Ringed sideroblasts

ALA synthase, the rate-limiting enzyme, requires pyridoxine (vitamin B ). Deficiency of pyri-doxine is associated with isoniazid therapy for tuberculosis and may cause sideroblastic anemia with ringed sideroblasts. 

Lead inactivates many enzjnnes including ALA dehydrase and ferrochelatase (hetne synthase), and can produce a microcytic sideroblastic anemia with ringed sideroblasts in the bone marrow. Other symptoms include ... 

There have been several cases of sideroblastic anemia, characterized by an excess of ringed sideroblasts in the bone marrow, as a suspected adverse effect of trientine (8,9). 

Azacitidine is a DNA demethylation agent, that causes hypomethylation of DNA and direct cytotoxicity on abnormal hematopoietic cells in bone marrow. Azacitidine is indicated in the treatment of myelodysplastic syndrome subtypes refractory anemia or refractory anemia with ringed sideroblasts (if accompanied by neutropenia or thrombocytopenia or requiring transfusions), refractory anemia with excess blasts, refractory anemia with excess blasts in transformation, and chronic myelomonocytic leukemia. 

In swine, copper deficiency leads to a microcytic, hypochromic anemia that resembles that of iron-deficiency anemia except that it cannot be effectively treated by the administration of iron. Indeed, it may occur in pigs with an excess of iron stores and 70 -80% ringed sideroblasts in the marrow, unless copper is administered (Erslev 1986). 

In lead-induced anemias, there is usually a reticulocy-tosis along with the presence of basophilic stippling, and ringed sideroblasts, although none of the above are jia-thognomonic for lead-induced anemia. 

The findings of basophilic stippling in circulating red blood cells (usually found in 1 to 5% of red cells following marrow injury), and detedion in the bone marrow of what are termed ringed sideroblasts must be taken seriously, as they have been noted in recent years to be premonitory signs of subsequent leukemia. 

Hematologic Anemia has been attributed to linezolid in two cases. In a patient with laryngeal cancer the hemoglobin concentration fell from 12.5 to 5.9 g/dl over 2 months of linezolid therapy there were ringed sideroblasts in the bone marrow and the hemoglobin slowly increased after linezolid withdrawal [152" ]. A 2-year-old boy with infective endocarditis took linezolid for 4 weeks and his hemoglobin concentration fell to 6.5 g/dl with markedly reduced erythropoiesis he recovered 19 days after linezolid withdrawal [153" ]. 

Defects in mitochondrial iron transport and utilization can result in mitochondrial iron overload. There is extensive iron accumulation in erythroblast mitochondria of both patients with X-linked sideroblastic anemia due to defective erythroid-speeifie 5-aminolevulinic acid synthase (eALAS) and those with ring sideroblasts associated with myelodysplastic syndrome. Mitochondrial iron overload has also been documented in patients with Friedreich s ataxia with defective frataxin" and in those with sideroblastic anemia with ataxia from defects in the Fe-S transporter ABC7. In addition, studies with yeast, the best studied eukaryotic model of Fe-S cluster synthesis, showed that defects in any of the enzymes of the Fe-S cluster assembly pathway caused mitochondrial iron accumulation and lack of normal mitochondrial function. ... 

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