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)

This study attempts to evaluate the adequacy of the erythropoietin (EPO) response in 42 anaemic patients with advanced human immunodeficiency virus (HIV) infection [30 with acquired immunodeficiency syndrome (AIDS) and 12 with AIDS-related conditions] by comparing their serum EPO levels with those found in a non-HIV reference population consisting of 36 patients with anaemia of chronic disorders (ACD) and 57 with iron deficiency anaemia (IDA). Although the average Hb concentration was similar in the three groups, the EPO level for HIV patients (mean +/- SEM, 64.3 +/- 7.7 mU/ml) did not differ significantly from that in ACD patients (45.3 +/- 8.3 mU/ml, P > 0.1), and both groups had a lower mean EPO level (P < 0.05 and P < 0.01 respectively) than IDA subjects (133.5 +/- 18.7 mU/ml). Thirteen HIV patients on zidovudine therapy showed similar mean Hb and EPO levels to those in the untreated patients. A significant inverse correlation between the log of serum EPO and the Hb values was observed in the three groups. However, this relationship was found to be stronger in IDA patients than in either HIV or ACD subjects (P < 0.001), with no difference between the two latter groups (P > 0.2). These data suggest that the EPO response is blunted in the anaemia associated with advanced HIV infection.
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PMID:Serum erythropoietin levels in anaemic patients with advanced human immunodeficiency virus infection. 148 42

Erythroid alterations were studied in 136 patients with rheumatoid arthritis (RA). Anemia was present in 75 cases. A definite diagnosis was determined in 65. The most frequent anemia was that of chronic disease (ACD) (43 cases); 14 patients with ACD presented with moderate to severe anemia. Prevalence of deficiencies were also high (15 cases had iron deficiency anemia, IDA). Serum erythropoietin levels were different in patients with RA compared with a healthy control group (p < 0.00001). Serum erythropoietin was increased in ACD (49 +/- 28.8 U/l) with respect to both RA (38.6 +/- 12.7 U/l, p = 0.0036) and controls (18.2 +/- 7.6 U/l, p < 0.00001). Although hemoglobin (Hb) was similar in ACD and IDA, serum erythropoietin in ACD was lower than in IDA (p = 0.01). There was a negative relationship between Hb and serum erythropoietin in ACD (r = -0.42, p = 0.005). In conclusion, almost 50% of patients with RA have anemia and ACD is the most frequent. As serum erythropoietin in ACD is blunted, patients with moderate to severe ACD are possible candidates for erythropoietin treatment.
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PMID:Erythroid abnormalities in rheumatoid arthritis: the role of erythropoietin. 149 87

To assess the effects of decreased erythrocyte production on the levels of serum erythropoietin in children, we measured simultaneous hemoglobin concentrations and erythropoietin in 18 children with iron deficiency anemia, 17 children with transient erythroblastopenia of childhood (TEC), and 7 children with aplastic anemia. In all but two patients (one with TEC; one with aplastic anemia), erythropoietin was measured at diagnosis, before institution of specific therapy for the anemia. There was a statistically significant inverse linear correlation between log10 erythropoietin and hemoglobin values for all patient groups (r = 0.904 to 0.912; p less than 0.005). A comparison of the slopes of the regressions for each patient group by analysis of covariance revealed a significantly steeper slope for the iron deficiency group (-0.553) versus the TEC (-0.287) and aplastic anemia (-0.256) groups (p = 0.0001). The difference in erythropoietin levels appeared greatest in patients whose presenting hemoglobin level was greater than 5 gm/dl. Decline in serum erythropoietin levels was more precipitous in the less severely anemic patients with iron deficiency anemia than in the patients with TEC or aplastic anemia. These data reveal quantitative and qualitative differences in the relationship between serum erythropoietin and hemoglobin levels when children with severe iron deficiency anemia versus those with TEC or aplastic anemia are considered, even though all three conditions are characterized by hypoproliferation of erythrocytes.
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PMID:Comparison of the erythropoietin response in children with aplastic anemia, transient erythroblastopenia, and iron deficiency. 155 89

ACD is probably the most common anemia among hospitalized medical patients. It is variably defined by its clinical and, particularly, its laboratory manifestations. The most consistent features are low serum iron and normal or increased serum ferritin levels, reflecting normal or increased iron stores and distinguishing ACD from iron deficiency anemia. ACD often coexists with iron deficiency and the anemia of renal insufficiency. Most patients have an underlying infectious, inflammatory, or neoplastic disease, but as many as one quarter of patients do not. Several mechanisms have been proposed, the most significant of which are a block in reutilization of hemoglobin iron for red cell production and relative deficiency of erythropoietin, but the pathogenesis and mediators involved remain uncertain. The anemia itself seldom requires treatment and is ameliorated by successful treatment of the underlying disease.
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PMID:Anemia of chronic disease. 157 57

Nine patients with myelodysplastic syndromes and one patient with agnogenic myeloid metaplasia have been treated with recombinant human erythropoietin (rhEpo), at the dose of 150 U/kg/day. Although serum Epo levels were correlated with hemoglobin concentrations in the whole population of patients, they clearly appeared inadequate in some instances, if compared to those of a group of control subjects with iron deficiency anemia. Moreover, no correlation was found between serum Epo and reticulocytes. Six patients showed a partial or complete response to the treatment and the outcome was not correlated with the pre-therapy serum Epo levels; however, serum Epo was less than 100 mU/ml in three of four patients who achieved a complete response. The mechanism(s) by which Epo stimulated erythrocyte production in myelodysplastic patients is unclear, because the number of both the reticulocytes and erythroid progenitors remained unchanged during and at the conclusion of a three months' therapy. Further studies are needed to better define the optimal dosage required to correct anemia in myelodysplastic syndromes, and to clarify rhEpo mechanism of action in these diseases.
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PMID:Recombinant human erythropoietin for treatment of myelodysplastic syndromes. 158 94

Anaemia in rheumatoid arthritis (RA) is a common and debilitating complication. The most common causes of this anaemia are iron deficiency and anaemia of chronic disease. Investigations have suggested that interleukin 1 (IL-1) or tumour necrosis factor (TNF), or both, from monocytes associated with chronic inflammation are responsible for the anaemia of chronic disease. On bone marrow examination anaemia of chronic disease is characterised by the diversion of iron from the erythropoietic compartment into marrow macrophages. This phenomenon is termed failure of iron utilisation. In this study, CFU-E (colony forming unit erythroid; late red cell precursors) and BFU-E (burst forming unit erythroid; early red cell precursors) stem cells were cultured from 10 normal marrow samples and 12 marrow samples from patients with RA with iron deficiency anaemia and 10 samples from patients with RA with failure of iron utilisation. All patients with RA were anaemic (haemoglobin less than 100 g/l), Potential accessory or inhibitory cells of erythropoiesis (CD4, CD8, or CD14 positive cells) were removed before culture. Control marrow samples were studied in a similar manner. Normal marrow samples yielded 377 (17) CFU-E and 133 (6) BFU-E (mean (SD)) colonies for each 2 x 10(5) light density cells plated. CD4 ablation caused reductions of 62 and 100% in CFU-E and BFU-E colonies respectively. CD14 removal resulted in considerable but lesser reductions of 46% for CFU-E and 25% for BFU-E. In both groups of patients with RA, CFU-E colony numbers were significantly lower than those seen in normal control subjects, 293 (17) for patients with iron deficiency anaemia and 242 (35) for patients with failure of iron utilisation. BFU-E colony numbers were 102 (13) and 108 (20) respectively. In patients with RA, CD4 removal caused a significantly greater loss of CFU-E colonies compared with normal control subjects. Cytolysis of CD14 positive cells caused a reduction in CFU-E colonies in the two RA groups which was similar to that seen in normal subjects. In conclusion, patients with RA seem to have fewer CFU-E progenitors but essentially normal numbers of BFU-E stem cells. Our data suggest a stimulatory role for marrow CD4 and CD14 cells in erythropoiesis in patients with RA. Monocytes-macrophages (CD14 positive) are known to be producers of IL-1 or TNF, or both, however, the predicted increase in the CFU-E colonies on removal of CD14 cells is not seen. Therefore, if IL-1 or TNF, or both, are responsible for the impairment of erythropoiesis in patients with RA, marrow macrophages are unlikely to be the source. Moreover, these results indicate the probability of erythropoietin resistance on the basis of diminished CFU-E colony formation in patients with RA.
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PMID:Anaemia of chronic disease in rheumatoid arthritis: effect of the blunted response to erythropoietin and of interleukin 1 production by marrow macrophages. 161 58

We evaluated the relationship between erythropoietin (EPO) and hemoglobin (Hb) concentrations in 156 normal subjects ranging from 60 to 98 years old. EPO was determined by a radioimmunoassay. The serum EPO concentration in subjects with Hb concentrations greater than 12.0 g/dl (26.9 +/- 15.2 mU/ml), was significantly higher than that in younger controls (15.8 +/- 5.0 mU/ml, p less than 0.001). No sex difference in serum EPO level was detected. In addition, there was an inverse semilogarithmic relationship between EPO and Hb concentrations in subjects with Hb concentrations less than 12.0 g/dl (r = -0.559, p less than 0.001). EPO concentrations in the elderly were lower than those in young subjects with iron deficiency anemia with the same Hb level. Thus, in the elderly, a high EPO concentration may be preventing a decrease in the Hb concentration. However, a decreased EPO response to low Hb concentrations may be a contributing factor in anemia in the elderly.
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PMID:Serum erythropoietin levels in the elderly. 176 84

The effect of iron supplementation, 66 mg elemental iron daily, from the 16th week of gestation to delivery, on iron status markers during uncomplicated pregnancies was assessed in a randomised, double-blind, placebo controlled study of 207 healthy women (100 iron treated, 107 placebo treated) and their newborn babies. Haemoglobin (Hb) and serum (S-) human placental lactogen (HPL) were measured in all 207 females, while transferrin saturation, S-ferritin and S-erythropoietin (EPO) were measured in 120 females at monthly intervals. Hb: from 27th week of gestation to eight weeks post partum, the placebo treated group had significantly lower Hb levels than the iron treated group (p less than 0.001). Iron status markers: in the placebo group (n = 57), 92% developed exhausted iron stores (i.e. S-ferritin less than or equal to 20 micrograms/l), 65% latent iron deficiency (i.e. S-ferritin less than or equal to 20 micrograms/l and transferrin saturation less than 15%), and 18% iron deficiency anaemia (i.e. S-ferritin less than or equal to 20 micrograms/l, transferrin saturation less than 15% and Hb less than 110 g/l). In the iron treated group (n = 63), 54% developed exhausted iron stores, 6% latent iron deficiency, and none iron deficiency anaemia. S-EPO: the placebo group had significantly higher values than the iron treated group from the 27th week of gestation to one week post partum (p less than 0.01). S-HPL: levels were identical in placebo and iron treated females. Babies of iron treated mothers had higher S-ferritin than babies of placebo treated mothers (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Iron supplementation during pregnancy. Effect on iron status markers, serum erythropoietin and human placental lactogen. A placebo controlled study in 207 Danish women. 180 36

Pathophysiological and therapeutic properties of anemia in rats with adjuvant-induced arthritis (AA) were investigated. Both anemia and chronic inflammation were induced in rats by a single injection of Freund's complete adjuvant. This study confirmed other earlier data that these anemic rats with AA had reduced serum iron levels and that the anemia was characterized as mild, non-progressive, hypochromic, microcytic. In addition, our studies showed that these anemic rats had slightly but significantly enhanced erythropoietin titers, but not renal failure; there was no significant difference in blood urea nitrogen and creatinine levels in anemic and normal groups. The anemia in rats with AA was improved by recombinant human erythropoietin (r-HuEPO) at 30 and 100 U/kg/day, given i.v. for 5 days. In contrast, iron-chondroitin-sulfate colloid (10 mg/kg/day, i.v. for 5 days) failed to improve the anemia and to enhance the effects of r-HuEPO. These data suggest that anemia in rats with adjuvant-induced arthritis is distinguished, pathophysiologically and therapeutically, from iron deficiency anemia, hemolytic anemia, and renal anemia.
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PMID:Recombinant human erythropoietin, but not iron supplementation, improves anemia in rats with adjuvant-induced arthritis. 181 58

One of the most important factors for the proliferation and hemoglobin synthesis of erythroid cells is iron atom. This atom is tightly bound to serum transferrin (Tf) and is taken up by erythroblasts and reticulocytes through transferrin receptor (TfR). Both Tf and TfR are reutilizable and have roles for the efficient intracellular accumulation of iron. In addition to the reutilization (recycling), the expression of TfR is also regulated by cytoplasmic iron concentration; the increase of iron downregulate the synthesis of TfR at the translational level and vice versa. This mechanism was recently explained by the binding between "iron responsive element (IRE)" in the 5' end of TfR mRNA and IRE binding protein by a transacting manner. Johnstone et al, and we found that TfR was externalized from sheep reticulocyte and human erythroleukemia cell, K562, respectively. Furthermore, we confirmed that this shed TfR was detected in blood and concluded that the quantitation of TfR in serum is a useful index for evaluating the erythropoiesis. The serum TfR was increased in iron deficiency anemia, hemolytic anemia and polycythemia and was decreased in aplastic anemia. In renal anemia, it was increased after the administration of erythropoietin (Epo). By the in vitro liquid culture of peripheral blood stem cells using interleukin 3 and Epo, it was found that soluble TfR was derived from the erythroblasts during the maturation process.
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PMID:[Expression and extracellular release of transferrin receptors on erythropoiesis]. 189 Jul 32


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