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)

The duodenal mucosa of genotypically normal iron replete and iron deficient mice and mice with sex-linked (sla) and microcytic anemias (mk) was examined for the presence of iron-binding proteins. Following continuous, 15 or 120 minute, in vivo intraenteric exposure of a closed duodenal loop to 59Fe, a high speed supernatant of homogenized mucosal tissue was chromatographed on G-200 Sephadex. Two major peaks of 59Fe activity were observed. The molecular weight, and immunological properties of peak I were similar to ferritin whilst those of peak II were similar to transferrin. The distribution of 59Fe between peaks I and II in mk/mk animals was similar to that in genotypically normal iron deficient animals indicating that the intramucosal mechanisms for iron transport were reacting appropriately to the iron deficient state of mice with microcytic anemia. In contrast, the distribution of 59Fe between peaks I and II in sla/Y animals was the reverse of that found in genotypically normal iron deficient animals suggesting the possibility of an intramucosal iron binding protein defect in sex-linked anemia.
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PMID:Mucosal iron binding proteins in sex-linked anemia and microcytic anemia of the mouse. 28 79

The reliability of a radioimmunometric assay of serum ferritin concentration by a packaged kit was evaluated. In addition, application of the serum ferritin assay to the clinical evaluation of selected anemias was assessed. When appropriate serum dilutions were utilized, this method was sufficiently reproducible and reliable for application to the clinical laboratory. Serum ferritin was found to be a valuable tool in the differential diagnosis of anemia accompanied by hypoferremia, although iron depletion coexisting with either the anemia of chronic disease or active hepatocellular disease may not be clearly appreciated. The primary advantage of the determination was to help characterize the iron status of the patient with a hypochromic microcytic anemia or hypoferremia who would ordinarly require a bone-marrow examination for iron stores.
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PMID:Evaluation of a packaged kit assay of serum ferritin and application to clinical diagnosis of selected anemias. 69 76

Microcytic anemia is defined as the presence of small, often hypochromic, red blood cells in a peripheral blood smear and is usually characterized by a low MCV (less than 83 micron 3). Iron deficiency is the most common cause of microcytic anemia. The absence of iron stores in the bone marrow remains the most definitive test for differentiating iron deficiency from the other microcytic states, ie, anemia of chronic disease, thalassemia, and sideroblastic anemia. However, measurement of serum ferritin, iron concentration, transferrin saturation and iron-binding capacity, and, more recently, serum transferrin receptors may obviate proceeding to bone marrow evaluation. The human body maintains iron homeostasis by recycling the majority of its stores. Disruptions in this balance are commonly seen during menstruation, pregnancy, and gastrointestinal bleeding. Although the iron-absorptive capacity is able to increase upon feedback regarding total body iron stores or erythropoietic activity, this physiologic response is minimal. Significant iron loss requires replacement with iron supplements. The vast majority of patients respond effectively to inexpensive and usually well-tolerated oral iron preparations. In the rare circumstances of malabsorption, losses exceeding maximal oral replacement, or true intolerance, parenteral iron dextran is effective. In either form of treatment, it is necessary to replete iron stores in addition to correcting the anemia.
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PMID:Microcytic anemia. Differential diagnosis and management of iron deficiency anemia. 157 56

The dose of recombinant human erythropoietin (r-HuEPO) required to correct the anemia of end-stage renal disease (ESRD) varies among patients. The response to r-HuEPO is impaired if absolute or relative iron deficiency exists. Aluminum may cause a microcytic anemia in patients with ESRD, but the mechanism remains incompletely defined. Twenty-two patients in the Canadian Multicentre EPO trial were studied for 6 months. In this randomized double-blind placebo-controlled trial, free erythrocyte protoporphyrin (FEP) was used as an indicator of iron-deficient deficient erythropoiesis. The relationship of FEP to the estimates of iron availability (serum iron, transferrin saturation, ferritin) and iron utilization (corrected reticulocyte count, hemoglobin) was evaluated by multiple linear regression analysis. The effect of aluminum on FEP was evaluated by adjusting the statistical model for this variable. All patients were iron replete as assessed by serum ferritin. FEP was not related to serum aluminum before administration of r-HuEPO, but it was significantly correlated with aluminum in the treated group. In hemodialysis patients treated with r-HuEPO, the proportion of the variability explained by the parameters of iron utilization and iron availability was 0.27. The effect of aluminum increased this to 0.59. In hemodialysis patients not receiving r-HuEPO, the proportion of variability in FEP explained by the model increased from 0.16 to 0.28 by adjusting for aluminum. The data support the hypothesis that aluminum interferes with the bioavailability of stored iron for erythropoiesis and thus may result in a microcytic anemia in patients with ESRD or may blunt their response to r-HuEPO therapy.
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PMID:Bioavailability of iron in hemodialysis patients treated with erythropoietin: evidence for the inhibitory role of aluminum. 223 35

To investigate the possible causes of an increased incidence of red cell microcytosis in Asian children, 204 Gujarati Asian children and 88 European children attending community infant welfare clinics underwent initial screening tests for determination of red cell indices. Seventy six Asian (37%) and nine European (12%) children had microcytic red cells (mean corpuscular volume less than 74 fl). Further investigation showed that 16 of the Asian children (21%) with microcytosis had thalassaemia trait (eight were heterozygous for alpha thalassaemia and eight for beta thalassaemia), and 50 (66%) had suspected iron deficiency (confirmed by a response to oral iron in 41 cases): the remaining 'microcytic' children were aged less than 2 years, when mean corpuscular volume between 70 and 74 fl may be normal. Increased values for serum total iron binding capacity were more sensitive in detecting iron deficiency than reduced serum ferritin concentrations. Enthusiastic screening for microcytic anaemia in young children may mean that a substantial minority with thalassaemia genes are given unnecessary iron supplements. The response to a short course of oral iron should therefore be carefully monitored, and the possibility of thalassaemia trait as well as non-compliance with treatment should be reconsidered in all those in whom there is little or no response.
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PMID:Microcytosis, iron deficiency, and thalassaemia in preschool children. 237 18

The prevalence of iron deficiency anemia has decreased in recent years because of improved dietary habits. Yet, iron deficiency anemia is still the most common anemia. Among mature adults, anemia of chronic disease is probably more common. Mean corpuscular volume and red cell distribution width, along with a peripheral smear examination, can often distinguish iron deficiency anemia from other common microcytic anemias, such as thalassemia minor. A normal serum iron level excludes iron deficiency anemia and indicates other causes for microcytic anemia. Often, a low serum iron level and total iron-binding capacity are due to chronic disease, and measurement of serum ferritin or a bone marrow stain for hemosiderin will be necessary to diagnose iron deficiency. Iron therapy to restore the red cell mass should be continued until iron stores are replenished.
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PMID:Iron deficiency anemia. How to diagnose and correct. 240 79

In order to predict a haemoglobin (Hb) rise, in response to treatment with iron from simple erythrocyte and serological parameters, we treated 28 anaemic RA patients with oral iron during 6 weeks. Iron deficiency, present in 57% of patients, was assessed by staining a bone marrow aspirate for iron. Response rate in this group was 81% and median Hb increase was 0.8 mmol/l. After 6 weeks 69% of iron deficient patients were still anaemic. Patients without iron deficiency, considered as having anaemia of chronic disease (ACD), showed no significant Hb rise. The finding of a hypochromic microcytic anaemia was associated with a significant Hb rise. MCV showed highest specificity and predictive value (90 and 88%) and ferritin was the most valid predictor of a Hb rise within 6 weeks. Combination of low MCV and low ferritin resulted in a 100% specificity and predictive value indicating that patients with values below cut off point of these variables will definitely respond to treatment. Disease activity tended to decrease after 6 weeks, but this was not correlated with a Hb rise. It was concluded that a Hb rise can be predicted accurately by blood parameters. Using certain combinations, bone marrow aspiration is rarely necessary. Iron treatment is only useful in iron deficient RA patients, although active RA limits maximal Hb rise. In contrast to earlier findings, iron treatment had no deleterious effects on disease activity.
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PMID:Prediction and evaluation of the effect of iron treatment in anaemic RA patients. 280 11

16 chronic haemodialysis patients (group I), with non-microcytic anaemia (mean haemoglobin 7.2 g/dl, SD 1.0, range 5.8-9.8), moderate aluminium overload (serum aluminium 44 micrograms/l, SD 16, range 21-74), and normal or high iron stores (ferritin 800 micrograms/l SD 464, range 34-2013) were treated with intravenous desferrioxamine 1 g at the end of each dialysis for six months. 8 patients with similar characteristics served as controls (group II). After six months group I showed a rise in haemoglobin to 9.1 (SD 2.5) g/dl and a decrease in blood transfusion requirements, both significant, whereas group II showed no changes. Other significant changes observed in group I, but not group II, were a rise in reticulocytes and in red cell creatine and a fall in red cell protoporphyrin and serum ferritin. Ferritin decreased more in the patients whose anaemia improved. Minor increases in serum aluminium in group I did not differ from those in the control group. Desferrioxamine may benefit the anaemia of chronic haemodialysis patients through improvement of erythropoiesis. The effect seems not to be related to chelation of a heavy aluminium overload.
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PMID:Improvement in the erythropoiesis of chronic haemodialysis patients with desferrioxamine. 289 66

A method for measuring erythrocyte aluminum content was developed. Erythrocyte aluminum levels correlated with plasma aluminum concentrations in normal controls and in patients undergoing dialysis (r = 0.90, p less than 0.001). In vitro studies showed that erythrocyte aluminum concentrations were not altered by contamination of blood samples, which is a common problem with plasma determinations. The need for anticoagulation and rapid processing were disadvantages of this assay. In the dialysis population studied, the correlative data between mean cell volume and both plasma and erythrocyte aluminum levels (r = -0.50, p less than 0.001; and r = -0.69, p less than 0.001) and lack of correlation with serum ferritin suggested that aluminum overload and not iron deficiency was the cause of microcytic anemia. Patients undergoing continuous ambulatory peritoneal dialysis had lower plasma and erythrocyte aluminum levels and absence of microcytic anemia compared with patients undergoing hemodialysis. Therapy with deferoxamine in 13 patients with aluminum-related microcytic anemia resulted in a decrease in erythrocyte and plasma aluminum content in all patients (265.5 +/- 69.2 micrograms/L to 22.6 +/- 9.7 micrograms/L and 196 +/- 30 micrograms/L to 129 +/- 13.8 micrograms/L). The relatively smaller decrease in plasma aluminum levels suggested mobilization of aluminum from tissues other than erythrocytes. Aluminum chelation most probably occurred from premature erythrocytes, because in vitro studies showed that deferoxamine was unable to chelate aluminum from mature erythrocytes. Hemoglobin level, hematocrit measurement, and mean cell volume showed significant improvement (p less than 0.001). Ten patients showed normalized mean cell volume after 6.2 +/- 2 months of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Application of an erythrocyte aluminum assay in the diagnosis of aluminum-associated microcytic anemia in patients undergoing dialysis and response to deferoxamine therapy. 290 50

The level of haemoglobin, serum iron, total iron binding capacity and ferritin were measured in patients with rheumatological conditions who were anaemic at the time of upper gastrointestinal endoscopy. These parameters were similar in patients with or without lesions of their upper gastrointestinal tract, and in patients with a positive or negative faecal occult blood result. Lesions of the upper gastrointestinal tract were not more frequent in patients with a microcytic anaemia when compared to those with a normocytic anaemia, nor were they found more frequently in patients with a positive faecal occult blood test. Lesions visible at upper gastrointestinal endoscopy are not an important cause of microcytic anaemia in patients with arthritis. The finding that patients with normocytic anaemia are more likely to proceed to lower bowel examination than patients with microcytic anaemia is a reflection of the difficulty in interpretation of these simple haematological tests and showed they were unhelpful in determining which patients warrant investigation of the lower bowel. The frequency of further investigation of the lower bowel was significantly reduced by a positive endoscopy report, irrespective of the nature of the lesion, but was not significantly increased by finding faecal occult blood. We suggest that patients with arthritis selected for investigation of possible gastrointestinal blood loss should follow an organized plan of investigation that includes examination of both upper and lower bowel, and which should proceed uninfluenced by pro tem results. Unfortunately the selection of patients for such further investigation is hampered by a lack of simple discriminatory tests.
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PMID:Anaemia in patients with arthritis: are simple investigations helpful? 291 44


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