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. 2021 Mar 15;193(3):637–658. doi: 10.1111/bjh.17361

Fig 1.

Fig 1

Transfusion‐dependent patients with β‐thalassaemia (β‐thal), sickle cell disease (SCD) and spherocytosis (SPH) are hallmarked by haemolysis and haem scavenger depletion. (A–C) Measurement of total cell‐free Hb/haem, haptoglobin and haemopexin in sera of healthy subjects (Ctrl), and patients with β‐thal major and intermedia (int). (D) Correlation between haemopexin and haem includes data from Ctrls and patients with β‐thal. (E,F) Total µmol/l Hb and haem binding capacity of haptoglobin and haemopexin and ‘free’ unbound Hb/haem (NHBHb, NHBH) in patients with β‐thal major and int (calculated as described in Methods). (G) Representative Western blot for haemopexin in sera of healthy subjects (Ctrl), as well as patients with β‐thal major, SCD (SCD 1 and 2), and SPH; (H,I) Measurement of total cell‐free Hb/haem and haemopexin in sera of Ctrls and patients with SPH and SCD (SCD 1 and 2). Few samples of patients with β‐thal major were included for comparison. (J) Correlation of haemopexin with haem includes data from Ctrls, and patients with SCD1 and 2. Values represent mean ± SD. *P < 0·05; **P < 0·01; ***P < 0·001; ****P < 0·0001.