Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of erythrocyte carbonic anhydrase isozymes (CA-B and CA-C) were determined by a quantitative immunochemical technique in order to elucidate their clinical significances in patients with iron deficiency anemia. The specific antibodies against rabbit CA-B and CA-C were also obtained, and the levels of rabbit erythrocyte carbonic anhydrase B and C isozymes were assayed immunochemically in experimental hemolytic and bleeding anemia. Simultaneously carbonic anhydrase isozymes were synthesized in vitro using rabbit reticulocyte-lysate. 1 The levels of erythrocyte CA-B per gram hemoglobin, CA-B per ml erythrocyte and CA-C per gram hemoglobin all increased but CA-C per ml erythrocyte did not increased in iron deficiency anemia. Erythrocyte CA-B and CA-C expressed per gram hemoglobin were inversely correlated to hemoglobin levels. 2 In experimental bleeding anemia and hemolytic anemia of rabbits, erythrocyte CA-B increased with the progression of anemia and with increase in reticulocyte count. However the levels of CA-C did not increased with progression of anemia. 3 In experimental bleeding anemia, it was found that the level of erythrocyte CA-B was correlated to the esterase activity and erythrocyte zinc content. 4 Most of the rabbit erythrocyte CA-B was distributed in younger erythrocytes. 5 It was confirmed that CA isozymes were synthesized in rabbit reticulocyte-lysate. The content of CA-B synthesized in lysates was much higher than that of CA-C. 6 In iron deficiency anemia, the increase of erythrocyte CA is speculated to be compensatory mechanism, which brought about the transportation of CO2 and right shifts of O2 dissociation curve.
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PMID:[Erythrocyte carbonic anhydrase isozymes in patients with iron deficiency anemia and their clinical significances (author's transl)]. 10 34

The effects of iron deficiency anemia and iron treatment on blood gas and acid-base balance at rest and during exercise were studied. Eight Sri Lankan males and 13 females were randomly divided into an iron treatment or placebo group. Their initial hemoglobin (Hb) levels were 6.2 +/- 0.5 and 5.5 +/- 0.7 g/100 ml (mean +/- SEM) with serum iron levels of 41 +/- 8 and 30 +/- 6 micrograms/100 ml, respectively. Hemoglobin concentration was increased significantly within 7 days after iron treatment to 7.2 +/- 0.4 g/100 ml. Resting lactate was higher than normal, while base excess, buffer base, and actual bicarbonate were lower, maintaining a normal pH. Heart rates during exercise at a given work load and lactate production following exercise decreased after the elevation of Hb. Venous blood PCO2 rose as Hb concentration increased, preceding a significant increase in resting O2 content, 16 days after iron treatment. With anemia, O2 delivery is potentially maintained by a shift of the O2-dissociation curve to the right due, in part, to 2,3-diphosphoglycerate. There was no significant change in PO2 or Hb-O2% saturation following exercise or iron treatment. These data suggest that severe iron deficiency anemia results in lactate accumulation in blood even at rest but pH is maintained within normal limits. It was also suggested that severe anemia may impair CO2 transport capacity of blood which could limit continuation of muscle metabolism.
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PMID:Characteristics of blood gas in response to iron treatment and exercise in iron-deficient and anemic subjects. 641 78