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PubMed2002

Neurologic manifestations of iron deficiency in childhood.

Iron deficiency is a common disorder in pediatric patients. Although the most common manifestation is that of anemia, iron deficiency is frequently the source of a host of neurologic disorders presenting to general pediatric neurologic practices. These disorders include developmental delay, stroke, breath-holding episodes, pseudotumor cerebri, and cranial nerve palsies. Although frequent, the identification of iron deficiency as part of the differential diagnosis in these disorders is uncommon and frequently goes untreated. The purpose of the current review is to highlight what is understood regarding iron deficiency and it's underlying pathophysiology as it relates to the brain, and the association of iron deficiency with common neurologic pediatric disease.

Anemia, Iron-Deficiency↗
PubMed1987

Iron deficiency in cystic fibrosis.

Iron state was measured as part of the comprehensive assessment of 165 patients with cystic fibrosis. Of 127 patients, 41 (32%) had low serum ferritin concentrations and at least this proportion were iron deficiency. Iron state did not correlate with clinical score, radiological score, or results of sputum culture. There was no evidence that patients with iron deficiency were either in better or worse clinical condition than those with better iron stores.

Adolescent↗
PubMed1993

Modulation of uptake of heme by rat small intestinal mucosa in iron deficiency.

Although body iron status modulates whole body retention of heme derived iron, it is not known with certainty whether modulation occurs by regulation of mucosal uptake of heme. In vivo uptake from perfused intestine of heme labeled with 14C in the porphyrin ring was studied in groups of rats of differing iron status ranging from fully replete to markedly iron deficient. Heme extraction from infusate and mucosal heme uptake were significantly different between test groups (P < 0.005 and 0.001, respectively). Marked iron deficiency induced a 4.8-fold rise in heme extraction relative to iron-replete animals; rats with latent iron deficiency showed a smaller but still significant rise. Heme extraction correlated negatively with indicators of iron status: hemoglobin (r = -0.76, P < 0.001) and serum iron (r = -0.56, P < 0.05). The specific binding of [14C]heme to purified brush borders from iron-replete and iron-deficient rats was 1.4-fold higher in deficient rats when expressed per milligram of protein (P = 0.046) and 3.3-fold higher when expressed relative to alkaline phosphatase activity (P = 0.014). Thus mucosal uptake of heme in iron deficiency is increased because of an increase in its binding to the brush border.

Animals↗
PubMed2001

[Changes of serum transferrin receptor in children with iron deficiency and its response to iron supplementation].

OBJECTIVES: To study the level of serum transferrin receptor (sTfR) in children with different stages of iron deficiency, as well as in the normal children, to observe its response to iron supplementation, and to explore the role of sTfR in surveillance of iron status and assessment of iron supplementation in population. METHODS: By determining iron status index, 1,006 children aged 6-14 years in Fangshan District, Beijing were divided into four groups, control group, iron depletion (ID) group, iron deficiency erythropoiesis (IDE) group and iron deficiency anemia (IDA) group, and 239 of them were measured for sTfR with Quintikine enzyme immunoassay (R&D system, Minneapolis, MN) and sTfR/logserum ferratin (SF) was estimated. Iron supplementation (NaFeEDTA capsules, containing 60 mg iron element per capsule) was administered for the children with ID and IDE per capsule once weekly and for the children with IDA per capsule thrice weekly for nine weeks. Iron status index and sTfR were measured before and after iron supplementation. RESULTS: The levels of sTfR and sTfR/log SF in children with ID, IDE and IDA were (20.03 +/- 2.33) nmol/L, (24.52 +/- 1.07) nmol/L, (33.28 +/- 6.09) nmol/L and (18.15 +/- 5.31), (20.98 +/- 8.88), (29.08 +/- 8.57), respectively, significantly higher than those in the control group [sTfR(18.74 +/- 3.06) nmol/L and sTfR/log SF(9.89 +/- 1.74)]. Statistical analysis showed that sTfR correlated to free erythrocyte protoporphyrin and hemoglobin. sTfR levels in normal children was (12.5-23.5) nmol/L. After iron supplementation, sTfR levels in children with ID was (16.37 +/- 3.10) nmol/L, significantly decreased than those before iron supplementation, but no change in sTfR was observed in children with IDE and IDA. sTfR/log SF were decreased significantly in all children with ID group(11.42 +/- 3.12), IDE (16.54 +/- 4.70) and IDA (23.59 +/- 9.93). CONCLUSION: sTfR is a specific indicator for identifying IDE and IDA, and sTfR/log SF is a sensitive index for assessing the effects of iron supplementation.

Adolescent↗
PubMed2006

Decreased hephaestin activity in the intestine of copper-deficient mice causes systemic iron deficiency.

Copper and iron metabolism intersect in mammals. Copper deficiency simultaneously leads to decreased iron levels in some tissues and iron deficiency anemia, whereas it results in iron overload in other tissues such as the intestine and liver. The copper requirement of the multicopper ferroxidases hephaestin and ceruloplasmin likely explains this link between copper and iron homeostasis in mammals. We investigated the effect of in vivo and in vitro copper deficiency on hephaestin (Heph) expression and activity. C57BL/6J mice were separated into 2 groups on the day of parturition. One group was fed a copper-deficient diet and another was fed a control diet for 6 wk. Copper-deficient mice had significantly lower hephaestin and ceruloplasmin (approximately 50% of controls) ferroxidase activity. Liver hepcidin expression was significantly downregulated by copper deficiency (approximately 60% of controls), and enterocyte mRNA and protein levels of ferroportin1 were increased to 2.5 and 10 times, respectively, relative to controls, by copper deficiency, indicating a systemic iron deficiency in the copper-deficient mice. Interestingly, hephaestin protein levels were significantly decreased to approximately 40% of control, suggesting that decreased enterocyte copper content leads to decreased hephaestin synthesis and/or stability. We also examined the effect of copper deficiency on hephaestin in vitro in the HT29 cell line and found dramatically decreased hephaestin synthesis and activity. Both in vivo and in vitro studies indicate that copper is required for the proper processing and/or stability of hephaestin.

Anemia, Iron-Deficiency↗
PubMed1996

Abnormalities in adenosine triphosphatase of the erythrocyte membrane in iron deficiency anaemia.

During iron deficiency rat and human erythrocyte membrane enzyme activities (Total ATPase and Ouabainsensitive Na+.K+ ATPase) showed significant (P < 0.001) decrease. The influence of iron deficiency on erythrocyte Na+ and K+ was also studied in rats and humans. The former parameter showed a significant (P < 0.01) increase while the latter showed a downward trend. Plasma Fe and Total Iron Binding capacity (TIBC) in iron deficiency varied significantly (P < 0.05) from normal values. These results suggest a defect in erythrocyte membrane function and a possible potentiating effect of intracellular Na+, plasma Fe and TIBC on ATPase activity in iron deficiency. Values obtained for rats and humans showed differences in the activities of membrane ATPase in iron deficiency anaemia.

Adult↗
PubMedDate not supplied

Iron-deficiency anemia resistant to iron therapy.

Iron-deficiency anemia resistant to iron administration is a common clinical problem. This paper analyzes the causes of primary failure of iron therapy. From a practical point of view, the main recommendation is that a physician should not be satisfied with simplistic explanations for "refractoriness". In fact, failure to respond to treatment is always the result of a diagnostic or therapeutic error which must be corrected in order to achieve the natural result of all substitution therapies: replenishment.

Absorption↗
PubMed2004

Recombinant human lactoferrin treatment for global health issues: iron deficiency and acute diarrhea.

Iron deficiency and diarrhea are two of the most significant issues for global health. Iron deficiency anemia is the most common nutritional deficiency in the world, affecting nearly 25% of the world population (UNICEF/WHO 1999). The prevalence of iron deficiency in developing countries is illustrated by comparison with other deficiencies: iron deficiency affects 3.5 billion people, while vitamin A and iodine deficiency affect 0.3 billion people and 0.8 billion people, respectively. The prevalence is highest among young children and women of childbearing age (particularly pregnant women). It is estimated that national productivity levels could be raised as much as 20% by correcting iron deficiency in developing countries. Recombinant human lactoferrin (rhLF), expressed and extracted from rice seed, is being evaluated by Ventria Bioscience for use as a dietary supplement to treat iron deficiency and/or iron deficiency anemia. Diarrhea is also a major world health issue. Sixty percent of children who die under age five die of pneumonia, diarrhea or measles. World Health Organization oral rehydration solution (WHO-ORS) is one of the major medical advances in the past 50 years, saving the lives of 1 to 2 million children annually. Many studies have demonstrated similar efficacy of rice-based ORS. There are studies documenting the reduced frequency of diarrhea in breast-fed children and this health improvement is attributed to the antimicrobial action of the human milk proteins lactoferrin and lysozyme. In vitro data document the growth inhibition of the diarrheal associated organisms: rotavirus, ETEC, cholera, salmonella, and shigella by human lactoferrin (hLF) and human lysozyme. Using Ventria's ExpressTec system, we have expressed human lactoferrin and human lysozyme in rice. In a rice-based ORS formulation, these proteins have the potential to provide not only the benefits of reduced stool volume and improved weight gain, but also shorten the course of diarrheal episodes via antimicrobial activity against the causative agent.

Anemia, Iron-Deficiency↗
PubMed2004

Outer hair cell activity of the cochlea in patients with iron deficiency anemia.

OBJECTIVE: Iron deficiency anemia is a common disorder, which has been reported to affect the auditory system. However, there are some conflicting points related with the pattern of hearing impairment. The aim of this study is to analyze the outer hair cell activity of the cochlea in patients with iron deficiency anemia. METHOD: Pure-tone audiometry (PTA) (250-6000 Hz) and distortion product otoacoustic emission (DPOAE) results of 42 patients with iron deficiency anemia and 22 healthy, age and sex matched subjects for the control group were compared. Cubic DPOAEs (2f1-f2) were obtained at 65 and 55 dB sound pressure level (SPL). DP grams were plotted as a function of f2 and signal-to-noise ratio (SNR) was specified as the difference in decibels SPL between DPOAE amplitude and the ambient noise level at a given f2. In DP grams, DP amplitudes and noise levels obtained from the baseline measurements were presented as the upper and lower limits of DP amplitude and noise level that were the 10th and 90th percentiles calculated by adding and subtracting standard deviations and from mean baseline DP amplitude and noise level. Independent-samples t-test is used for comparison of the groups. RESULTS: Pure-tone audiometry was normal in patients with iron deficiency anemia and control subjects and there was no significant difference in comparison of DPOAE in both groups and both sides and the results were between two percentiles (P > 0.05). CONCLUSION: The results of the present study did not support a casual relationship between the iron deficiency anemia and the auditory dysfunction on the basis of DPOAE.

Adult↗
PubMed2003

Impact of parturition on iron status in nonanaemic iron deficiency.

BACKGROUND: Iron-deficient nonanaemic parturients risk underdiagnosis as a result of the reliance on postpartum ferritin and haemoglobin as markers of iron status. Ferritin is an acute-phase protein whose levels increase during the inflammatory response, as occurs after delivery. Our aims were to evaluate the impact of parturition on iron status, erythropoiesis and the inflammatory response, and identify the optimal parameters and timing for diagnosing iron deficiency in the presence of postpartum inflammation. MATERIALS AND METHODS: Conventional parameters of iron status, erythropoiesis and the inflammatory response (serum ferritin, serum iron, transferrin saturation, C-reactive protein) were compared with more recent parameters [soluble transferrin receptors (sTfR), hypochromic red cells, reticulocyte indices] within 48 h either side of delivery in 64 iron-deficient nonanaemic women (defined by a prepartum serum ferritin < or =15 microg L(-1), and a pre- and postpartum haemoglobin of > or =11.0 g dL(-1) and > or =10.0 g dL(-1), respectively). RESULTS: Mean sTfR decreased pre to postpartum from 7.3 to 5.8 microg mL(-1) (P<0.01), while mean serum ferritin increased from 9.7 to 16.9 microg L(-1) (P<0.01). Serum ferritin did not correlate with haemoglobin pre or postpartum (r=0.04, P=0.7; r=0.2, P=0.09), but a correlation persisted postpartum between hypochromic red blood cells and haemoglobin (r=-0.26; P<0.05). The percentage of hypochromic red cells remained virtually unchanged pre- and postpartum (4.0% vs. 3.8%; NS). Postpartum mean reticulocyte haemoglobin content (CHr) was 27.1 +/- 1.6 pg. CONCLUSION: Iron status should be tested prepartum, in the absence of an inflammatory response, rather than in the early postpartum. A valuable additional parameter, where available, might be the hypochromic red cell percentage, which is virtually uninfluenced by the inflammatory response. Furthermore, hypochromic red cell percentage, CHr and sTfR can be helpful to differentiate between functional iron deficiency and depleted iron stores.

Adult↗
PubMed1987

Iron deficiency in the elderly.

Iron deficiency in the elderly almost always results from blood loss. The loss of iron can be viewed as occurring in four stages, which are reflected in the different tests used to diagnose iron deficiency. Tests used to diagnose iron deficiency have certain limitations regarding their ability to detect iron deficiency before the overt anaemia occurs. The tests which diagnose iron deficiency most accurately are low serum ferritin and reduced iron staining of a bone marrow aspirate. Because iron is present in many metabolic processes besides the production of haemoglobin, iron deficiency results in a variety of defects which are manifested at biochemical, tissue, and functional levels. Iron is a component of several enzymes in the respiratory electron transport chain. Adequate haem and iron levels are necessary to control cytoplasmic and mitochondrial protein synthesis. Iron deficiency results in tissue defects, including those affecting the gastrointestinal tract, and defects of mitochondria and lymphocytes. Normal iron levels seem to be necessary for normal work capacity. A deficiency of iron, independent of the anaemia, results in reduced exercise capacity that can be measured in both physiological and economic terms. Elderly patients complaining of increased fatigue should therefore be screened for iron deficiency. There is evidence to suggest that iron deficiency may predispose individuals to certain infections. Other information points to the promotion of certain bacterial and parasitic infections after rapid correction of iron deficiency. Thus elderly patients having iron replacement therapy should be followed closely. A deficiency of iron has been shown to result in certain behavioural and learning abnormalities. Iron deficiency has been shown to result in impaired control of body temperature, resulting in an increase in catecholamine levels. The impairment in heat-generating ability was shown to result from reduced conversion of T4 to T3 in the peripheral tissues.

Aged↗
PubMed1984

Serum iron, serum transferrin and transferrin saturation in healthy children without iron deficiency.

Serum iron, serum transferrin and transferrin saturation were studied in 253 healthy, non-anaemic children 4, 8 and 13 years old, and in 60 healthy, non-anaemic adults having serum ferritin values greater than or equal to 15 micrograms/l. One hundred and ninety-six children had serum ferritin values greater than or equal to 15 micrograms/l (i.e. replete iron stores), 35 had intermediate ferritin values from 10-14 micrograms/l and 22 had ferritin values less than 10 micrograms/l (i.e. depleted iron stores). Iron replete children showed a gradual rise in serum iron and transferrin saturation values with age. Serum iron and transferrin saturation values were lower (P less than 0.001, P less than 0.0001) and transferrin values higher (P less than 0.0001) in iron replete children compared to adults. Iron replete children had a 2.5 centile transferrin saturation value of 5%; 19.9% of these children had saturation values less than 15% and 8.2% had values less than 10%. In iron depleted children a transferrin saturation value less than 7% yielded the highest diagnostic efficiency as regards exhausted iron stores, although with a low predictive value of a positive test. The transferrin saturation is unsuitable as a single diagnostic criterion in the evaluation of iron deficiency in children and should always be combined with other indicators of iron status.

Adolescent↗
PubMed2002

Neurobehavioral analysis of developmental iron deficiency in rats.

Iron deficiency (ID) in early life alters the course of behavioral and cognitive development in humans, causing decreased physical activity and responsiveness to the environment. The effects of ID on behavior are similar in rats and hypothesized to be related to ID-related impairments in central dopamine pathways. The objective of this study was to examine the association between brain iron measures of dopamine function, and behavioral measures of activity and reactivity. Male and female weanling rats were fed either an iron deficient diet or control diet for 6 weeks. The iron deficient rats showed significantly decreased activity and increased anxiety-like behaviors. Iron deficient rats also showed significant decrements in brain iron content in the corpus striatum, prefrontal cortex, and midbrain and decreases in dopamine receptors and the transporter in the same areas. Multiple regression analysis showed ventral midbrain iron concentration and dopamine D(1) receptor density to be highly associated with exploration and repeated movements, respectively. In addition, the results showed anxiety-like behaviors to be related to prefrontal cortex dopamine transporter and dopamine D(1) receptor densities. We conclude from these analyses that iron concentration in dopamine containing regions and densities of dopamine receptors and the transporter, are significant predictors of measures of activity and reactivity. These observations also strengthen the argument that the Fe-dopamine link is fundamental to understanding biobehavioral difficulties seen in children with ID anemia.

Animals↗
PubMed2001

[Economic assessment of iron deficiency. Replacement of ferritin and serum iron by other parameters].

Economic assessment of iron deficiency. Replacement of serum iron and ferritin by other parameters. Serum iron and ferritin are still widely used parameters for the assessment of iron deficiency, in spite of their poor diagnostic performance. Compared to the combined use of ferritin, zinc protoporphyrin and soluble transferrin receptors an increase of the percentage of hypochromic erythrocytes (PEH) was found to be highly sensitive and specific for iron deficiency. We suggest to use it in a two phase strategy. Normal PEH excludes iron deficiency. Increased PEH may be confirmed by zinc protoporphyrin and/or soluble transferrin receptors.

Anemia, Hypochromic↗
PubMed2001

Does iron-deficient erythropoiesis in pregnancy influence fetal iron supply?

BACKGROUND: It was investigated whether the iron status in newborns is negatively influenced by iron-deficient erythropoiesis of the mother during pregnancy. METHODS: The iron status is characterized by hemoglobin, erythrocyte zinc protoporphyrin and serum ferritin values. Iron-deficient erythropoiesis of the mother is characterized by erythrocyte zinc protoporphyrin values. Measurement of erythrocyte zinc protoporphyrin was performed in 103 non-anemic females within 24 hours after delivery. The iron status of their newborns was measured in cord blood. RESULTS: Erythrocyte zinc protoporphyrin concentrations were normal in 62% and elevated in 38% of the females, hence 39 women had iron-deficient erythropoiesis. There were no significant differences in mean values of the iron status parameters between neonates born to females with iron-deficient erythropoiesis and neonates born to females not having iron-deficient erythropoiesis. No correlation was found between maternal erythrocyte zinc protoporphyrin values and any of the neonatal parameters. CONCLUSION: It is concluded that fetal iron supply is not negatively influenced by iron-deficient erythropoiesis in the mother.

Anemia, Iron-Deficiency↗
PubMed1997

Gastric as well as duodenal biopsies may be useful in the investigation of iron deficiency anaemia.

BACKGROUND: Iron absorption is known to be impaired in the setting of gastric achlorhydria, yet gastric atrophy is not usually considered an aetiological factor for iron deficiency anaemia. We aimed to determine the prevalence of achlorhydric gastric atrophy in patients with iron deficiency and no identifiable source of gastrointestinal blood loss, and to assess whether gastric, as well as duodenal, biopsies should be routinely performed in these patients. PATIENTS: Forty-one consecutive patients with iron deficiency anaemia and no specific gastrointestinal symptoms or evidence of a bleeding lesion on faecal occult blood testing or upper gastrointestinal or colonic endoscopy. METHODS: As well as routine duodenal biopsies, samples were taken from gastric corpus and antrum for evidence of gastric atrophy. Achlorhydria was considered to be present if plasma gastrin measured on a sample obtained with the patient fasting was over 200 ng/l. Serum was tested for intrinsic factor and gastric parietal cell antibodies. RESULTS: Haemoglobin concentrations ranged from 4.1 to 10.9 g/dl. Eight (20%) of the 41 patients had corpus-predominant or generalized atrophy and high plasma gastrin levels, of whom six had serum intrinsic factor and/or gastric parietal cell antibodies: two also had Giardia lamblia organisms in duodenal biopsies. Four other patients (10%) had villous atrophy of the duodenum. CONCLUSIONS: As well as confirming the importance of seeking coeliac disease in patients with iron deficiency anaemia, our results suggest that achlorhydric gastric atrophy is also a common association. Gastric biopsies should be taken in patients with no other explanation for anaemia. The finding of Giardia organisms in two achlorhydric patients, with a possible contributory role, suggests that duodenal biopsies should be obtained even if serum coeliac-related antibodies are absent.

Adolescent↗