Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.16.3.1 (ceruloplasmin)
 5,074 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentrations of three trace elements (iron, copper and zinc) involved in hematopoiesis were studied in 200 patients with iron-deficit anemia, hemolytic anemia and Biermer's anemia, in comparison with a group of normal subjects. The method used was atomic absorption spectrophotometry. The results obtained showed that in iron-deficit anemia resistant to iron therapy the copper and ceruloplasmin serum concentrations are at the lowest limit of normal. This copper deficit has a negative effect on the disease by preventing hemoglobin synthesis. In iron-deficit anemias responding to iron therapy the relatively low (about 90 gamma %) zinc values have a negative effect by blocking the iron in the iron reserve. In hemolytic anemia the very high zinc serum concentrations (over 200 gamma %) may lead to a shortening of the erythrocytes life span due to its "entatic state". In Biermer's anemia zinc by its high concentration has a positive role owing to carbonic anhydrase which eliminates more rapidly carbon dioxide from the organism.
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PMID:Possible correlation between the zinc and copper concentrations involved in the pathogenesis of various forms of anemia. 228 64

Six of eight patients with Addisonian pernicious anemia were found to have diminished corticosteroid-binding globulin (CBG) concentrations, which returned within 2 weeks to normal after the im administration of cobalamin. T4-binding globulin was found to be completely normal before and after cobalamin replacement. Other estrogen-responsive proteins, i.e. ceruloplasmin, alpha 1-trypsin inhibitor, haptoglobin, transferrin, and alpha 2-macroglobulin, also did not follow CBG concentration in a parallel fashion. The immunoglobulins similarly did not follow a course parallel to that of CBG. The CBG concentration in two untreated patients had a normal increase in response to estrogen administration, similar to that described in CBG deficiency from other causes. No clue was found regarding the mechanism by which B12 influences the putative hepatic control of CBG concentration. It is speculated that at least two control points may be necessary for a normal CBG concentration. Patients with a genetic deficiency of CBG may also have to have cobalamin deficiency in order for them to reach a concentration approaching zero.
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PMID:Vitamin B-12 (cobalamin) deficiency: a heretofore undescribed control mechanism for plasma corticosteroid-binding globulin concentration in man. 617 43