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)

Knowledge of disturbancies of iron utilization has been considerably extended by histochemical-ultrastructural findings and the results of immunoradiometric assays for serum ferritin. -- In chronic anaemia due to infections or neoplastic diseases hyposideraemia and normal unsaturated iron binding capacity were associated with increased iron retention in macrophages and slightly to highly increased serum ferritin (500--4000 ng/ml). -- 117 patients with sideroblastic anaemia formed a heterogenous group of diverse aetiology. The iron granules of ringed sideroblasts contained nonferritin iron in mitochondria. At diagnosis, a normal iron status was found in single cases. More frequently, praelatent and latent iron overload with ferritin levels up to more than 2000 ng/ml were observed. Manifest iron overload with tissue damage was mostly the result of numerous transfusions (ferritin 4700 bis 9500 ng/ml). -- After i.v. application of colloidal iron endothelial siderosis was a regular finding. The typical uniform granules representing nonferritin-iron in lysosomes disappeared in the course of 1--3 years completely. In contrast, the colloidal iron taken up simultaneously by the macrophages was rapidly transformed into ferritin and easily used up for haemoglobin synthesis when required. The corresponding increase of serum ferritin up to maximal 4000 mg/ml was dose related. Continued blood losses lead to residual endothelial siderosis after exhaustion of macrophageal iron and recurrence of iron deficiency anaemia. The serum ferritin fell to low levels (0--12 ng/ml) as observed in untreated cases.
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PMID:[Disturbancies of iron utilization: chronic anaemia, sideroblastic anaemia, and residual endothelial siderosis (author's transl)]. 73 33

A multicentre study was carried out in a sample population of healthy volunteers in order to assess the usefulness of assaying serum ferritin to monitor the extent of reserves in subjects with a risk of iron deficiency. A total of 317 subjects were included in the study. Ninety-nine were children with a mean age of 19 months, 121 were adolescents with a mean age of 18 years and 7 months, and 97 were women with a mean age of 28 years and 9 months. Levels of serum ferritin below the normal minimum levels for each age bracket, an indication of the exhaustion of the body's reserves, were found in 29% of children, 32.2% of adolescents and 27.8% of women. This study therefore confirm the frequent onset, even in our modern society, of iron-deficient states at particular times of life and that these are easily overlooked. The measurements of serum ferritin levels, in addition to being a confirmatory test in cases of suspected sideropenic anemia, has the peculiar characteristic of being the only test able to identify risk subjects before they become symptomatic. This enables rapid treatment to be commenced or better, efficient prevention.
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PMID:[Multicenter study of serum ferritin assay for the surveillance of subjects at risk of iron deficiency]. 194 3

Determination of serum ferritin is an important means of assessing body iron stores. Trace amounts of ferritin normally present in serum are detectable by sensitive radioimmunoassay techniques or an enzyme immunoassay procedure. Ferritin normally accounts for no more than a very small fraction of the total iron in serum, but generally maintains a stable concentration that is proportional to the much larger pool of storage iron in tissues. The serum ferritin assay, in contrast to other measurements of iron status such as hemoglobin, serum iron and iron-binding capacity, can distinguish differences in iron stores within the physiological range. In iron deficiency anemia, the concentration is below 10 ng per ml. Increased concentrations (above 200 ng per ml) are found in conditions with increased iron stores. The information it provides is similar to that obtained from bone-marrow aspirates stained for iron. In contrast to the percent transferrin-saturation and concentration of erythrocyte protoporphyrin, ferritin concentrations become abnormal before exhaustion of mobilizable iron stores and before the onset of anemia. Serum ferritin also provides a practical means of assessing new programs of iron supplementation, since it reflects various degrees of iron deficiency and overload.
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PMID:The measurement and interpretation of serum ferritin. 700 32

While the crucial role of haemoglobin in aerobic exercise has been well accepted, there is still a great deal of controversy about the optimal haematological parameters in the athletic population. The initial part of this review will examine the question of anaemia in athletes. The most common finding in athletes is a dilutional pseudoanaemia that is caused by a plasma volume expansion, rather than an actual blood loss. It is not a pathological state and normalises with training cessation in 3 to 5 days. This entity should be distinguished from conditions associated with lowered blood counts, such as intravascular haemolysis or iron deficiency anaemia. The evaluation of true anaemia states in the athlete must take into account not only blood losses secondary to exercise, such as foot strike haemolysis or iron losses through sweat, but non-athletic causes as well. Depending on the age and sex of the athlete, consideration must be given to evaluation of the gastrointestinal or genitourinary systems for blood loss. Finally, a comprehensive nutritional history must be taken, as athletes, especially women, are frequently not consuming adequate dietary iron. The second section of the paper will deal with the very contentious issue of sickle cell trait. While there have been studies demonstrating an increased risk of sudden death in people with sickle cell trait, it is still quite rare and should not be used as a restriction to activity. Further, studies have demonstrated that patients with sickle cell trait have an exercise capacity that is probably normal or near normal. However, in the cases of sudden death, it has been secondary to rhabdomyolysis occurring among sickle cell trait athletes performing at intense exertion under hot conditions, soon after arriving at altitude. The recommendations are that athletes with sickle cell trait adhere to compliance with the general guidelines for fluid replacement and acclimatisation to hot conditions and altitude. The final section of the paper examines the issue of haematological manipulation for the purposes of ergogenic improvement. Although experiments with blood doping revealed improvements in running time to exhaustion and maximal oxygen uptake, the introduction of recombinant erythropoietin has rendered blood doping little more than a historical footnote. However, the improvements in performance are not without risk, and the use of exogenous erythropoietin has the potential for increased viscosity of the blood and thrombosis with potentially fatal results. Until a definitive test is developed for detection of exogenous erythropoietin, it will continue to be a part of elite athletics.
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PMID:Sports haematology. 1068 81

This is to introduce a new method for determining the amount of blood loss by measuring the storage iron decrease rate (SID), as obtained by following serum ferritin after intravenous iron therapy in a patient with iron deficiency anemia due to intestinal blood loss. The patient was followed from the day S, when iron therapy started, to the day E, when serum ferritin decreased to 12 microg/l, indicating the exhaustion of the iron stores. The SID was calculated from the formula: SID=(T-R)/D, where, T mg = total amount of injected iron, R mg = the difference in the iron in the hemoglobin (deltaHb) between day S and E, and D = days from S to E. The SID was thought to be iron loss only, as the contribution of iron absorption and iron loss to the SID, with the exception of bleeding, was believed to be negligible and as the serum ferritin decrease curve was exponentially linear. Using the formula, V = iron loss/iron in mean Hb, the amount of blood loss: V=29 ml/day was obtained. This method can also be used for the quantitation of blood loss in other patients with chronic blood loss, because the SID could also be determined in 12 cases of post-treatment iron deficiency anemia with chronic blood loss.
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PMID:[Method for determining the amount of blood loss using the storage iron decrease rate as obtained from serum ferritin after intravenous iron therapy]. 1560 83

The common nutritional deficiency, iron deficiency, causes Iron Deficiency Anemia (IDA) throughout the world especially in the developing countries. In Ayurveda, different herbal, mineral or herbomineral drugs have been emphasized to combat anemia (Panduroga). Trikatrayadi Lauha and Fersolate-CM (a modern medicine taken as standard control) were administered to the patients to evaluate their role in Panduroga. A simple random sampling method was followed for the clinical study. The 56 iron deficiency anemic patients of both sexes and age group between 16 to 70 years divided into two groups - Group-A (n=34) and Group-C (n=22) were treated with Trikatrayadi lauha and Fersolate-CM, respectively. Both drugs provided significant effect on the signs and symptoms of Shrama (fatigue), Shwasa (dyspnea on exertion), Daurbalya (weakness), Pandu Varna (pallor/yellowish-whitish), Hridspandana (palpitation), Hatanala (diminished digestive capacity), Bhrama (giddiness), Aruchi (anorexia), Arohana Ayasa (exhaustion during climbing), Shiroruja (headache) and Shotha (edema). Trikatrayadi Lauha provided significant results on Hb gm%, RBC, PCV, MCV, serum iron, percent transferrin saturation and TIBC where as insignificant changes were found in MCH and MCHC. Fersolate-CM provided significant results on Hb gm%, RBC, PCV, MCV, MCH, serum iron, percent transferrin saturation and TIBC whereas insignificant change was found in MCHC. Trikatrayadi Lauha showed significant results on Panduroga and Iron Deficiency Anaemia (IDA).
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PMID:Efficacy of Trikatrayadi Lauha in Panduroga with reference to Iron Deficiency Anemia. 2304 86