[Iron deficiency anemia in a female gastrectomized for cancer. Involvement of iron deficiency factors].
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Anemia↗
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[Control of iron deficiency in developing countries].
Iron deficiency is the most prevalent nutritional disorder worldwide, especially in developing countries. It occurs when iron absorption cannot compensate iron requirements and losses. Requirements are especially high in pregnant women, infants, young children and adolescents who run a higher risk of being iron-deficient. In developing countries, the main cause of iron deficiency is the low iron bioavailability of the diet. The consequences of iron deficiency are many and serious, affecting not only individuals' health but also the development of societies and countries. The prevention and the control of iron deficiency and anemia in all groups of a population with different iron requirements imply to coordinate different interventions. Iron fortification of staple foods or condiments directed to the whole population is a sustainable and low cost-effective approach. However, at some periods of life, especially during pregnancy and in children from the age of 6 months, iron requirements are high. For pregnant women, the current approach favours the daily iron-folate supplementation during pregnancy but the results in terms of public health are disappointing. The preventive weekly iron-folate supplementation of women during their reproductive life, whose efficacy is recognized, offers a promising alternative; its impact in terms of public health is under current evaluation. For infants and young children, iron fortification of complementary food is effective but this food is generally imported and economically inaccessible to populations with limited resources. The production, by small private units from local products, of complementary foods of low viscosity, good nutritional quality, fortified with vitamins and minerals, and of low cost is at hand in several countries. When complementary foods are not available, the preventive iron supplementation from 6 to 18 months of age has to be advised. This approach should be strengthened by the advantages of the weekly approach. These interventions are more effective when they integrate other approaches like the improvement of the nutritional practices, infection control and the promotion of breast-feeding and when coupled with programs aiming to control other micronutrient deficiencies. The success of most interventions requires the active participation of the individuals. Information and education of the populations, especially through social mobilization campaigns, are essential because iron deficiency induces few visible symptoms, not easily recognizable by individuals. The implementation of national nutrition plans including the control of iron deficiency as one of the priorities and the participation of the public health and education sectors, food industries, the community and the media should contribute to the success of the interventions and to the control of iron deficiency.
Anemia, Iron-Deficiency↗
[Treatment of iron deficiency in infancy with iron-acetyl transferrin].
In twenty eight patients with iron deficiency the efficacy of iron-acetil-transferrin treatment (2-3 mg/kg/die) has been evaluated from the changes of the following variables: RBC and reticulocyte count, Hb concentration, MCV, MCH, serum ferritin, serum iron, TIBC, and ZnPP. These variables were assessed before and after three months of treatment in all patients, and after three months from the end of the treatment in thirteen patients. At the end of the treatment there was a significant increase of RBC count, Hb concentration, MCV, MCH, serum ferritin, serum iron, and TIBC, a significant decrease of ZnPP, while reticulocyte count remained essentially unchanged. After three months from the end of the treatment only serum ferritin and ZnPP underwent an additional significant increase and decrease, respectively. In twenty-six patients serum ferritin values returned to normal. The changes of RBC and reticulocyte count, Hb concentration, MCV, serum iron, and TIBC were larger the lower the initial values, suggesting that the efficacy of the treatment is greater the more serious the iron deficiency.
Analysis of Variance↗
Postweaning carnitine supplementation of iron-deficient rats.
Severe iron deficiency in the suckling and weanling rat is associated with lipid accumulation in serum and liver, impaired ketogenesis in the suckling pup and low levels of carnitine in some tissues. Carnitine has been effective in reducing high triacylglycerol levels in humans and rats. This study examined tissue triacylglycerol concentrations of iron-deficient rats supplemented with carnitine or iron. Iron-adequate (C) and iron-deficient (D) pups were weaned to diets containing 38 ppm Fe (c) or 6 ppm Fe (d) with or without 0.2% DL-carnitine (Carn) resulting in six experimental treatments: CcCarn, DdCarn, Cc, Cd, Dc, Dd. Males received the diets for 2 wk and female littermates for 4. After 2 and 4 wk, carnitine supplementation significantly increased carnitine content in liver, heart and skeletal muscle by 30-60% in rats from control and Fe-deficient dams. Carnitine treatment significantly lowered the triacylglycerol level in liver of 49-d-old Fe-deficient females, but did not affect other tissues at either time point compared to other dietary treatments. Fe supplementation did not increase carnitine content in tissues, but did reduce triacylglycerol levels in liver by 4 wk and in skeletal muscle at both time points. Possible mechanisms by which iron and carnitine may lower lipids are discussed.
Animals↗
Treatment of iron deficiency anemia with intravenous iron preparations.
OBJECTIVE: We aimed to determine the effects of intravenous iron therapy on blood parameters in pediatric patients who do not tolerate oral iron therapy for any reason. PATIENTS AND METHODS: The patient group consisted of candidates for elective operations requiring blood transfusions in order to raise hemoglobin (Hb) concentrations rapidly and for whom oral iron administration is useless and compliance with long-term treatment is definitely impossible due to sociocultural factors. Sixty-two children were included in the study. Venous blood samples were taken at diagnosis, and after 1 week and 1, 2 and 3 months. Hb, hematocrit, erythrocyte indices (mean erythrocyte volume, mean erythrocyte Hb and mean erythrocyte Hb concentration), serum iron (SI) levels, iron binding capacity, transferrin receptor (CD71) and serum ferritin levels were measured. Iron sucrose was used as an intravenous iron preparation. RESULTS: All children showed improvements in iron deficiency anemia. A statistically significant elevation occurred between the time of diagnosis and week 1 (p<0.05) in nearly all parameters. SI was raised until at least 1 month of therapy. There was no significant difference between transferrin receptors measured before and after the intravenous iron therapy. Ferritin did not exceed the values achieved in the 1st month. Mild side effects were encountered in only 8 (12.9%) patients. Treatment was not discontinued because of side effects in any case. The patients in the control group were given an oral form containing ferroglycine sulfate. CONCLUSION: Intravenous iron therapy can replace oral therapy in patients whose blood parameters must be raised rapidly and in situations where oral iron administration would not be appropriate for any reason. However, reinforcement with oral iron therapy or additional intravenous doses would be appropriate.
Adolescent↗
Effectiveness of iron-fortified infant cereal in prevention of iron deficiency anemia.
BACKGROUND: Iron deficiency continues to be a common problem among infants throughout the world. Iron-fortified formula is effective in preventing iron deficiency but the benefit of iron-fortified cereal is controversial. METHODS: We compared iron-fortified rice cereal to unfortified rice cereal in infants who were exclusively breast-fed for more than 4 months and to iron-fortified formula in infants who were weaned to formula before 4 months of age. The design was double blind in respect to the presence or absence of fortification iron in the cereal or formula and included 515 infants who were followed on the protocol from 4 to 15 months of age. Rice cereal was fortified with 55 mg of electrolytic iron per 100 g of dry cereal and infant formula with 12 mg of ferrous sulfate per 100 g of dry powder, levels approximating those in use in the United States. Measures of iron status were obtained at 8, 12, and 15 months. Infants with hemoglobin levels of < 105 g/L were excluded from the study and treated. RESULTS: Consumption of cereal reached plateaus at means of about 30 g/d after 6 months of age in the formula-fed groups and 26 g/d after 8 months in the breast-fed groups; these amounts are higher than the 19-g/d mean intake by the 73% of infants who consume such cereal in the United States. Among infants weaned to formula before 4 months, the cumulative percentages of infants excluded for anemia by 15 months were 8%, 24%, and 4%, respectively, in the fortified cereal, unfortified cereal and formula, and fortified formula groups (P < .01 unfortified vs either fortified group; the difference between the two fortified groups was not significant). In infants breast-fed for more than 4 months, the corresponding values were 13% and 27%, respectively, in the fortified and unfortified cereal groups (P < .05). Mean hemoglobin level and other iron status measures were in accord with these findings. CONCLUSION: Iron-fortified infant rice cereal can contribute substantially to preventing iron deficiency anemia.
Anemia, Hypochromic↗
[Relations between iron deficiency anemia and protein metabolism: experimental research in iron deficiency of swine].
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Anemia, Hypochromic↗
Iron deficiency, but not anemia, upregulates iron absorption in breast-fed peruvian infants.
Iron absorption in adults is regulated by homeostatic mechanisms that decrease absorption when iron status is high. There are few data, however, regarding the existence of a similar homeostatic regulation in infants. We studied 2 groups of human milk-fed infants using (57)Fe (given as ferrous sulfate without any milk) and (58)Fe (given at the time of a breast-milk feeding) stable isotopes to determine whether healthy infants at risk for iron deficiency would regulate their iron absorption based on their iron status. We studied 20 Peruvian infants at 5-6 mo of age and 18 infants at 9-10 mo of age. We found no effect of infant hemoglobin concentration on iron absorption with 5-6 mo-old infants absorbing 19.2 +/- 2.1% and 9- to 10-mo-old infants absorbing 25.8 +/- 2.6% of the (57)Fe dose. For (58)Fe, 5- to 6-mo-old infants absorbed 42.6 +/- 5.0% and 9 to 10-mo-old infants absorbed 51.9 +/- 10.3%. Following log transformation, iron absorption from (57)Fe (r = -0.61, P = < 0.001) and (58)Fe (r = -0.61, P = < 0.001) were inversely correlated to serum ferritin (S-Ft). For both the (57)Fe and (58)Fe doses, infants with S-Ft <12 mg/L (n = 11) had significantly higher iron absorption than those with S-Ft >12 mg/L. We concluded that iron absorption in infants is related to iron status as assessed by serum ferritin but not hemoglobin concentration. Infants with low iron status upregulate iron absorption from breast milk at both 5-6 and 9-10 mo of age.
Absorption↗
Assessment of iron deficiency in populations.
Iron deficiency constitutes a major problem of Public Health affecting 10 to 20% of the world population. Although developing countries are specially susceptible, developed countries are also at risk. The use of reliable indicators of iron status is essential for assessing the magnitude and the distribution of iron deficiency in populations, and for developing effective public health measures. In this paper, the different indicators of iron status are briefly reviewed. The signification of these indicators, as reflect of a change in different body iron compartmentalization is also presented. In addition, their limitations in epidemiological surveys have been evaluated. It appears that no single iron parameter monitors the entire spectrum of iron deficiency. A combination of indicators, depending on the objectives of the study, the characteristics of the study population and the working conditions is required to measure the body iron content of individuals and to evaluate the iron status of the population.
Adolescent↗
[Free radical processes in patients with iron deficiency anemia treated with iron medication].
AIM: To study the effects of iron salts drugs (ISD) sorbifer durules and ferro-folgamma on free radical processes in 44 patients with iron deficiency anemia (IDA). MATERIAL AND METHODS: IDA was diagnosed as a rule in women with uterine myomas, endometriosis, dysfunctional hemorrhage and other menorragias. Generation of active oxygen forms (AOF) was estimated by hemoluminescence (CL) before and after therapy. Lipid peroxidation was assessed by malonic dialdehyde (MDA) in plasma, antiperoxide plasma activity (APA)--by CL intensity in interaction with nitric peroxide. The system of antioxidant defense in ISD treatment was estimated by the activity of key antioxidant enzymes: superoxidedismutase, glutathion peroxidase and catalase. RESULTS: The studied ISD normalized hemoglobin 3-4 weeks after the treatment onset. MDA decreased. Generation of AOF and activity of plasmic antioxidant enzymes did not change much. CONCLUSION: ISD modulate free radical processes without oxidant stress.
Adolescent↗
Disaccharidase levels in normal epithelium of the small intestine of rats with iron-deficiency anemia.
Iron-deficiency anemia is the nutritional deficiency most frequently occurring throughout the world, which manifests as a complex systemic disease involving all cells, affecting enzyme activities and modifying protein synthesis. In view of these considerations, the objective of the present study was to determine the effects of iron-deficiency anemia on disaccharidases and on the epithelial morphokinetics of the jejunal mucosa. Newly weaned male Wistar rats were divided into 4 groups of 10 animals each: C6w received a standard ration containing 36 mg elemental iron per kg ration for 6 weeks; E6w received an iron-poor ration (5-8 mg/kg ration) for 6 weeks; C10w received an iron-rich ration (36 mg/kg ration) for 10 weeks; E10w received an iron-poor ration for 6 weeks and then an iron-rich ration (36 mg/kg) for an additional 4 weeks. Jejunal fragments were used to measure disaccharidase content and to study cell proliferation. The following results were obtained: 1) a significant reduction (P < 0.001) of animal weight, hemoglobin (Hb), serum iron and total iron-binding capacity (TIBC) in group E6w as compared to C6w; reversal of the alterations in Hb, serum iron and TIBC with iron repletion (E10w = C10w); animal weights continued to be significantly different in groups E10w and C10w. 2) Sucrase and maltase levels were unchanged; total and specific lactase levels were significantly lower in group E6w and this reduction was reversed by iron repletion (E10w = C10w). 3) The cell proliferation parameters did not differ between groups. On the basis of these results, we conclude that lactase production was influenced by iron deficiency and that this fact was not related to changes in cell population and proliferation in the intestinal mucosa.
Anemia, Iron-Deficiency↗
Value of routine duodenal biopsy in diagnosing coeliac disease in patients with iron deficiency anaemia.
BACKGROUND: Iron deficiency anaemia (IDA) is a recognised feature of coeliac disease in adults and can be its only presentation. OBJECTIVE: To determine the yield of routine distal duodenal biopsies in diagnosing coeliac disease in adult and elderly patients with IDA whose endoscopy revealed no upper gastrointestinal cause of iron deficiency. STUDY DESIGN: Prospective study in a teaching hospital endoscopy unit. METHOD: Altogether 504 consecutive patients with IDA, aged 16-80 years, attending for endoscopy were included in this study. At least two distal duodenal biopsies were taken if endoscopy revealed no cause of iron deficiency. RESULT: In nine (1.8%) patients duodenal biopsies revealed typical histological features of coeliac disease. Of these, five patients were above 65 years old. CONCLUSION: In adult and elderly patients undergoing endoscopy for IDA, the endoscopist should take distal duodenal biopsies to exclude coeliac disease if no upper gastrointestinal cause of anaemia is found. Coeliac disease is not an uncommon cause of IDA in patients >65 years of age and a history of chronic diarrhoea increases diagnostic yield in this age group.
Adolescent↗
Usefulness of certain red blood cell indices in diagnosing and differentiating thalassemia trait from iron-deficiency anemia.
Iron-deficiency anemia and thalassemia are among the most common microcytic anemias. Differentiating these anemias by means of hemogrant indices is imprecise. Powerful statistical computer programming now enables sensitive discriminant analyses to aid in the diagnosis. Laboratory results from 383 adults were examined retrospectively and grouped according to their original diagnoses: normal (n = 78); beta-thalassemia (n = 134); alpha-thalassemia (n = 106); and iron-deficiency anemia (n = 65). Statistical analysis of results evaluated only RBC indices: RBC count, hemoglobin level, mean corpuscular volume, mean corpuscular hemoglobin, and RBC distribution width. Stepwise multivariate discriminant analysis determined those indices that best differentiated the 4 groups. The Fisher linear discriminant function for each group was calculated and tested casewise. Discriminant analysis identified mean corpuscular hemoglobin, RBC count, mean corpuscular volume, and RBC distribution width as the best set of indices for differentiating the 4 diagnoses. Casewise testing of the calculated Fisher linear discriminant function resulted in mean-weighted sensitivity of 80.4%. The present study demonstrates that a set of linear discriminant functions based on routine hemogram data can effectively differentiate between alpha-thalassemia, beta-thalassemia, and iron-deficiency anemia, with a high degree of accuracy.
Anemia, Iron-Deficiency↗
Iron deficiency among active men.
Iron deficiency in active men is well documented. To assess the relative importance of dietary iron intake, iron absorption, and iron loss in the pathogenesis of this iron deficiency, we compared a group of iron-deficient athletes to a group with normal iron stores. Iron absorption was assessed by an iron tolerance test. Serum haptoglobin was used as a measure of hemolysis. The presence of hemoglobinuria reflected urinary iron loss. Iron intake was determined by a 3-day dietary record as well as a food frequency questionnaire. Results showed iron absorption to be inversely correlated with iron stores. Iron-deficient athletes had higher absorption, suggesting a normal regulation mechanism. Major hemolysis (serum haptoglobin below 40 mg/dl) was found in 28% of subjects with no relationship to iron stores. No hemoglobinuria was detected after a usual training session. Iron intake was elevated in relation to high caloric intake, but iron intake in the form of meat was lower in iron-deficient athletes, as compared to those with normal or repleted iron stores. It is our opinion that inadequate iron intake is an important determinant of iron deficiency in athletes.
Absorption↗
Changes in the cochlear iron enzymes and adenosine triphosphatase in experimental iron deficiency.
The influences of iron deficiency on the cochlear iron enzymes and adenosine triphosphatase were studied in 68 iron-deficient rats and 68 control rats (normal and with chronic anemia). A disorderly or topographic distribution and reduction or disappearance of the cochlear succinic dehydrogenase and peroxidase reaction products were found in 37.8% of the rats fed on a basic iron-deficient diet for 14 to 100 days. The activity of cochlear sodium-potassium-dependent adenosine triphosphatase in iron-deficient rats was slightly increased, compared to that in normal controls. These results suggest that iron deficiency would produce significant abnormalities of succinic dehydrogenase and peroxidase activity, which in turn would disturb cell respiration and initiate peroxidative damage to the inner ear cells, result in sensorineural hearing loss, or provide a pathologic basis for cochlear deafness.
Anemia, Hypochromic↗
[Diagnosis and treatment of iron deficiency].
The investigation of iron deficiency should be oriented by clinical background. In group at risk (infants and children, women of childbearing age, pregnant women) management is limited to nutritional inquiry and gynaecologic examination and oral iron treatment. In men and post menopausal women iron deficiency is assumed to be the result of occult gastro-intestinal blood loss; so, in these patients, upper and lower gastro-intestinal endoscopy are required. Benign lesions are more frequently found in upper digestive tract than lower digestive tract. When these investigations are negative and iron treatment unsuccessful, enteroscopy is recommended. Oral iron treatment is performed with ferrous salts (200 mg/d). Duration of treatment depends on severity of iron deficiency: three months for iron stores deficiency an iron deficient erythropoisis, six months for iron deficiency anaemia.
Female↗
The effect of iron deficiency on skeletal muscle metabolism of the rat.
Using 31P magnetic resonance spectroscopy we compared skeletal muscle bioenergetics in Wistar rats made chronically anaemic by being fed a diet deficient in iron for 6 weeks with chronically iron deficient animals given a normal diet as well as 5 mg iron dextran at 2 or 7 days before experimentation. Spectra of the gastrocnemius muscle were taken at rest and during stimulation of the sciatic nerve at 2 Hz for 10 min. Relative concentrations of intracellular phosphate (Pi), phosphocreatine (PCr) and ATP were determined. Iron deficiency increased PCr breakdown and production of acid in stimulated skeletal muscle. Recovery of PCr and Pi concentrations after exercise was slow. These metabolic changes are consistent with either a reduction in supply of oxygen to the muscle cell or altered oxidative phosphorylation by the mitochondria. The latter may be mediated by defective function of iron-containing proteins crucial in oxidative phosphorylation and this is suggested both by the observation that treatment with iron, sufficient to correct the anaemia, does not completely reverse the metabolic changes and that there is a different time course for such metabolic improvements and the observed increase in haemoglobin concentration.
Adenosine Diphosphate↗
Iron deficiency and immune responses.
Iron deficiency is often associated with the impairment of the immune system, particularly the functioning of T-cell lymphocytes. Studies were therefore carried out in mice to investigate the involvement of iron in T-cell functions. Iron deficiency in mice was induced nutritionally by feeding diets differing in iron content for 4 weeks to produce normal, moderately low and severely low haematological indices. The proliferation of lymphocytes stimulated by Con A from these groups of mice was significantly affected by the degree of iron deficiency. Iron depletion also resulted in decreased production of interleukin 2 (IL-2) in the proliferating cells. The implications of these findings in the manifestation of iron deficiency anaemia are discussed.
Animals↗