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At least 19 recordsLinked to original sources
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↗
PubMed1999

Gastrointestinal tract evaluation in patients with iron deficiency anemia.

Iron deficiency anemia is the most common form of anemia encountered in clinical practice and is an extremely common manifestation of chronic occult gastrointestinal bleeding. Current evidence suggests that a large proportion of men and postmenopausal women with iron deficiency anemia harbor significant gastrointestinal tract pathological lesions as the source of blood loss. As such, the evaluation of patients with iron deficiency anemia is generally focused on the gastrointestinal tract. Importantly, the diagnosis of iron deficiency anemia should be firmly established before an extensive evaluation is undertaken. Management strategies for patients with iron deficiency anemia are reviewed; an important general point is that clinical features (ie, symptoms) may help direct specific investigation. The role of small-intestinal investigation in patients with iron deficiency anemia is controversial and should probably be reserved for patients with iron deficiency anemia and persistent gastrointestinal symptoms or those who fail to respond to appropriate therapy. The treatment and prognosis of patients with iron deficiency anemia and the majority of gastrointestinal tract lesions are straightforward. However, patients with vascular ectasias as the source of blood loss can represent a true management challenge.

Adenocarcinoma↗
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↗
PubMed2001

Serum free carnitine and total triglycerid levels in children with iron deficiency anemia.

Iron deficiency anemia and hyperlipidemia are common public health problems in Turkey. The connection between iron and lipid metabolisms has not been clarified yet. The aim of the study was to determine the effect of iron deficiency on carnitine and lipid metabolism. Study group was consisted of 70 children (mean age 14.7 +/- 1.3 months) suffering from iron deficiency anemia and 20 healthy children (mean age 13.7 +/- 1.2 months) attended to outpatient clinics of Cumhuriyet University, Sivas were enrolled the study as the control group. Assessments of serum free carnitine concentrations, total triglyceride, total cholesterol and VLDL levels were made in both groups. The mean serum free carnitine concentration was significantly lower than the control group (18.9 +/- 0.43 nmol/ml and 45.9 +/- 1.47 nmol/ml respectively, t = 17.5 p < 0.01). Results of our study also indicated higher serum total triglyceride, total cholesterol and VLDL levels in iron deficient patients than the healthy controls. Regression analyses indicated a negative correlation between serum free carnitine and total triglyceride levels in iron deficient patients. This study confirms that iron deficiency anemia may be linked to the endogenous carnitine synthesis in pediatric age group, and thus hyperlipidemia appears to be a risk factor for premature cardiovascular diseases.

Anemia, Iron-Deficiency↗
PubMed2004

Cerebral sinovenous thrombosis in children: another reason to treat iron deficiency anemia.

Iron deficiency anemia is a rare cause of cerebral sinovenous thrombosis in children. We report three cases of cerebral sinovenous thrombosis and iron deficiency anemia treated at Primary Children's Medical Center in Salt Lake City, Utah, between 1998 and 2001. The children were 9, 19, and 27 months old at the time of admission. Hemoglobin levels ranged from 6.6 to 7.0 g/dL, mean corpuscular volume levels from 45 to 56 fL, and platelet counts from 248,000 to 586,000/microL. Magnetic resonance imaging and magnetic resonance venography revealed thrombosis of the straight sinus and internal cerebral veins in all three children, with the addition of the vein of Galen, left transverse and sigmoid sinuses, and upper left internal jugular vein in one child. Recovery ranged from excellent to poor in 3 months to 3 years of follow-up. Four additional cases, ages 6 to 22 months, were found in the English-language literature. Evaluation for prothrombotic disorders was negative in all children, including the current cases. Treatments have included thrombectomy, corticosteroids, mannitol, heparin, low-molecular-weight heparin, warfarin, aspirin, blood transfusion, and iron supplementation, but there is no consensus regarding therapy, other than to correct the anemia and treat iron deficiency. Iron deficiency anemia, a preventable cause of cerebral sinovenous thrombosis, deserves consideration when cerebral sinovenous thrombosis is detected in young children.

Anemia, Iron-Deficiency↗
PubMed1988

Amylophagia and iron deficiency anemia.

Iron deficiency anemia may be associated with dietary practices such as amylophagia, which is seen frequently in women of certain ethnic origins. Starch eating may be a direct or indirect cause or symptom of iron deficiency anemia. Orofacial symptoms of amylophagia and iron deficiency anemia are discussed. A case in which anemia and dietary aberration were incidental to the admitting diagnosis is presented.

Adolescent↗
PubMed1996

Effect of iron-supplemented total parenteral nutrition in patients with iron deficiency anemia.

Iron deficiency anemia is common among hospitalized patients, and blood losses from diagnostic phlebotomy increase the likelihood of a negative iron balance. The role for iron supplementation of total parenteral nutrition (TPN) in these patients is unclear. Twenty-three patients with iron deficiency anemia were identified. Twelve patients were randomized to receive TPN without iron (group 1) and 11 received TPN supplemented with 10 mg of iron as iron dextran daily (group 2). Both groups were matched for age, serum iron studies, red cell indices, and hemogram. After a 7-d period, the mean serum iron in group 2 increased from 10 to 26 micrograms/dL, with an increased transferrin saturation from 7.3 to 15.3% (each, p < 0.05). No changes in total iron binding capacity, ferritin, reticulocyte count, hemoglobin, hematocrit, or mean corpuscular volume were observed in the two groups. The incidence of infectious complications was not different between both groups. We conclude that iron supplementation of TPN appears safe and is effective in increasing serum iron levels. The use of iron-supplemented short-term TPN needs to be further studied given no change in red cell indices, hemoglobin, hematocrit, or transfusion requirement.

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↗
PubMed1987

Substrate-dependent functional defects and altered mitochondrial respiratory capacity in hearts from guinea pigs with iron deficiency anemia.

Iron deficiency anemia was induced by dietary means in weanling guinea pigs. A 25% higher ventricular wall mass per 100 g body mass was seen after 6 weeks of feeding. Myocardial performance was determined in isolated perfused hearts using an isovolumic Langendorff preparation. All hearts exhibited a 25% decrease in left ventricular developed pressure (LVDP) and decreased dP/dt when substrate was switched from 10 mM pyruvate to 16.6 mM glucose. The glucose reduction in LVDP resulted from decreased systolic pressure, which completely reversed when hearts again metabolized pyruvate. With glucose as substrate, left ventricular developed pressure-end diastolic volume relationships were indistinguishable. However, with pyruvate, iron-deficient hearts appeared to be less responsive to the increased energy demands required by elevated diastolic volumes. Rates of state 3 respiration were 18% below control with glutamate + malate as substrate, and 38% lower with pyruvate + malate in mitochondria isolated from anemic animals. No differences in respiration were noted with succinate. Cytochrome a + a3 content, cytochrome oxidase activity and total mitochondrial protein content appeared to be unchanged. In contrast, cytochromes b, c + c1, and the flavoproteins were significantly decreased. The data suggest that iron deficiency anemia induces cardiac hypertrophy with a fixed but defective mitochondrial population, potentially placing the heart in an energetic imbalance. These differences in mitochondrial function were expressed by decreased myocardial performance when the heart metabolizes pyruvate, an exclusively aerobic substrate.

Anemia, Hypochromic↗
PubMed1982

Evaluating iron deficiency anemia.

Iron deficiency anemia is the most common of all the anemias and can be created easily once it is diagnosed. Diagnosis is a multistep procedure since there are many other clinical entities that have similar symptomatology and physical findings. The history and physical examination can provide clues to additional procedures or tests that may need to be ordered. If anemia is identified as the cause of symptoms, then the type of anemia must be differentiated. When iron deficiency is confirmed, the underlying pathology must be identified if treatment is to be successful. Successful treatment requires correction of cause in addition to use of iron supplements.

Adolescent↗
PubMed2002

Twenty-four-hour motor activity in human infants with and without iron deficiency anemia.

Iron deficiency anemia (IDA) is a very common nutritional problem that alters motor activity. The aim of this study was to compare 24-h motor activity in the home in healthy 6-month-old infants with and without IDA. Activity was assessed via actigraphs on the leg during 24 continuous hours in 17 Chilean infants with IDA and 18 with normal hemoglobin levels. All infants were given oral iron, and activity was reassessed at 12 and 18 months. The frequency of movement units per minute was determined for each waking/sleep state during the day and night, and the duration of each state was computed. At 6 months of age, there were no differences between anemic and nonanemic infants in time per state. However, infants with IDA showed an overall increase in motor activity compared to controls. These differences were no longer observed at 12 and 18 months of age. Increased activity during the period of IDA raises the issue of a shared underlying mechanism with restless legs syndrome, a sensorimotor dysfunction where iron deficiency increases the severity of the symptoms and iron supplementation ameliorates them. Due to previous findings of decreased motor activity in the laboratory at 12 months during the waking time surrounding an afternoon nap, we also compared those data to a nap in the home. Infants with IDA were less active in the laboratory than in the home. The home versus laboratory results suggest that contextual factors affect the motor activity of IDA infants to a larger extent than controls.

Anemia, Iron-Deficiency↗
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↗
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↗
PubMed2005

Anemia, iron deficiency, and iron deficiency anemia in 12-36-mo-old children from low-income families.

BACKGROUND: Iron deficiency (ID) is the most common nutritional deficiency in the world and remains relatively common in at-risk groups in the United States. The actual prevalence of anemia, ID, and iron deficiency anemia (IDA) in California remains unclear. OBJECTIVE: The objective was to determine the prevalence of anemia, low iron stores, ID, and IDA in children participating in the Special Supplemental Nutrition Program for Women, Infants and Children (WIC) population, and to assess the value of using hemoglobin to predict ID. DESIGN: This was a cross-sectional study of a convenience sample of 12-36-mo-old children from WIC clinics in 2 California counties. RESULTS: The prevalence of anemia was 11.1% (hemoglobin <110 g/L at 12-24 mo or <111 g/L at 24-36 mo). Study- and literature-determined abnormal values for iron measures were as follows: serum ferritin or=8.4 or >10.0 microg/mL, and transferrin saturation or=2 abnormal iron measures) were 16.2% and 8.8%, and of IDA (ID with low hemoglobin) were 3.4% and 3.2% on the basis of study- and literature-determined cutoffs, respectively. Hemoglobin concentration was used to predict study- and literature-determined ID on the basis of receiver operating characteristic curves. The sensitivity of low hemoglobin in predicting study- and literature-determined ID was low (23.2% and 40.0%, respectively). CONCLUSIONS: Anemia and ID were prevalent in this WIC sample, but IDA was uncommon. Low hemoglobin is a poor predictor of ID.

Anemia↗
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

[Iron deficiency anemia].

Iron deficiency anaemia is characterized by the conjunction of a microcytic, typically are generative anaemia and a biochemical syndrome in which sideropoenia is associated with transferrin increase. It is usually due to a chronic exsudative gastrointestinal or gynaecological bleeding. Diagnosing the mechanism of anaemia is easy in most cases, but difficulties arise from association with a pathology, such as chronic inflammatory syndrome, disturbing the haematological or biochemical data. The prognosis of iron deficiency anaemia depends on its cause. Treatment is aetiological (the cause of chronic bleeding is suppressed) and symptomatic (the body's iron reserves are quickly restored).

Anemia, Hypochromic↗