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Pathology - Sideroblastic Anemia (Lead Poisoning)
Sideroblastic anemia is owing to lead poisoning, most likely from pica (an abnormal need for non-nutritive items) for ingesting lead paint chips from an old inner city structure. Lead is absorbed through the GI tract from ingestion (or in the lungs from inhalation) and accumulates in the bones and teeth of youngsters (as detected on physical examination). Radiographs will show lead lines in the epiphyses of long bones. GI and neurologic (including encephalopathy) symptoms can emerge. Lead impacts enzyme function, including aminolevulinic acid (δ-ALA) dehydrase, causing increased δ-ALA and ferrochelatase, blocking the incorporation of iron into the heme molecule, resulting in increased protoporphyrin. Inhibition of ribonuclease results in persistence of ribosome in the RBC and generates coarse basophilic stippling. Sideroblastic anemia can potentially be the result of an X-linked mutation in the δ-ALA synthase gene, or vitamin B6 deficiency (a cofactor for δ-ALA synthase). Increased iron buildup in the mitochondria due to faulty heme production results in ringed sideroblasts.
Sideroblastic anemia is owing to lead poisoning, most likely from pica (an abnormal need for non-nutritive items) for ingesting lead paint chips from an old inner city structure. Lead is absorbed through the GI tract from ingestion (or in the lungs from inhalation) and accumulates in the bones and teeth of youngsters (as detected on physical examination). Radiographs will show lead lines in the epiphyses of long bones. GI and neurologic (including encephalopathy) symptoms can emerge. Lead impacts enzyme function, including aminolevulinic acid (δ-ALA) dehydrase, causing increased δ-ALA and ferrochelatase, blocking the incorporation of iron into the heme molecule, resulting in increased protoporphyrin. Inhibition of ribonuclease results in persistence of ribosome in the RBC and generates coarse basophilic stippling. Sideroblastic anemia can potentially be the result of an X-linked mutation in the δ-ALA synthase gene, or vitamin B6 deficiency (a cofactor for δ-ALA synthase). Increased iron buildup in the mitochondria due to faulty heme production results in ringed sideroblasts.
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