Alcohol Ring sideroblasts may be found in the bone marrow of malnourished anemic alcoholics, usually in the presence of associated folate deficiency. In contrast, binge drinking or chronic alcohol ingestion in subjects with good nutrition is not associated with sideroblastic abnormality. Sideroblastic change is never the sole cause for the anemia of alcoholism. Alcohol has a direct toxic effect on hematopoiesis. An increased or high-normal MCV and vacuolation of red blood cell precursors is often seen in addition to the ring sideroblast abnormality. Red blood cells show dimorphic morphology; evidence in the marrow of folate deficiency is present in half of cases. Transferrin saturation and marrow iron stores tend to be increased but may be low if gastrointestinal bleeding is present. The ring sideroblasts gradually disappear over 4 to 12 days when alcohol is withdrawn; during this period, there may be a rebound erythroid hyperplasia, reticulocytosis, and thrombocytosis. Folic acid should be given for the associated megaloblastic changes after blood is taken for vitamin B12 and folate assays.

Alcohol consumption lowers the plasma concentration of pyridoxal phosphate, a cofactor for ALAS2, needed in the first step in heme synthesis. Conversion of ethanol to acetaldehyde is necessary for this effect, and acetaldehyde acts by accelerating the degradation of intracellular pyridoxal phosphate in the liver, lowering plasma levels of this coenzyme.

Chronic alcoholics have an altered heme metabolism with increased urinary excretion of coproporphyrin, mainly isomer III, but normal urinary excretion of uroporphyrin, ALA, and PBG. Acute and chronic ethanol ingestion markedly depresses the activity of ALA dehydratase in peripheral blood. Ethanol administration to normal subjects results in increased activity of leukocyte ALAS and erythrocyte PBGD, the two rate-controlling enzymes of the pathway. The activities of each of the other four enzymes are depressed. FECH, the enzyme that inserts iron into protoporphyrin to form heme, shows the most marked depression, and in alcoholism there is prolonged depression of uroporphyrinogen decarboxylase, which provides a rationale for the role of ethanol in the etiology of PCT. As expressed earlier, ethanol is a major precipitating fac tor in acute porphyria.

Isoniazid

 Administration of the antituberculous drug isoniazid has occasionally been associated with development of a sideroblastic anemia after 1 to 10 months of therapy. The anemia is hypochromic and microcytic, with a dimorphic blood smear and ring sideroblasts in the marrow. This complication is thought to occur only in slow acetylators of isoniazid, allowing this drug to react nonenzymatically with pyridoxal and to form a hydrazone that is rapidly excreted in the urine. The anemia can be fully reversed by coadministration of pyridoxine (25 to 50 mg/day) with isoniazid or by withdrawing isoniazid. Another antituberculous drug, pyrazinamide, may also cause a sideroblastic anemia, which is caused by inhibition of ALAS2 and responds to pyridoxine therapy.

Chloramphenicol

Chloramphenicol is an antibiotic that produces a reversible suppression of erythropoiesis after several days of therapy (plasma levels of 10 to 15 μg/mL). This effect is predictable and separate from the rare idiosyncratic side effect of aplastic anemia in approximately 1 of 20,000 exposed persons. Nearly all patients given chloramphenicol (>2 g/day) develop vacuolation of the erythroid precursors and ring sideroblasts. These effects are thought to arise from suppression of mitochondrial respiration. Chloramphenicol inhibits mitochondrial protein synthesis and reduces cytochrome a, a3 , and b levels. Serum iron concentrations are increased, and reticulocyte numbers are sub normal; these changes revert on stopping the antibiotic.

Other Drugs

 A reversible acquired sideroblastic anemia has been described with penicillamine, linezolid, and with the use of triethylene tetramine hydrochloride, a copper-chelating agent used in the treatment of Wilson disease. Acquired sideroblastic anemia has also been precipitated by progesterone given to a patient on two separate occasions 15 years apart, and this anemia promptly reversed on withdrawal of the drug.

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مواضيع ذات صلة

Morphologic Expression of Megaloblastosis

Presentations Associated with Sideroblastic Anemia or Porphyrinuria

Addison’s Disease

Cushing’s Disease

Sideroblastic anemias

Osteoporosis

Pathophysiology of Beta-Thalassemia Syndromes

Etiology and Pathophysiology of Anemia of Chronic Inflammation

Goitre and Thyroid nodules

Pathogenesis of Cobalamin Deficiency

Clinical Manifestations of Iron Overload

Pathobiology of Acquired Iron Overload