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So basically what you are asking is,

Why doesnt HbA2 replace HbA?

I mean that makes complete sense right HbA2 replacing whole of HbA since its defective but instead we get a rise in HbF which is only capable of delivering oxygen when O2 stats are high and it has high affinity for oxygen which is bad for the tissues and 2,3-BPG has no effect on HbF

This makes complete sense Happy-2 I dont know man I am surprised I never thought of this :happy:

Two or Three things are there I can think of:

1.HbF is high during the first 6months so being high its protective I guess and its high in everyone but its HIGH like you said

2.Since normally the HbA2 is only 2.5% while the majority of the rest is HbA when hematopoisis occurs in the medullary tissues so I think when in Beta thalassemia major extra medullary hematopoisis sets in the old fetal days are back so HbF is then synthesized

3.We treat this patients with HYDROXYUREA which causes are rise in levels of HbF, so levels are HIGH

I guess number 2 but I dont know man...very good point :cool:
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