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PubMed2002

Upper and lower gastrointestinal endoscopical investigation in elderly patients with iron deficiency anaemia.

Iron deficiency anaemia is frequently observed in male adults and postmenopausal women due to chronic occult bleeding, usually from the gastrointestinal tract. Practically, as endoscopical investigation of the gastrointestinal system is an invasive procedure, iron replacement treatment was generally started without investigation of the underlying aetiology even in first-line health institutions. This study evaluates the role of endoscopy in the investigation of the aetiology of anaemia in 95 patients (51 males, 44 females), aged 64.9+/-12.5 years (range 50-90 years). All patients having iron deficiency anaemia were investigated by upper gastrointestinal endoscopy and colonoscopy. Upper and lower gastrointestinal pathologies were seen in 10 (10.6%) and 55 (57.8%) patients, respectively. However, no gastrointestinal lesion was found in 30 (31.6%) patients with iron deficiency anaemia. Out of the 95 patients, 16 (16.9%) had erosive gastritis, 15 (15.8%) duodenal ulcer, 8 (8.4%) gastric ulcer, 7 (7.3%) gastric tumours, 7 (7.3%) oesophagitis. 5 (5.4%) colon tumours, 3 (3.2%) haemorrhoids, 2 (2.1%) non-tropical sprue, 1 (1%) colonic polyp, and 1 (1%) colitis. In the majority of elderly patients with iron deficiency anaemia, upper gastrointestinal system disease was found. In 12 (12.7%) patients in the study group, malignancies were detected. In elderly patients with iron deficiency anaemia, the aetiology should be highlighted before giving iron supplementation.

Aged↗
PubMed1980

Transferrin gene expression. Effects of nutritional iron deficiency.

Nutritional iron deficiency was produced experimentally by raising newly hatched chicks on an iron-deficient diet for several weeks. During this time, hematocrit and hemoglobin values declined, iron stores were depleted, and the circulating level of transferrin increased 2- to 4-fold. The increase in serum transferrin was related to a similar increase in the rate of transferrin synthesis in liver. In addition, the level of transferrin mRNA sequences, as determined by hybridization to a specific cDNA, increased 2- to 3-fold, and more than 80% of the transferrin mRNA was associated with polyribosomes in both control and iron-deficient liver. These results demonstrate that the induction of transferrin synthesis in iron-deficient chicks is regulated directly by an increase in transferrin mRNA. The iron-mediated effects on transferrin also appear to be gene-specific since the rate of synthesis of serum albumin, the major secretory product of liver, was unaffected by any of the experimental conditions. Furthermore, when iron stores were rapidly replenished by the administration of iron-saturated ferritin, both the rate of transferrin synthesis and the level of transferrin mRNA returned to control values with 2 to 3 days.

Animals↗
PubMed1999

Ferritin mutants of Escherichia coli are iron deficient and growth impaired, and fur mutants are iron deficient.

Escherichia coli contains at least two iron storage proteins, a ferritin (FtnA) and a bacterioferritin (Bfr). To investigate their specific functions, the corresponding genes (ftnA and bfr) were inactivated by replacing the chromosomal ftnA and bfr genes with disrupted derivatives containing antibiotic resistance cassettes in place of internal segments of the corresponding coding regions. Single mutants (ftnA::spc and bfr::kan) and a double mutant (ftnA::spc bfr::kan) were generated and confirmed by Western and Southern blot analyses. The iron contents of the parental strain (W3110) and the bfr mutant increased by 1.5- to 2-fold during the transition from logarithmic to stationary phase in iron-rich media, whereas the iron contents of the ftnA and ftnA bfr mutants remained unchanged. The ftnA and ftnA bfr mutants were growth impaired in iron-deficient media, but this was apparent only after the mutant and parental strains had been precultured in iron-rich media. Surprisingly, ferric iron uptake regulation (fur) mutants also had very low iron contents (2.5-fold less iron than Fur+ strains) despite constitutive expression of the iron acquisition systems. The iron deficiencies of the ftnA and fur mutants were confirmed by Mössbauer spectroscopy, which further showed that the low iron contents of ftnA mutants are due to a lack of magnetically ordered ferric iron clusters likely to correspond to FtnA iron cores. In combination with the fur mutation, ftnA and bfr mutations produced an enhanced sensitivity to hydroperoxides, presumably due to an increase in production of "reactive ferrous iron." It is concluded that FtnA acts as an iron store accommodating up to 50% of the cellular iron during postexponential growth in iron-rich media and providing a source of iron that partially compensates for iron deficiency during iron-restricted growth. In addition to repressing the iron acquisition systems, Fur appears to regulate the demand for iron, probably by controlling the expression of iron-containing proteins. The role of Bfr remains unclear.

Aerobiosis↗
PubMed2005

Expression of iron-acquisition-related genes in iron-deficient rice is co-ordinately induced by partially conserved iron-deficiency-responsive elements.

Rice plants (Oryza sativa L.) utilize the iron chelators known as mugineic acid family phytosiderophores (MAs) to acquire iron from the rhizosphere. Synthesis of MAs and uptake of MA-chelated iron are strongly induced under conditions of iron deficiency. Microarray analysis was used to characterize the expression profile of rice in response to iron deficiency at the genomic level. mRNA extracted from iron-deficient or iron-sufficient rice roots or leaves was hybridized to a rice array containing 8987 cDNA clones. An induction ratio of greater than 2.0 in roots was observed for 57 genes, many of which are involved in iron-uptake mechanisms, including every identified or predicted step in the methionine cycle and the biosynthesis of MAs from methionine. Northern analysis confirmed that the expression of genes encoding every step in the methionine cycle is thoroughly induced by iron deficiency in roots, and almost thoroughly induced in leaves. A promoter search revealed that the iron-deficiency-induced genes related to iron uptake possessed sequences homologous to the iron-deficiency-responsive cis-acting elements IDE1 and IDE2 in their promoter regions, at a higher rate than that showing no induction under Fe deficiency. These results suggest that rice genes involved in iron acquisition are co-ordinately regulated by conserved mechanisms in response to iron deficiency, in which IDE-mediated regulation plays a significant role.

Blotting, Northern↗
PubMedDate not supplied

Cytological findings in iron deficiency anemia.

Iron deficiency anemia is a common condition in India. We made an attempt to study the cytological changes in the buccal mucosal cells of iron deficiency anemia, patients. Buccal mucosal cells were scraped from 40 iron deficiency anemia patients and were subjected to morphometric analysis. Results of the study showed there is an increase in the cellular diameter, nuclear diameter, and nuclear:cytoplasmic ratio of iron deficiency anemia patients when compared to the normal values.

Adult↗
PubMed1985

Problems in diagnosis of iron deficiency anemia.

Iron deficiency is the most common nutritional deficiency in children and is widespread in childhood populations throughout the world. Although many sophisticated tests have been devised for the diagnosis of iron deficiency the most reliable criterion of iron deficiency anemia is the hemoglobin response to an adequate therapeutic trial of iron. Following the reticulocytosis peak hemoglobin rises at an average of 0.25 to 0.4 g/dl/day and hematocrit at a rate of 1% per day. If the response to iron falls short of this response other causes of the anemia should be sought by detailed hematologic investigation. In addition to making a diagnosis of iron deficiency anemia it is incumbent on the physician to demonstrate its cause.

Anemia, Hypochromic↗
PubMed2002

Reversal of iron deficiency anemia-induced peripheral neuropathy by iron treatment in children with iron deficiency anemia.

The effects of iron deficiency anemia (IDA) on nerve conduction and efficiency of iron therapy were investigated by peripheral nerve-electrophysiological measurements. Eighteen children (10 boys, eight girls; mean age 31 +/- 1.3 months) with IDA and 12 healthy children (six boys, six girls; mean age 29 +/- 1.3 months) were enrolled into the study. Nerve conduction velocity was measured in the median and posterior tibial nerve. After nerve conduction values were determined in the patients and controls, 6 mg/kg/24 h ferrous sulphate was given orally to the patients for 3 months and nerve conduction velocity tests were performed again. Median/motor and sensory nerve conduction velocity and tibial/motor nerve distal-amplitute values of children with IDA were lower than for the control group (p < 0.05, p < 0.01 and p < 0.001 respectively). With iron supplementation these values increased to the normal levels and even higher than control levels for some parameters. In correlation studies between whole blood parameters and nerve conduction velocity results, there was a correlation between median/sensory nerve conduction velocity values and serum iron levels. Additionally there was a correlation between some nerve conduction velocity values and age. In conclusion, the evidence from this preliminary study suggests that peripheral neuropathy may develop in children with IDA. Peripheral neuropathy symptoms in these patients may be improved by iron therapy.

Administration, Oral↗
PubMedDate not supplied

Prevention of iron deficiency with carbonyl iron in female blood donors.

The effectiveness of elemental, nontoxic carbonyl iron in replacing iron lost at blood donation was examined. In a randomized double-blind design, 99 women, aged 18 to 40, were given placebo or low-dose carbonyl iron (100 mg orally) at bedtime for 56 days after phlebotomy. Compliance was equivalent for the two regimens. Mild side effects were slightly greater with carbonyl iron. At Day 56, estimated net iron absorption from therapy or diet, or both, was sufficient to replace iron in 85 percent of those receiving carbonyl iron but in only 29 percent of those taking placebo (p less than 0.001). The rates of deferral from repeat donation were 8 percent in the carbonyl iron group and 36 percent in the placebo group (p less than 0.01), and the positive predictive value of routine screening in identifying participants without iron deficiency was 83 versus 13 percent (p less than 0.01). It can be concluded that short-term carbonyl iron supplementation in female blood donors can replace the iron lost at phlebotomy, protect the women against iron deficiency, and enhance their ability to give blood.

Anemia, Hypochromic↗
PubMed1996

Use of whole gut perfusion to investigate gastrointestinal blood loss in patients with iron deficiency anaemia.

Iron deficiency anaemia may be due to occult bleeding into the gut. However, although clinical investigations may show a high frequency of gastrointestinal tract disease in these patients, the cause-effect relationship between the lesions detected and anaemia remain uncertain. This study aimed to establish whether lesions detected by endoscopy or imaging of the gastrointestinal tract in patients with unexplained iron deficiency anaemia are bleeding continuously. Routine clinical tests were performed in 42 patients with unexplained iron deficiency anaemia referred to this unit. Whole gut lavage and assay of haemoglobin in the gut perfusate were also performed. The main outcome measures were clinical diagnoses (by imaging and endoscopy of the upper gastrointestinal tract and colon); the concentration of haemoglobin in whole gut lavage fluid; and the calculated gastrointestinal blood loss per day. There were 73 clinical, dietary, or iatrogenic factors of possible aetiological importance in the 42 patients--poor diet (10), gross gastrointestinal abnormality (34 in 28 patients), malabsorption (14), coagulation problems (6), and NSAID use (9). The gut lavage test showed, however, that at the time the test was performed, only eight patients were losing more than 2 ml blood daily into the gut, including all four with colonic cancer, one with diffuse gastric vascular ectasia, and one with severe ulcerative oesophagitis. It is concluded that occult gastrointestinal bleeding sufficient to cause anaemia was evident in only 19% of 42 patients. There was a high frequency of other potential causes of iron deficiency in the remainder, suggesting that most of the gastrointestinal diseases and lesions detected in them were probably coincidental. Factors other than blood loss should be considered and treated in patients referred for anaemia assessment.

Adult↗
PubMed1992

A guide to primary care of iron-deficiency anemia.

Iron deficiency, the most common cause of anemia, is prevalent in 10 percent to 30 percent of the world's population. Inadequate intake of iron may be an important causative factor, particularly when the body requires more iron than usual (e.g., during infancy, early childhood, adolescence, pregnancy and periods of blood loss). The popular increase of fiber in diets may increase the incidence of iron-deficiency anemia because too much fiber in the diet renders available iron unabsorbable. Symptoms in children include skin or conjunctival pallor, excessive sleepiness, learning disabilities, diminished attention span, tiredness, irritability or inappropriate behavior, and pica. Adults may have shortness of breath, decrease in exercise tolerance, palpitations, tachycardia, angina, congestive heart failure, orthopnea and edema. Iron deficiency occurs in sequential states and is measured by many laboratory tests. The levels of hemoglobin and hematocrit are both decreased, while the red blood cell count may be normal initially, but will decrease as the iron-deficiency state continues. The steps of treatment include correction of the underlying disorder, administration of the amount of iron needed and observation of the response to treatment.

Adolescent↗
PubMed1980

Activity and T-maze performance in iron deficient rats.

Iron deficient rats were tested in a t-maze to see whether the changes in activity during the onset and progress of the deficiency would affect their performance in the maze. Increased exploratory activity in the initial stages of iron deficiency was reflected in enhanced t-maze learning, whereas the lower activity seen as the deficiency progressed was associated with normal maze-learning. The t-maze task may not be sufficiently sensitive to pick up differences between deficient and control animals due to reduced general activity in the later stages of iron deficiency.

Animals↗
PubMed2001

Iron deficiency anemia.

Iron deficiency anemia is the most common cause of anemia worldwide and results from inadequate iron supply for erythropoiesis. Iron deficiency is most prevalent during periods of rapid body growth: in infancy and again at puberty. Insufficient intake accounts for most cases. The clinical manifestations of iron deficiency anemia can be subtle, but irreversible delayed psychomotor development may occur if the anemia is severe and prolonged. The optimal approach is prevention and early treatment.

Adolescent↗
PubMed2006

The cardiomyopathy of iron deficiency.

Iron-deficiency anemia can have deleterious effects on the heart. Herein, we describe the effects of iron deficiency on the heart as corroborated with electrocardiography, radiology, echocardiography, and cardiac catheterization. We review the pathophysiology, clinical features, and management of iron-deficiency-induced cardiomyopathy.

Adult↗
PubMed2004

Intestinal permeability to lactulose and mannitol in growing rats with iron-deficiency anemia.

Iron deficiency can have nonhematological manifestations, some of which may affect the gastrointestinal tract. The aim of this study was to determine if iron-deficiency anemia in growing rats affected small-bowel permeability as assessed by the urinary ratio of lactulose and mannitol. Thirty-seven male Harlan Sprague-Dawley rats (21 d of age) were randomly divided into two groups and fed either an iron-deficient (n=19) or an iron-sufficient diet (n=18) that contained either 13.5 or 43.8 mg of iron/kg diet, respectively. Animals were evaluated between 25 and 38 d of dietary treatment. Intestinal permeability was assessed by measuring the lactulose/mannitol urinary ratio following administration of a solution that contained the two sugars. At the end of the study, the mean body weight of rats fed the low-iron diet was approx 95% that of the controls. The mean hemoglobin (g/dL) was significantly lower in the low-iron diet group (11.2+/-1.4) than in the control group (16.9+/-0.8) (p=0.001). The liver iron concentration (microg/g) of the anemic group (41.4+/-4.7) was also statistically (p=0.001) lower than in the control group (116.6+/-18.2). The lactulose/mannitol ratio was lower in the anemic rats (2.0+/-0.7) than in the control group (2.6+/-0.7) (p=0.008), a finding that is not suggestive of intestinal mucosal atrophy, previously described in anemic children.

Anemia, Iron-Deficiency↗
PubMed2005

Blood lead levels in iron-deficient and noniron-deficient adults.

Iron deficiency (ID) has been reported to increase lead absorption. This relationship has been investigated in detail in children but not in adults. This study was designed to investigate whether blood lead levels are significantly higher in iron-deficient adults. ID-parameters (haemoglobin, mean corpuscular volume, mean corpuscular haemoglobin, serum iron, total iron-binding capacity, iron-binding saturation, soluble transferrin receptors, washed zinc protoporphyrin and ferritin) together with whole blood lead were measured in three different adult groups - blood donors (n = 73), pregnant women (n =74) and haemodialysis patients (n = 72). Of a total of 219 subjects tested, 7.7% was found to have a lead level above 10 microg/dl (maximum 16 microg/dl). No association was found between blood lead level and ID [iron-deficient subjects (n: 139), mean: 5.6 microg/dl (SD: 3 microg/dl) and noniron-deficient subjects (n: 80), mean: 5.4 microg/dl (SD: 3 microg/dl)]. The results suggest that the inverse association between blood lead and serum iron in studies carried out on children does not occur in adults.

Adult↗
PubMed2005

Only a small proportion of anemia in northeast Thai schoolchildren is associated with iron deficiency.

BACKGROUND: Iron deficiency is assumed to be the major cause of anemia in northeast Thailand, but other factors may be involved. OBJECTIVE: We determined the prevalence of anemia among schoolchildren in northeast Thailand and the role of hemoglobinopathies, selected micronutrient deficiencies, and other factors in hemoglobin status. DESIGN: Blood samples were collected from 567 children aged 6-12.9 y attending 10 primary schools for the determination of a complete blood count and hemoglobin type [Hb AA (normal hemoglobin), Hb AE (heterozygous for Hb type E), and Hb EE (homozygous for Hb type E)] and the measurement of serum ferritin, transferrin receptor, retinol, vitamin B-12, and plasma and erythrocyte folate concentrations. Children with a C-reactive protein concentration > or = 10 mg/L (n = 12), which indicated infection, were excluded. RESULTS: The prevalence of anemia was 31%. Age, hemoglobin type, and serum retinol were the major predictors of hemoglobin concentration. Hb AA and Hb AE children with anemia had lower (P < 0.01) hematocrit, mean cell volume, and serum retinol values than did their nonanemic counterparts; no significant differences in serum ferritin were found by hemoglobin type. Only 16% (n = 22) of the anemic Hb AA and Hb AE children were iron deficient. Hb AA and Hb AE children with a serum retinol concentration <0.70 micromol/L (n = 14) had a significantly higher geometric mean serum ferritin concentration than did those with a retinol concentration > or = 0.70 micromol/L (P = 0.009); no significant difference in transferrin receptor concentrations was found between these 2 groups. CONCLUSIONS: Hemoglobinopathies, suboptimal vitamin A status, and age were the major predictors of hemoglobin concentration. The contribution of iron deficiency to anemia was low, and its detection was complicated by coexisting suboptimal vitamin A status.

Anemia, Iron-Deficiency↗