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PubMed1992

[Iron-deficiency anemia: diagnosis and therapy].

Iron deficiency is the most frequent cause of anemia. The correct diagnosis is based on history, peripheral blood findings and investigations of the iron status. Anemia occurs only when iron stores are empty. Iron deficiency anemia is a microcytic, hypochromic anemia. Red blood cells show poikilo- and anisocytosis with predominance of small erythrocytes. In one third of the patients the anemia is accompanied by slight leukopenia. The platelet counts may be normal, increased or decreased. Iron deficiency is documented by decreased serum iron, increased transferrin and decreased iron saturation. Ferritin below 15 ng/ml confirms the depletion of iron. Once the diagnosis of iron deficiency is established, its cause must be investigated. Pregnancy and bleeding are the most frequent conditions leading to iron deficiency. Therapy of iron deficiency involves treatment of the underlying condition as well as reestablishment of iron stores. Oral therapy is the most safe and economical method of correcting iron deficiency. Parenteral therapy should be confined to exceptional situations.

Anemia, Hypochromic↗
PubMed1998

Iron-deficient intestine is more susceptible to peroxidative damage during iron supplementation in rats.

Redox-active forms of iron are known to catalyze free radical mediated peroxidative reactions. There is scanty information on such effects at the sites of iron absorption. This was tested in iron-deficient WKY female rats supplemented for 15 days with FeSO4 equivalent to 8 mg of iron (D+) and compared with iron deficient (D) and iron adequate (C) rats. The levels of intestinal MDA and protein carbonyls and the activities of various antioxidant enzymes were estimated. As markers of functional integrity, the activities of alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were evaluated. In addition, we measured the concentrations of ferritin, transferrin, and ceruloplasmin levels in serum and in intestinal mucosa. It was observed that correction of iron deficiency resulted in significant increase in MDA and protein carbonyl formation. Activities of both alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were significantly decreased in D+ compared to C. The increase in catalase and decrease in Gpx was found to be sensitive to iron administration. Neither iron deficiency nor its correction had any effect on the activity of SOD and GSH levels. Iron supplementation has resulted in decreased mobilization of stored iron as reflected by increased mucosal ferritin level and decreased serum ceruloplasmin ferroxidase activity contributing to greater peroxidative stress in the intestine. These results suggest that iron-deficient intestine of rat is more susceptible to iron-mediated peroxidative damage and functional impairment during correction of deficiency with iron.

Administration, Oral↗
PubMed1982

Clinical evaluation of iron deficiency.

While the prevalence of iron deficiency has remained relatively constant, there has been continuing refinement in its laboratory recognition, especially with the recent introduction of serum ferritin and FEP measurements. It is helpful to classify iron deficiency into three stages. Storage iron depletion is identified by marrow examination or serum ferritin, iron deficient erythropoiesis by TS, FEP, or MCV, and iron deficiency anemia by hemoglobin concentration or therapeutic iron trial. Combinations of these measurements have been used in prevalence studies to obtain a quantitative measure of body iron stores. The optimal laboratory approach to diagnosing iron deficiency depends on the clinical setting. In the office or outpatient clinic, iron depletion is best recognized by the serum ferritin, although the TS, FEP, and MCV are helpful in gauging its severity. In hospitalized patients with overt anemia, the TS, FEP, and MCV are much less helpful because similar changes are seen in the anemia of chronic disease. Examination of marrow iron remains the method of choice, especially in patients with infection, chronic disease, malignancy, or liver disease, although in many clinical situations the same information can be obtained from a serum ferritin. Serial measurements of serum ferritin have been particularly useful in monitoring patients at high risk of iron deficiency such as those with rheumatoid arthritis, chronic inflammatory bowel disease, or chronic renal failure.

Adult↗
PubMedDate not supplied

[Disordered lymphoid regulation of hematopoiesis in iron-deficiency anemia].

Iron-deficiency anemia (IDA) in rats is attended by secondary cellular immunodeficiency. The authors studied the importance of lymphocyte dysfunction in the pathogenesis of hematological disorders in rats with IDA. Transplantation of lymphocytes from intact donors subjected to hypoxia to syngeneic recipients led to stimulation of erythropoiesis in them. The effect of "iron deficiency' cells was less manifest. It was established that the hematological disorders in IDA are lymphocyte-determined. This was also demonstrated in experiments on rats with IDA and changed functional condition of the lymphoid tissue.

Anemia, Hypochromic↗
PubMed1995

Brain iron, transferrin and ferritin concentrations are altered in developing iron-deficient rats.

To study the iron, transferrin, and ferritin distribution at subcellular levels in response to acute dietary iron deficiency, we tested the hypothesis that early post-weaning iron deficiency can change iron and iron regulatory protein concentrations in rat brain. Male Sprague-Dawley rats were fed diets containing either 2 or 35 micrograms iron/g for 2, 3 or 4 wk starting at 21 d of age. Brain iron, transferrin and ferritin concentrations in cytosolic and microsomal fractions of either whole brain or pons and cerebellum were then determined. After 14 d of dietary iron restriction, brain iron concentrations were 50% lower in the microsomal fraction and 30% lower in cytosol compared with controls. Brain cytosolic transferrin concentration almost doubled in the same animals. Brain ferritin concentration in fractions from rats fed the iron-deficient diet for 14 d was lower than in controls, but then remained fairly constant. Absolute brain weight and total brain protein contents were unaffected by iron restriction. This study extends previous research by demonstrating that the brain responds to changes in body iron status with a change in transferrin concentration. If the dietary restriction is quite severe, this adaptation is insufficient. This study also notes that brain ferritin decreases with decreasing body iron status, though it was less responsive than nonheme iron in liver. The concept that iron enters the brain through a highly regulated endocytotic process at the blood brain barrier, that undoubtedly involves the regulation of transferrin receptors in capillary endothelial cell, is supported by our observation of elevated transferrin concentrations in brain of iron-deficient rats.

Anemia, Iron-Deficiency↗
PubMed2004

A 69-year-old woman with persistent iron deficiency anemia.

In women, iron deficiency anemia-a result of chronic iron loss-is most common during the reproductive years because of physiologic demands such as menstrual blood losses and pregnancy. In other cases, iron deficiency anemia is generally attributed to occult gastrointestinal bleeding. Common causes of chronic gastrointestinal blood loss include erosive esophagitis, gastric and duodenal ulcers, vascular ectasias, colon adenomas, and cancers. Bleeding from the small intestine at sites beyond the duodenal bulb is uncommon. The lesions of the small intestine are responsible for approximately 4% of gastrointestinal bleeding [7]. In this report we describe a case of persistent iron deficiency anemia due to carcinoid tumor of the small intestine.

Aged↗
PubMed2003

Iron deficiency and erythropoiesis: new diagnostic approaches.

Iron deficiency anemia is one of the most common diseases worldwide. In the majority of cases, the presence of hypochromic microcytic anemia and biochemical evidence for depletion of body iron stores makes the diagnosis relatively straightforward. However, in several clinical conditions, classic biochemical indices such as serum iron, transferrin saturation, and ferritin may not be informative or may not change rapidly enough to reflect transient iron-deficient states (functional iron deficiency), such as the ones that develop during recombinant human erythropoietin (r-HuEPO) therapy. The identification and treatment of iron deficiency in settings such as r-HuEPO therapy, anemia of chronic disease, and iron deficiency of early childhood may be improved by the use of red cell and reticulocyte cellular indices, which reflect in almost real time the development of iron deficiency and the response to iron therapy. In the anemia of chronic disease, measurements of plasma cytokines and iron metabolism regulators such as hepcidin (when available) may be helpful in the characterization of the pathophysiologic basis of this condition. The ratio of serum transferrin receptor (sTfR) to serum ferritin (R/F ratio) has been shown to have excellent performance in estimating body iron stores, but it cannot be used widely because of the lack of standardization for sTfR assays. The combination of hematologic markers such as reticulocyte hemoglobin content, which decreases with iron deficiency, and R/F ratio may allow for a more precise classification of anemias.

Anemia, Iron-Deficiency↗
PubMed1988

The effect of iron therapy on the exercise capacity of nonanemic iron-deficient adolescent runners.

Iron-deficiency anemia impairs exercise capacity, but whether nonanemic iron depletion decreases endurance performance is unclear. In 14 iron-deficient (serum ferritin level, less than 20 micrograms/L [less than 20 ng/L])nonanemic runners, hematologic and treadmill running values were followed up during a competitive season. Following a four-week control period, runners were treated for one month in a double-blind protocol with ferrous sulfate (975 mg/d) or placebo. During treatment, the mean ferritin level rose from 8.7 to 26.6 micrograms/L (8.7 to 26.6 ng/mL) in those patients taking iron and fell from 10.6 to 8.6 micrograms/L (10.7 to 8.6 ng/mL) in the placebo group. Treadmill endurance times improved significantly in the iron-treated runners compared with controls. Endurance time declined in all seven controls (range, 0.07 to 1.30 minutes), while six of seven iron-treated subjects improved their performance (range, 0.03 to 1.92 minutes). No significant differences in maximal or submaximal oxygen consumption, ventilation, or heart rate were observed between the groups except for a 4% increase in maximum oxygen consumption during placebo treatment. These data indicate that nonanemic iron deficiency impairs exercise performance but does not influence gas exchange or cardiac measures.

Adolescent↗