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A cost effective approach to the biochemical diagnosis of iron deficiency.

Serum iron, total iron binding capacity (TIBC) and serum ferritin were measured on 419 samples to evaluate the value of these measurements and to develop a cost effective strategy for diagnosis of iron deficiency. If transferrin saturation (PS) of less than 16% and TIBC of greater than 70 mumol/L were used as diagnostic criteria for iron deficiency, 93% of the 59 patients who fulfilled these criteria were iron deficient; 49 had low serum ferritin and six were iron deficient with normal serum ferritin levels. When we used PS of greater than or equal to 22% and TIBC less than or equal to 70 mumol/L to exclude iron deficiency, 99% of those patients who fulfilled these criteria had normal serum ferritin levels. We, therefore, suggest that for biochemical diagnosis of iron deficiency serum iron and TIBC should be done first, and serum ferritin is not required when the PS is less than 16% and TIBC greater than 70 mumol/l or if PS is greater than or equal to 22% and TIBC less than or equal to 70 mumol/L. In all other cases serum ferritin is measured to detect iron deficiency. This approach will save 35 to 40% of reagent costs.

Anemia, Hypochromic↗

Zinc protoporphyrin/heme ratio for diagnosis of preanemic iron deficiency.

OBJECTIVE: Iron deficiency anemia is known to impair cognitive and psychomotor development. The zinc protoporphyrin/heme (ZPP/H) ratio is a simple, accurate, and sensitive laboratory screening test that detects early iron depletion before the onset of anemia. The objective of this work was to evaluate this test in a primary pediatric practice setting. METHODS: The iron status of a cohort of 361 children was screened during routine examinations at a community pediatric practice. Whole blood hemoglobin concentration, hematocrit ratio, serum transferrin saturation, ferritin concentration, and the ZPP/H ratio were measured. The ZPP/H ratio then was evaluated as a single indicator of iron status by comparing it with other tests for detecting the onset of iron deficiency and for monitoring recovery after iron supplementation. RESULTS: Significant age- and sex-related differences in the ZPP/H ratio were found. In this cohort, serum ferritin concentration and the ZPP/H ratio independently identified the same fraction of iron-deficient patients (3%-4%), and both tests were more specific than was either hemoglobin or hematocrit. A concordance of three iron status parameters changed the prediction of iron deficiency to </=1%. Children <3 years of age and adolescent girls had significantly higher ZPP/H results. CONCLUSION: The prevalence of iron deficiency anemia in the typical healthy American pediatric population is low, but iron deficiency without anemia remains relatively common at some stages of development. Increase in the ZPP/H ratio is demonstrated to be a sensitive, specific, and cost-effective test for identifying preanemic iron deficiency in a community pediatric practice. anemia, nutrition, development.

Adolescent↗

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↗

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↗

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↗

Globus pallidus: a target brain region for divalent metal accumulation associated with dietary iron deficiency.

Recently, iron deficiency has been connected with a heterogeneous accumulation of manganese in the rat brain. The striatum is particularly vulnerable, for there is a significant negative correlation between accumulated manganese and gamma-aminobutyric acid levels. The effect of dietary iron deficiency on the distribution of zinc and copper, two other divalent metals with essential neurobiological roles, is relatively unexplored. Thus, the primary goal of this study was to examine the effect of manipulating dietary iron and manganese levels on the concentrations of copper, iron, manganese and zinc in five rat brain regions as determined with inductively coupled plasma mass spectrometry analysis. Because divalent metal transporter has been implicated as a transporter of brain iron, manganese, and to a lesser extent zinc and copper, another goal of the study was to measure brain regional changes in transporter levels using Western blot analysis. As expected, there was a significant effect of iron deficiency (P < 0.05) on decreasing iron concentrations in the cerebellum and caudate putamen; and increasing manganese concentrations in caudate putamen, globus pallidus and substantia nigra. Furthermore, there was a significant effect of iron deficiency (P < 0.05) on increasing zinc concentration and a statistical trend (P = 0.08) toward iron deficiency-induced copper accumulation in the globus pallidus. Transporter protein in all five regions increased due to iron deficiency compared to control levels (P < 0.05); however, the globus pallidus and substantia nigra revealed the greatest increase. Therefore, the globus pallidus appears to be a target for divalent metal accumulation that is associated with dietary iron deficiency, potentially caused by increased transporter protein levels.

Animals↗

[Increased erythron transferrin uptake associated with ineffective erythropoiesis in iron deficiency state--the common factors to iron deficiency anemia and portal hypertensions].

We calibrated the erythron transferrin uptake (ETU) and efficiency ratio (R-Ef) in erythropoiesis on the basis of ferroerythrokinetic data in 90 patients with iron deficiency anemia (IDA) and 64 patients with noncirrhotic and cirrhotic portal hypertension with splenomegaly (PH). Then we analyzed the data to elucidate how iron deficiency (ID) status effects variation of these values. ETU was significantly higher and R-Ef was lower in IDA subgroup before treatment (n = 71) than those with any recent treatment (n = 19), and in PH with anemia of ID type (PH-ID n = 39) than those without ID state (n = 34). A remarkable inverse correlation was obtained between ETU and R-Ef in both IDA and PH-ID and iron replacement therapy effected synchronous improvement of these values. We deduced the quantitative parameter of ID status (ID-x) on blood chemistry data in IDA by multiple regression of ETU and of R-Ef respectively. These calibration formulae were extrapolated to the data in PH-ID. Thus we delineate the factor which represents ID status in common to these two diseases to increase ETU and decrease R-Ef, although the contribution of ID-x was greater in IDA than PH-ID. Additional factors to enhance or modify these values were shortened survival of erythrocytes, splenomegaly and hepatic dysfunction.

Anemia, Iron-Deficiency↗

Lactic acidosis as a result of iron deficiency.

Iron-deficient rats have an impaired work performance, even when their anemia is corrected by exchange transfusion. Muscle activity is associated with a higher blood lactate concentration than is observed in iron-replete animals. The accumulation of lactate is a result of excessive production as lactate clearance from the blood was shown to be unaffected. By adjusting the work load to a lower level, it was possible to divide iron-deficient animals into two groups, one capable of continued treadmill running and another in which animals stopped before 20 min. In the former, blood lactate concentration reached a plateau at moderate levels, whereas it continued to increase in the latter until the animal stopped running. Levels of alpha-glycerophosphate oxidase in skeletal muscle mitochondria were found to be much lower in the second group (P < 0.001). Lactate infusion into normal animals was shown to interfere with work performance, and maintenance of a normal pH in iron-deficient and iron-replete animals did not prevent the impairment in work associated with high blood lactate concentrations. Additional evidence was obtained that energy substrate (blood glucose and free fatty acids, muscle glycogen) was adequate in irondeficient animals. Oxygen tension in their vena caval blood was higher than in controls. Furthermore, the in situ behavior of electrically stimulated gastroenemius and soleus muscles appeared similar to that of control animals. Because the stimulation of the single muscle in the iron-deficient animal did not result in appreciable elevation of blood lactate and did not show impaired contractility further supported the hypothesis that the elevation of blood lactate caused the decreased work performance. It is concluded that iron deficiency by a depletion in the iron-containing mitochondrial enzyme, alpha-glycerophosphate oxidase, impairs glycolysis, resulting in excess lactate formation, which at high levels leads to cessation of physical activity.

Acidosis↗

Geophagia in Turkey: iron and zinc deficiency, iron and zinc absorption studies and response to treatment with zinc in geophagia cases.

A brief summary of the research carried out on the problem of geophagia is reported in this paper. Geophagia was a common finding among Turkish children and women in villages, associated with severe iron deficiency anemia in addition to zinc depletion. The syndrome characterized by geophagia, iron deficiency anemia, growth retardation, hypogonadism and zinc deficiency has been observed in both sexes in Turkey for several decades. Zinc deficiency has been also shown by our group in this syndrome. The decreased concentrations of zinc in serum, plasma, RBC, hair and urine were measured by atomic absorption spectrophotometer. Oral iron (both inorganic and radioactive iron) and zinc absorption tests were carried out with and without clay and revealed decreased iron and zinc absorption in some cases with prolonged geophagia. Therefore, malabsorption of iron and zinc was considered to be an additional and/or a new finding in the syndrome. Furthermore, Turkish clay most probably inhibits zinc absorption in a way similar to its inhibition of iron absorption. It was worthy of observation that some Turkish patients with this syndrome had a thalassemia-like appearance with similar skull-bone changes. Finally, growth retardation and delayed puberty were shown to be corrected by oral zinc treatment for 6-month terms. Linear growth and sexual maturation were found to be greater in the zinc-treated group than in the controls.

Adolescent↗