Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Therapy with recombinant human erythropoietin (rEPO) can correct anemia in RDT patients. However, iron deficiency can develop making treatment unsuccessful. Eighteen non-transfused RDT patients with hematocrit less than 26% were treated with rEPO to raise the HCT to 30-35%; then the dose was individually adjusted to maintain the HCT. The mean HCT rose from 22.3% to 31.5%. Ten patients received iron substitution before rEPO. During rEPO therapy five further patients had to be supplemented with iron; all patients needed an increase in the oral iron doses and three required i.v. iron. During the correction phase mean serum ferritin dropped from 203 micrograms/l to a minimum of 71 micrograms/l and was 102 micrograms/l after six months. Serum iron and TIBC changed only moderately. It thus appears that iron demand rises markedly during rEPO therapy, requiring iron substitution in most patients. Serum ferritin is the most sensitive parameter for development of iron deficiency.
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PMID:Iron metabolism under rEPO therapy in patients on maintenance hemodialysis. 234 53

Serum erythropoietin (EPO) was measured in 64 children with chronic renal failure (CRF) by means of the fetal mouse liver cell assay. The results were compared with two control groups consisting of 20 healthy children and 10 with nonrenal anemia. EPO was analyzed according to the mode of treatment and the degree of uremia, anemia, hypoxemia, hyperparathyroidism, and body iron load. Mean EPO was 36 U/liter on conservative treatment (CT) (N = 30), similar to that in healthy children (35 U/liter) and in 15 children with renal transplants (TP, 39 U/liter), but significantly higher than that in 19 patients on regular dialysis (RDT; 16 U/liter) and lower than that in children with nonrenal anemia but with similar hemoglobin (230 U/liter). On CT, EPO was higher with severe uremia (SCr greater than 4 mg/dl) compared with moderate CRF and was inversely correlated with hemoglobin, but on a lower level compared with control, whereas on RDT the correlation became positive. By serial measurements, the decrease of EPO from CT to RDT was confirmed. An inverse relationship between EPO and p50 or the oxygen transport index was detected only on CT and after TP. EPO was inversely correlated with serum ferritin levels on HD. Between EPO and PTH, no correlation was found. Data demonstrate a negative feedback between EPO and the degree of hypoxia in children with CRF. On CT, this regulatory mechanism of erythropoiesis is acting on a lower level than it does in control subjects and is lost on RDT.
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PMID:Serum erythropoietin levels in children with chronic renal failure. 658 79

In RDT hemosiderosis appears to be an inevitable complication only in the small number of patients in need of frequent transfusions. To prevent clinical consequences (e.g. cardiomyopathy) known from polytransfused patients without renal disease, transplantation should be considered in RDT patients in need of frequent transfusions. Iron substitution - preferably oral - to replace dialysis-related iron loss does not cause clinically significant hemosiderosis provided iron stores are monitored adequately. A sufficient method of controlling iron stores in RDT patients under iron substitution or regular transfusion therapy is a twice annual determination of serum ferritin concentration. The treatment of choice for hemosiderosis in nontransfused RDT patients is discontinuation of iron substitution. When polytransfused RDT patients with severe hemosiderosis cannot be transplanted and submitted consecutively to phlebotomy, DFO treatment is indicated. Quantitative data regarding optimal dosage and application of DFO in RDT patients are not yet available. Constant infusion of DFO during hemodialysis may be superior to bolus application.
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PMID:Therapy and monitoring of hypersiderosis in chronic renal insufficiency. 671 93