No. Acute Intermittent & cutanea tarda both are due to defective enzymes on the cytoplasmic side of the pathway. X-linked involves a defective mitochondrial enzyme. Sideroblastic anemia is due to mitochondrial enzyme defects only - causing the basophilic stippling.
Ive actually wondered this too...wouldnt the Iron still just sit around in the mitochondria waiting for protoporyphrin to be made and hence accumulate to form the ringed sideroblasts = sideroblastic anemia? As a big picture point it seems that the emphasis of the path on sideroblastic anemia is the mitochondrial enzymatic steps (ferrocheletase, ALAS, B6 def from INH) or the mitochondria itself (alcohol)
No. Acute Intermittent & cutanea tarda both are due to defective enzymes on the cytoplasmic side of the pathway. X-linked involves a defective mitochondrial enzyme. Sideroblastic anemia is due to mitochondrial enzyme defects only - causing the basophilic stippling.
So only defects in the mechanisms of the first and last three steps can lead to sideroblastic anemias? All the porphyrias besides cutanea tarda and acute intermittent?
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