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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients receiving erythropoietin therapy require large quantities of iron to keep pace with the demands of the bone marrow during active erythropoiesis. If this iron supply to the marrow is not maintained, the response to erythropoietin is impaired, and indeed iron insufficiency is the most common cause of a poor response to this drug. Iron deficiency may be either absolute, which is defined as a reduction in total body iron stores, or functional, which implies adequate iron stores but a failure to supply available iron to the marrow or a failure in the utilization of this iron in the process of erythropoiesis. The detection of absolute or functional iron deficiency is difficult because there is no absolutely reliable marker of iron status, with the exception of an unequivocally low serum ferritin level. Measurement of serum ferritin and transferrin saturation are the most widely used methods, but both have drawbacks. Monitoring of the percentage of hypochromic erythrocytes in the circulation also seems promising, but the technology is of limited availability, and other methods (eg, monitoring erythrocyte ferritin, free erythrocyte protoporphyrin, and erythrocyte zinc protoporphyrin levels) lack widespread validation. Treatment of iron insufficiency is accomplished by intensifying iron supplementation either orally or intravenously, and in many instances the latter route becomes necessary. The high cost of erythropoietin demands that iron deficiency be screened for on a regular basis and treated to maximize the benefits of this drug.
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PMID:Monitoring of iron status and iron supplementation in patients treated with erythropoietin. 788 86

Treatment of renal anemia with recombinant human erythropoietin (rEPO) frequently raises arterial blood pressure. The objective of this study was to determine whether this is a direct effect of rEPO or a consequence of the expansion of erythrocyte mass. Twenty-three chronic hemodialysis patients receiving maintenance rEPO therapy who had uncontrolled anemia due to iron deficiency were studied. It was anticipated that repletion of iron stores with iv iron dextran would restore rEPO responsiveness, leading to a gradual rise in hematocrit to the target values (0.30 to 0.33). The effect of the increase in hematocrit on arterial blood pressure could then be dissected from the direct effect of rEPO in patients receiving constant doses of rEPO throughout the study period. To this end, arterial blood pressure, iron indices, hematocrit, and measures of fluid balance were monitored at baseline and for a 10-wk period after iron repletion. In eight patients, the hematocrit transiently rose above 0.33, triggering a reduction in rEPO dosage. In the remaining 15 patients, rEPO dosage was held constant during the study period. In this subgroup, repletion of iron stores led to a rise in hematocrit from 0.25 +/- 0.04 to 0.32 +/- 0.04 (P < 0.001) within 4 wk. Despite the significant rise in hematocrit, both systolic and diastolic blood pressure values remained virtually unchanged. Likewise, body weight and interdialytic fluid gain were unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of erythrocyte mass on arterial blood pressure in dialysis patients receiving maintenance erythropoietin therapy. 791 37

The serum transferrin receptor (TfR) level reflects iron status and the rate of erythropoiesis. This study was undertaken to assess the role of serum TfR in the iron status and erythropoiesis in very-low-birth-weight infants under conditions in which erythropoiesis is stimulated by large doses of recombinant human erythropoietin (rHuEPO) and oral iron. The first 34 infants were followed from the 3rd to 11th wk of life or until discharged. They received iron at a rate of 3 mg/kg/d. The subsequent 21 infants were given rHuEPO (300 U/kg three times a week s.c.) and iron at a rate of 6 mg/kg/d from the 3rd or 4th wk of life for a mean of 3.4 wk. With this treatment, the need for transfusion was reduced from 1.4 +/- 0.4 to 0.1 +/- 0.1 transfusions per infant (p = 0.02). The serum TfR concentrations in the rHuEPO-treated infants increased gradually to values several-fold higher than those in the untreated infants. This increase was not related to intrauterine or postnatal growth, protein intake, or serum albumin concentration. Neither was an association observed between Hb and TfR concentration. In the treated infants, the serum ferritin concentration was lower at the 4th, 5th, and 7th wk of life than in the untreated infants. The very-low-birth-weight infants who were given large doses of rHuEPO and iron had a marked rise in serum TfR concentration and a small decline in serum ferritin concentration. These events have been related to iron deficiency.
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PMID:Early rise in serum concentration of transferrin receptor induced by recombinant human erythropoietin in very-low-birth-weight infants. 793 43

Anemia does not correct in many kidney transplant recipients, probably due to iron deficiency or inadequate erythropoietin (Epo) production. We evaluated effects of iron (Fe) availability on correction of anemia in renal transplant recipients and sought to characterize patterns of early Epo production by transplanted kidneys as related to peritransplant factors. In a prospective randomized trial, 51 consecutive renal transplant patients were followed for 6 months. Epo was measured on days 0, 3, 14, 48 and 168 posttransplantation. Fe status was monitored on days 14, 48 and 168. Pts were randomized at day 14 based on Fe status. Iron-deficient (FeD) patients (n = 24) were randomized to receive daily Fe supplementation (FeDs, n = 12) or no supplementation (FeDns, n = 12). Those with normal Fe status (FeN, n = 27) were followed as controls. No differences were found between groups at day 0 for Hct, Cr, Epo, age, dialysis history, or type of donor. Day 3 Creatinine and Hct were similar among groups, while Epo was significantly higher in FeD groups vs FeN (p < 0.004), and continued higher at 6 months. Though each pt improved Hct, most FeDns and FeN were anemic and Fe deficient at 6 months while all FeDs patients had corrected their anemia (p < or = 0.009) and Fe status. Four FeDs patients developed polycythemia. Epo production correlated inversely to cold ischemia time in cadaver renal allografts (p < 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting erythropoietin production and correction of anemia in kidney transplant recipients. 794 39

Erythropoietin has been shown to be effective both in the reversal of anaemia in patients with end-stage renal failure and to increase the volume of autologous red blood cells donated preoperatively as well as to decrease the units of homologous blood transfused. This review analyzes the side effects of erythropoietin reported in the literature for long-term administration (mainly in patients with end-stage renal failure) as well as for acute/short-term administration (in patients participating in an autologous predeposit programme). The most important adverse events reported for long-term administration are as follows: (a) arterial hypertension; (b) cerebral convulsion/hypertensive encephalopathy; (c) thrombo-embolism; (d) iron deficiency; (e) influenza-like syndrome. The numbers given for these side effects are mainly taken from the first and dose-finding studies in patients with renal failure. These figures differ very much from the data given in controlled studies analyzing adverse events as well. Summarizing the results from controlled, multi-center trials in patients with end-stage renal failure or in AIDS patients, no significant differences have been observed between the control group and the patients treated with erythropoietin. The overall-incidence of side effects occurring in either group of these two studies was of approximately 83% and 95%, respectively. In contrast to these results the data published for the dose finding/treatment studies is approximately 30% for development of arterial hypertension, approximately 5% for occurrence of cerebral convulsion/hypertensive encephalopathy, approximately 10% for thrombo-embolic complications/clotting of vascular access, approximately 50% for development of iron deficiency, and approximately 10% for symptoms summarized as influenza-like syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse events of erythropoietin in long-term and in acute/short-term treatment. 795 Jan 71

The aim of this study was to investigate the effects of recombinant human erythropoietin (rh-EPO) in patients with cancer-related anaemia. Thirty-six ambulatory patients who had malignant neoplasms and haemoglobin (Hb) values of < 11 g/dl (Pretoria is 1,310 m above sea level) entered the study. Patients with renal insufficiency or anaemia caused by bleeding or haemolysis, and patients with iron deficiency or megaloblastic anaemia, were not entered in the study. 22 IU/kg rh-EPO was given subcutaneously 3 times/week. The dose was escalated if Hb values did not rise after 4 weeks. All 36 patients were evaluable for toxicity. Side effects ascribed to rh-EPO were pain or discomfort at the site of injection (12 patients), heart palpitations (3 patients), skin rash (2 patients) and hypertension, deep vein thrombosis, and myalgia in 1 patient each. Thirty of the 36 patients who entered the study were evaluable for response. There were 16 females and 14 males among the evaluable patients. Median age was 64.5 years. Response, defined as an increase of Hb of at least 2 g/dl or to 12.5 g/dl, for at least 1 month, was documented in 12 patients. This was accompanied by an improvement in performance status and occurred within 1 month in 5 of the 12 patients who responded. rh-EPO has a limited but measurable therapeutic value for patients with cancer-associated anaemia.
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PMID:Recombinant human erythropoietin in the treatment of cancer-related anaemia. 797 Apr 93

Various studies have shown that peritoneal dialysis patients may require less erythropoietin (rHuEPO) than maintenance hemodialysis patients. Iron deficiency in hemodialysis patients may contribute to the difference in response. This study compares the response to rHuEPO in 24 patients on CAPD to 33 patients on hemodialysis. All the hemodialysis patients received intravenous iron to prevent iron deficiency. Peritoneal dialysis patients received rHuEPO subcutaneously twice weekly. Erythropoietin was administered intravenously thrice weekly in hemodialysis patients. In peritoneal dialysis patients, hematocrit was 23.1% and 30.1%, rHuEPO dose was 80.9 and 89.0 u/kg/wk, while in hemodialysis patients hematocrit was 22.2% and 31.2%, and rHuEPO dosage was 140.2 and 154.3 u/kg/wk at initiation, and six months after therapy (p < 0.05 for dose, hemodialysis vs CAPD). Serum iron and transferrin saturation remained normal both in peritoneal and hemodialysis patients. These findings suggest that hemodialysis patients require a higher dosage of rHuEPO than peritoneal dialysis patients for a comparable rise in hematocrit, even when iron deficiency is prevented with parenteral iron. The improved efficacy of rHuEPO in CAPD patients may be due to the better removal of the inhibitors of erythropoiesis and/or the subcutaneous route of administration.
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PMID:Improved response to erythropoietin in peritoneal dialysis patients as compared to hemodialysis patients: role of iron deficiency. 799 11

Recombinant human erythropoietin (EPO) is an effective and safe therapy for correction of anemia in end-stage renal disease (ESRD). Clinical trials reported to date suggest that EPO improves anemia in over 90% of hemodialysis patients with anemia (Eschbach 1989). Factors which have been identified that appear to inhibit the effectiveness of EPO are infection [Muirhead N et al. 1990], iron deficiency, hyperparathyroidism, aluminium excess [Casati 1991] and persistent GIT bleeding. The development of reticulocytosis in response to EPO in the absence of a rise in hematocrit should alert the clinician to the possibility of either hemolysis or occult blood loss. We present a case in which, despite the development of a reticulocytosis of 5% in response to EPO and the absence of hemolysis, we had difficulty in identifying the presumed source of blood loss.
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PMID:Chronic occult intra-alveolar hemorrhage: a rare cause of failure to respond to erythropoietin. 800 33

Prior to beginning to administration erythropoietin (EPO) in 1989, we examined the relationships of hematocrit (HCT), mean corpuscular volume (MCV), and serum ferritin (FER) in one group of hemodialysis patients (group A, n = 117) and replicated the findings in a second group (group B, n = 73). The groups had similar mean (+/- SD) HCT (A: 25.7 +/- 5.3%; B: 25.2 +/- 5.1%), MCV (A: 83.3 +/- 6.5 fl; B: 83.5 +/- 7.5 fl) and FER (A: 607 +/- 1446 micrograms/l; B: 374 +/- 601 micrograms/l). For group A, iron stores [log (FER)] correlated inversely with HCT (r = -0.44, p < 10(-4)) and directly with MCV (r = 0.32, p < 10(-3)). After dividing group A into octiles by the FER level, the lowest octile (mean FER 17.8 +/- 6.2 micrograms/l) had the highest mean HCT (29.5 +/- 6.4%) and lowest mean MCV (80.8 +/- 7.1 fl), while the highest octile (mean FER 3,312 +/- 3,005 micrograms/l) had the lowest mean HCT (21.9 +/- 2.8%) and the second-highest mean MCV (86.4 +/- 4.9 fl). The trends were similar in group B. We conclude that increased erythropoiesis appeared to cause or, at least, unmask iron deficiency in HD patients even prior to the advent of EPO therapy. Variations in the level of erythropoiesis among these patients (presumably due to variation in EPO levels, chronic inflammation) strongly influenced the determinants of iron stores (i.e., marrow utilization of iron, transfusion need); iron stores, in turn, influenced MCV.
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PMID:Serum ferritin, hematocrit and mean corpuscular volume in hemodialysis. 805 64

The level of plasma erythropoietic activity was determined in healthy and iron deficiency anemia children by bioassay in vitro. The erythropoietic activity in healthy children was 13.6 +/- 2.9 (5.0-24.8) mU/ml and the lowest activity was in two month (6.3 +/- 0.7) and three month (6.9 +/- 1.4) mU/ml healthy children. The erythropoietic activity was increased from 40.5 to 715.0 mU/ml in iron deficiency anemia children and its level distinctly depends on anemia stage and iron deficiency. From this study we suggest, that erythropoietin is produced in response of anemia. The results also demonstrate the necessity of erythropoietin treatment in iron deficiency anemia in early infants.
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PMID:[Plasma erythropoietic activity in healthy children and in children with iron-deficiency anemia]. 805 70


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