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PubMed1994

Zinc protoporphyrin and iron-deficient erythropoiesis.

Iron-deficient erythropoiesis may occur in patients with adequate levels of storage iron as well as those with tissue iron deficiency. Here we compare two methods of detecting iron-deficient erythropoiesis. The measurement of percent hypochromic cells in the full blood count provides a direct indicator of iron-deficient erythropoiesis. The zinc protoporphyrin (ZPP) determination is simple, precise and reproducible, and also appears to provide a sensitive index of iron-deficient erythropoiesis. There was a significant correlation between ZPP levels and percent hypochromic cells in patients with iron deficiency anaemia, rheumatoid arthritis and with patients with renal failure undergoing dialysis and receiving erythropoietin. However in the latter group ZPP levels were raised in almost all patients, suggesting that there may be interference by other metabolites in the assay. This may be overcome by washing the red cells before assay, but the procedure becomes cumbersome. If the laboratory is equipped to determine percent hypochromic cells during the blood count this direct measure of iron-deficient erythropoiesis dispenses with the need to determine ZPP. Otherwise ZPP determinations on washed cells may be of diagnostic use.

Anemia, Hypochromic↗
PubMed2006

[The iron letter--an update on the treatment of iron deficiency anemia].

Iron deficiency is a frequent complication in chronically ill patients and in pregnant women. Iron status can now be characterised precisely and relatively easily by determining serum ferritin, transferritin saturation and if necessary hypochromic erythrocytes and the haemoglobin content of erythrocytes (CHr). Oral iron replacement is usually restricted by limited absorption and low tolerability. Intravenous iron therapy is possible in such cases and can be combined with rHuEPO (e.g. EPREX/Epoetin alfa) in severe cases. Iron saccharate Switzerland and this permits high dose iron replacement without any danger of anaphylaxis or acute iron toxicity.

Administration, Oral↗
PubMed1993

The immune response in iron-deficient young children: effect of iron supplementation on cell-mediated immunity.

The effects of iron deficiency on immunity remain controversial. This study was designed to assess the impact of iron supplementation on the immune status, in 81 children aged 6 months-3 years, at high risk for iron deficiency, using a longitudinal double blind randomised and placebo-controlled study. Lymphocytes of iron-deficient children produced less interleukin-2 in vitro. Iron supplementation for 2 months increased mean corpuscular volume, serum ferritin and serum transferrin, but had no effect on the parameters of T-cell mediated immunity. The lower interleukin-2 levels in iron-deficient suggest that cell-mediated immunity may be impaired in iron deficiency.

Anemia, Hypochromic↗
PubMed2006

Non haematological effects of iron deficiency - a perspective.

Iron deficiency is a continuum beginning from lowering of tissue stores to the phase of exhausted tissue stores, interference with iron driven biochemical reactions in the body, microcytosis, hypochromia, increasing severity of anaemia with all its attendant consequences. Iron deficiency anaemia is a very well known concept but what is often not appreciated is the effect of broad canvas of iron deficiency on various tissues, organs and systems in our body in addition to iron deficiency anaemia leading to concept of "Iron deficiency disease". In this condition not only tissue delivery of oxygen is compromised but proliferation, growth, differentiation, myelinogenesis, immunofunction, energy metabolism, absorption and biotransformation are compromised leading to abnormal growth and behaviour, mental retardation, reduced cardiac performance and work efficiency, infection etc which ultimately leads to the concept that "iron deficiency not only breaks the machine but also wrecks the machinery."

Cell Respiration↗
PubMed1991

Reduced cortisol secretion in patients with iron deficiency.

The iron-containing protein cytochrome P-450 is present in high concentration in the adrenal cortex and is involved in the synthesis of corticosterone. This study was designed to determine the cortisol response to adrenocorticotropin (ACTH) in patients with severe iron deficiency. Eleven patients with iron deficiency and 15 normal controls were studied. Fasting blood samples were taken from all the subjects before and 30, 60 and 120 min after infusion of 25 units of ACTH for plasma cortisol determination. Six patients had blood samples collected at night, too. The same test was performed in 6 patients with iron deficiency, 7 days after therapy with 800 mg of ferrous sulfate. No significant differences were observed between patients and controls for the baseline cortisol values. The cortisol secretion and the increment at 30, 60 and 120 min after ACTH infusion were significantly lower in patients than in controls, either before or after ferrous sulfate therapy. There were no significant differences between baseline and stimulated cortisol values in patients before and after 7 days of ferrous sulfate therapy. There was no change in cortisol secretion rhythm in patients with iron deficiency (cortisol level at night = 5.1 +/- 4.3 micrograms/dl). In conclusion, the results of the present study showed that, in patients with severe iron deficiency, the cortisol secretion after ACTH stimulation was decreased.

Adrenocorticotropic Hormone↗
PubMed2005

The prevalence of coeliac disease as detected by screening in children with iron deficiency anaemia.

AIM: Iron deficiency anaemia is a frequent finding seen in coeliac disease, which can be diagnosed alone or with other findings. In this study, our aim was to determine the prevalence of coeliac disease in children with iron deficiency anaemia without significant gastrointestinal symptoms. METHODS: There were 135 children with iron deficiency anaemia in the patient group (group 1), and 223 healthy children without iron deficiency anaemia in the control group (group 2) in this study. Antiendomysial antibody (EMA) IgA test was given to both groups. Antiendomysial antibody-positive patients underwent small intestine biopsy. RESULTS: The mean age was 7.2+/-4.6 (2-16) y in the patient group (group 1) and 8.2+/-3.8 (2-16) y in the control group (group 2), and no significant difference between the two groups was detected. In terms of gender, there was a significant difference between groups 1 and 2 (M/F: 74/61 and 98/125, respectively) ( p<0.05). EMA was positive in six cases in group 1 (4.4%), and villous atrophy and/or inflammation in the lamina propria with increased intraepithelial lymphocytes was seen on small intestine biopsy in these patients. In the control group, EMA was negative in all children. In detailed histories of patients with coeliac disease diagnosis, recurrent iron deficiency anaemia/pica was found in four patients (66.7%) and occasionally foul-smelling or watery stool attacks were seen in four patients (66.7%). Three of these six patients (50%) had short stature. CONCLUSION: The prevalence of coeliac disease was high in patients with iron deficiency anaemia; therefore, gastrointestinal findings should be further examined for coeliac disease, and the possibility of coeliac disease should be investigated in patients with recurrent iron deficiency anaemia and short stature.

Adolescent↗
PubMed1976

[Malformations, anomalies and variations in patients with severe iron deficiency].

In severe iron deficiency which frequently occurs in the population of Turkey, malformations, anomalies and variations are often observed. In 190 patients with severe iron deficiency of long duration such abnormalities could be found in 107 cases. The abnormal changes were of different character and occured in various parts of the body. In the majority multiple changes, ranging from 2 to 7 and more could be registered. 100 persons showing no iron deficiency and no anemia presented a much lower incidence of the same changes; in a second group of 54 patients suffering from a severe anemia without iron deficiency the incidence was still lower. These observations suggest that the occurrence of the abnormalities is closely connected with the iron deficiency. The character of the abnormal changes which are not susceptible to iron treatment are pointing to a prenatal origin. The diversity of the changes, the occurrence in various parts of the body and skeleton as well as the multiplicity of incidence are showing that they are due to impairment of the process of development in the embryonic organism. This view is supported by the results of the examination of the chromosomes. A distinct relation could be established between the incidence of the malformations and the occurrence of the chromosomal aberrations. As the iron deficiency in the Turkish population is mainly caused by an insufficient supply of iron with the food it is likely that by sufficient iron supply in pregnant women the incidence of malformations and anomalies caused by the iron deficiency can be prevented and by a general amelioration of the nutrition their occurrence in the population markedly reduced.

Adolescent↗
PubMed1999

Neutrophil hypersegmentation in iron deficiency anaemia: a case-control study.

Neutrophil hypersegmentation (NH) is an important haematological feature of cobalamin or folate deficiency. As iron deficiency and folate deficiency often occur in the same target groups it is important to establish whether iron deficiency alone is a cause of NH. We report a case-control study which addresses this issue. Two groups of hospital patients were studied. Group 1 comprised 50 patients with iron deficiency anaemia (IDA). Group II comprised 50 control age- and sex-matched patients who were haematologically normal without evidence of iron deficiency from the iron studies. Patients with other factors which could affect the degree of neutrophil segmentation (cobalamin/folate deficiency, renal failure, infection and drug exposures) were excluded from the study. A total of 10 000 neutrophils were examined, 100 from each patient. NH was defined as the presence of five or more five-lobed neutrophils per 100, or any neutrophils with six or more lobes. The results were as follows: IDA, mean neutrophil lobe count 3.36; number of patients with NH 31/50 (62%): controls, mean neutrophil lobe count 2.96, number of patients with NH 2/50 (4%). These differences were statistically significant. We conclude that NH is common in IDA. The mechanism whereby iron deficiency results in NH is not clear.

Adolescent↗
PubMed1991

Iron status of inner-city elementary school children: lack of correlation between anemia and iron deficiency.

The iron status of 103 inner-city third and fourth graders was evaluated. These children had significantly lower hemoglobin concentrations and significantly higher serum ferritin concentrations than values previously reported. Mean erythrocyte protoporphyrin concentrations agree with previous results whereas mean corpuscular volume was significantly lower than in some previous studies. Though 11 children (10.7%) were anemic, only 1 anemic child had another abnormal measure of iron status. Three children (2.9%) had a low serum ferritin concentration along with another abnormal measure of iron status. Four children (3.9%) had at least two abnormal measurements of iron status without an elevated blood lead concentration. These results agree with recent observations of decreasing rates of anemia in preschool children. The poor utility of hemoglobin measures to identify iron-deficient children suggests the need for alternate screening methods, and the relatively high serum ferritin concentration suggests a trend of rising iron stores in school-age children.

Anemia↗
PubMed1985

Decreased antibody formation in iron-deficient rat pups--effect of iron repletion.

Rats were fat diets containing 6, 12, or 250 ppm iron throughout gestation and lactation. On day 17, pups immunized with sRBC were used to determine antibody synthesis by the Jerne plaque assay. In both iron-deficient groups, antibody formation was decreased by at least 50% compared to controls. For 3 weeks beginning on day 21, iron-deficient pups were fed either a control diet (35 ppm iron) or the same iron-deficient diet as fed to the dam. IgG and IgM formation was only slightly improved in repleted rats and remained significantly below that of rats fed the control diet throughout the experiment. In contrast, 250 ppm iron pups fed an iron-deficient diet postweaning had significantly decreased IgG and IgM production compared to littermates fed a control diet postweaning. Maternal iron deficiency during the critical pre- and postnatal growth periods may result in long-term impairment of humoral immunity that is not corrected by dietary iron repletion after weaning.

Animals↗
PubMedDate not supplied

Evaluation and treatment of iron deficiency in adults.

Iron deficiency is prevalent in populations seen in primary practices. It is easily evaluated and treated, but often undiagnosed. Iron deficiency can lead not only to anemia but to decreased work capacity, abnormal neurotransmitter function, and altered immunologic and inflammatory defenses. Risk for iron deficiency is a function of iron loss, iron intake, iron absorption, and physiologic demands. Women of child-bearing age are at especially high risk for iron deficiency due to ongoing menstrual blood losses. This article presents and describes a simple algorithm incorporating dietary considerations for evaluation and treatment of iron deficiency in primary care settings.

Adult↗
PubMed1993

Red blood cell regeneration induced by subcutaneous recombinant erythropoietin: iron-deficient erythropoiesis in iron-replete subjects.

Limited red blood cell (RBC) regeneration often prevents collection of sufficient blood from autologous donors. We studied the effects of subcutaneous recombinant erythropoietin (rEPO) in subjects making frequent blood donations. Six healthy iron-replete male subjects took rEPO (200 U/kg) subcutaneously daily, and donated blood (450 mL) twice a week for 3 weeks. During a control study, these subjects also attempted twice-weekly blood donations without rEPO. Four other males given rEPO, including one with idiopathic hemochromatosis, waited until day 8 to begin blood donations. All healthy subjects took oral ferrous sulfate. Subcutaneous rEPO given with blood donations resulted in a marked reticulocytosis (mean peak value 568 +/- 159 x 10(9)/L v 235 +/- 77 x 10(9)/L, control study; P < .05), and enhanced RBC production at 28 days (1,208 +/- 227 mL v 719 +/- 161 mL, P < .05). rEPO in advance of blood donations was slightly less effective in normal subjects (941 +/- 139 mL, P < .05); however, the subject with hemochromatosis produced substantially more RBCs (1,764 mL) than any normal subject. rEPO-treated normal subjects (but not the rEPO-treated patient with hemochromatosis or untreated controls) produced iron-deficient RBCs with elevated zinc protoporphyrin levels and low hemoglobin content. These cells appeared within 1 week of rEPO administration and before laboratory confirmation of depleted iron stores. Thus, subcutaneous rEPO is an effective stimulant of erythropoiesis in nonanemic blood donors. However, in addition to eventual depletion of iron stores, early functional iron deficiency affects response to the drug.

Blood Donors↗
PubMed1999

[Storage iron decrease rates and their clinical significance in iron deficiency anemia patients following intravenous iron therapy].

A simple method was devised for determination of the storage iron decrease rate (SID) and the number of days to a recurrent state of iron deficiency. Several patients with iron deficiency anemia were given intravenous doses of iron, and their serum ferritin levels were periodically assayed. A serum ferritin decrease curve was plotted semi-logarithmically; back-extrapolation of that curve yielded the period of days (D) from the starting day of iron supplement therapy to the day by which serum ferritin had decreased to 12 ug/l. The amount of administered iron that was initially stored and eventually lost during period D was calculated by subtracting the amount of iron utilized for hemoglobin increase (R) from the total amount of iron administered (T) to each patient. R was calculated from values for patient body weight and change in hemoglobin concentration prior to and after therapy. SID values were obtained from the following formula: SID = (T-R)/mg/day. SID rates and the number of days to a state of recurrent iron deficiency were measured in 12 patients. SID rates ranged from 0.8 to 9.8 mg/day, and were larger in those patients who exhibited heavier blood loss. A correlation was observed between SID values and the half-times for serum ferritin decrease, as expressed by the equation, Y = 248.5X0.129 (r = 0.129). SID values reflected the negative iron balance of each patient. That observation suggested it should be possible to select a more appropriate intravenous iron does for individual patients if their SID values are taken into full account.

Anemia, Iron-Deficiency↗
PubMed2001

An approach to iron-deficiency anemia.

Iron-deficiency anemia is a common reason for referral to a gastroenterologist. In adult men and postmenopausal women, gastrointestinal tract pathology is often the cause of iron-deficiency anemia, so patients are frequently referred for endoscopic evaluation. Endoscopy may be costly and at times difficult for the patient. Therefore, physicians need to know what lesions can be identified reliably and, more importantly, the importance of ruling out life-threatening conditions such as occult malignancy. Over the past decade, a number of prospective studies have been completed that examined the yield of endoscopy in the investigation of iron-deficiency anemia. The present article provides a broad overview of iron-deficiency anemia, with particular emphasis on hematological diagnosis, etiology, the use of endoscopy in identifying lesions and iron-repletion therapy. Other clinical scenarios, including assessment of patients on anti-inflammatory or anticoagulation therapy and patients with bleeding of obscure origin, are also addressed. The present article provides a diagnostic algorithm to iron-deficiency anemia, which describes a more systematic manner in which to approach iron-deficiency anemia.

Anemia, Iron-Deficiency↗
PubMed1999

Low-dose oral iron absorption test in anaemic patients with and without iron deficiency determined by bone marrow iron content.

The low-dose oral iron absorption test (OIAT) was performed in 85 consecutive anaemic patients referred for bone marrow examination in order to investigate the ability of the test to predict bone marrow iron stores and to differentiate between different categories of anaemia. Eight patients were excluded for technical reasons. Test results from 77 patients are presented as Cmax (micromol/l): the maximum increase in S-iron measured during a 3 h period after administration of 10 mg oral iron sulfate. Iron deficiency was defined as the absence of stainable iron in bone marrow aspirates. Cmax was higher in 46 iron deficient patients [3 (median); 0 and 13 (1st and 3rd quartiles); 0-40 (range)] than in 31 non-iron-deficient patients (0; 0 and 2; 0-4) (P<0.01). 27 patients had primary bone marrow disease, 25 patients had absent bone marrow iron stores accompanied by inflammation, 17 patients had anaemia of chronic disease (ACD) and 8 patients had uncomplicated iron deficiency anaemia (IDA). Patients with IDA had higher Cmax (15; 13 and 28; 6-40) than patients with ACD (1; 0 and 2; 0-3), and than the 69 non-IDA patients (1; 0 and 3; 0-19) (P<0.001). Cmax values above 5 micromol/l always indicated absent bone marrow iron stores.

Adult↗
PubMed2000

Hookworms, malaria and vitamin A deficiency contribute to anemia and iron deficiency among pregnant women in the plains of Nepal.

Anemia and iron deficiency during pregnancy are prevalent in developing countries, but their causes are not always known. We assessed the prevalence and severity of anemia and iron deficiency and their association with helminths, malaria and vitamin A deficiency in a community-based sample of 336 pregnant women in the plains of Nepal. Hemoglobin, erythrocyte protoporphyrin (EP) and serum ferritin were assessed in venous blood samples. Overall, 72.6% of women were anemic (hemoglobin < 110 g/L), 19.9% had moderate to severe anemia (hemoglobin < 90 g/L) and 80.6% had iron deficiency (EP > 70 micromol/mol heme or serum ferritin < 10 microg/L). Eighty-eight percent of cases of anemia were associated with iron deficiency. More than half of the women (54.2%) had a low serum retinol concentration (<1.05 micromol/L), 74.2% were infected with hookworms and 19.8% had Plasmodium vivax malaria parasitemia. Hemoglobin, EP and serum ferritin concentrations were significantly worse and the prevalence of anemia, elevated EP and low serum ferritin was increased with increasing intensity of hookworm infection. Hookworm infection intensity was the strongest predictor of iron status, especially of depleted iron stores. Low serum retinol was most strongly associated with mild anemia, whereas P. vivax malaria and hookworm infection intensity were stronger predictors of moderate to severe anemia. These findings reinforce the need for programs to consider reducing the prevalence of hookworm, malaria infection and vitamin A deficiency where indicated, in addition to providing iron supplements to effectively control anemia.

Adolescent↗
PubMed1988

Selective alteration in blood-brain barrier and insulin transport in iron-deficient rats.

Nutritional iron deficiency induced in rats causes a significant reduction in level of brain nonheme iron and is accompanied by selective reduction of dopamine D2 receptor Bmax. Our previous studies have clearly demonstrated that these alterations can be restored to normal by supplementation with ferrous sulfate; however, neither brain nonheme iron level nor dopamine D2 receptor Bmax can be increased beyond control values even after long-term iron therapy. The possibility that iron deficiency can induce the breakdown of the blood-brain barrier (BBB) was examined. A 70 and 100% increase in brain uptake index (BUI) for L-glucose and insulin, respectively, were noted in iron-deficient rats. However, the BUI for valine was decreased by 40%, and those for L-norepinephrine and glycine were unchanged. In addition, it was demonstrated that in normal rats insulin is transported into the brain. The data show that iron deficiency selectively affects the integrity of the BBB for insulin, glucose, and valine transport. Whether the effect of iron deficiency on the BBB is at the level of the capillary endothelial cell tight junction is not yet known. However, this study has shown that an important nutritional disorder (iron-deficiency anemia) has a profound effect on the BBB and brain function.

Anemia, Hypochromic↗