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Sideroblastic anemia has been known to be caused by several genetic mutations mostly due to a defect in hemoglobin synthesis. Congenital sideroblastic anemia (CSAs) are inherited conditions due to mitochondrial dysfunction due to defects in heme biosynthesis, iron biogenesis, or even generalized mitochondrial protein synthesis.[1][3] Like most of the pathway to heme biosynthesis, this is an evolutionarily conserved mitochondrial pathway that involves multiple enzymes that reduce organic sulfur to sulfide, complexes it with iron and then delivers it to the mitochondria and cytosol. One of the best-characterized forms of CSA is the X-linked sideroblastic anemia, XLSA which is typically due to missense mutations in ALA synthase or ALAS2 which is the first step in heme biosynthesis.

However, most of the refractory anemia with ringed sideroblasts will have an evolution in two forms: MDS with a normal lifespan or MDS with development to a higher grade MDS or AML. The majority of cases belonging to the first category and will develop in only 7-10% of all RARs patients. Morphology at the time of diagnosis is crucial as it will drive the evolution of the disease. 153554b96e

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