.9 (7.4-8.5) g/dL in patients with α thalassemia vs 7.4 (6.8-8.1) g/dL in those without α thalassemia (P < .001). No significant difference was observed among BEN/BEN and SEN/SEN patients. Hb was significantly lower in CAR/CAR patients than in BEN/BEN patients in those with (P = .022) or without α thalassemia (P = .003). (E) LDH at baseline as a function of the number of α genes in the 3 major homozygous β haplotypes. The impact of α thalassemia on LDH was higher in CAR/CAR patients. Median (Q1-Q3) LDH was 773 (564-1018) IU/L in patients with α thalassemia vs 946 (686-1274) IU/L in those without α thalassemia (P = .005). No significant difference was observed among BEN/BEN and SEN/SEN patients. LDH was significantly higher in CAR/CAR patients than in BEN/BEN patients with or without α thalassemia (P = .014).](https://ash.silverchair-cdn.com/ash/content_public/journal/bloodadvances/2/6/10.1182_bloodadvances.2017014555/4/advances014555f2.jpeg?Expires=1735512528&Signature=iFgkVr~HPMcRN1UPq7zb~S-K6cXGgGqIXPvmwJ6os-r0thg~c5u-8yUUjDKGFQnJqW8qyp4AvbJsQnIm87s544rjszQPZmK331O35S2Au~QRZ9OLdobPafReo3T90CGCH~c4YgXXm8QltOZ8uXX1nJ~Tu9NT9KFLbRsx4Vtc~WEkNzId-8RGnkfCyOdj4DxlLjZwCA1n-66cKnYCi1d2aZimyB-weR~~nNhkhYXxEz-ZdnEtOdEDb3DktqHNcww6ZQ9wcuhjR5LkI3DPBDG3jeuoickatOko08LOjfvJzC-mQo5rgGZ1~80zHLs4dtPyX6QzNLkL4VX0DMqhc3Wrcw__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Biological parameters at baseline. Impact of G6PD deficiency and the number of α genes and β haplotypes (boxplots showing the median and interquartile range for each biological parameter). (A) Hb at baseline as a function of the presence or absence of G6PD deficiency in the 3 major homozygous β haplotypes. Median (quartile 1 [Q1] to Q3) hemoglobin was significantly lower in CAR/CAR patients with G6PD deficiency (7.3 [6.6-7.8] g/dL) than in CAR/CAR patients with normal G6PD activity (7.9 [7.2-8.5] g/dL; P = .005), whereas no such difference was observed in BEN/BEN and SEN/SEN patients. (B) MCV at baseline as a function of the number of present α genes. In the absence of α thalassemia (4 α genes), median (Q1-Q3) MCV was 82.8 (77.8-88.0) fL, whereas MCV was significantly lower in patients with α thalassemia (76.8 [73.0-81.3] fL in patients with 1 deleted gene and 67.5 [63.1-70.2] fL in those with 2 deleted genes). (C) HbF at baseline as a function of the major homozygous β haplotypes. Median (Q1-Q3) HbF was significantly lower in CAR/CAR patients (8.8% [4.8-14.0%]) than in BEN/BEN patients (12.8% [7.9-20.0%]; P < .001) and SEN/SEN patients (15.1% [10.0-23.5%]; P < .001), whereas the difference between BEN/BEN and SEN/SEN was not significant (P = .058). (D) Hb at baseline as a function of α-thalassemia presence or absence in the 3 major homozygous β haplotypes. The impact of α thalassemia on Hb was higher in CAR/CAR patients. Median (Q1-Q3) hemoglobin was 7.9 (7.4-8.5) g/dL in patients with α thalassemia vs 7.4 (6.8-8.1) g/dL in those without α thalassemia (P < .001). No significant difference was observed among BEN/BEN and SEN/SEN patients. Hb was significantly lower in CAR/CAR patients than in BEN/BEN patients in those with (P = .022) or without α thalassemia (P = .003). (E) LDH at baseline as a function of the number of α genes in the 3 major homozygous β haplotypes. The impact of α thalassemia on LDH was higher in CAR/CAR patients. Median (Q1-Q3) LDH was 773 (564-1018) IU/L in patients with α thalassemia vs 946 (686-1274) IU/L in those without α thalassemia (P = .005). No significant difference was observed among BEN/BEN and SEN/SEN patients. LDH was significantly higher in CAR/CAR patients than in BEN/BEN patients with or without α thalassemia (P = .014).
