Iron Ingestion Research Articles

Juvenile ferric iron prevents microbiota dysbiosis and colitis in adult rodents

To assess whether juvenile chronic ferric iron ingestion limit colitis and dysbiosis at adulthood in rats and mice. Two sets of experiments were designed. In the first set, recently weaned mice were either orally administered ferrous (Fe²⁺) iron salt or ferric (Fe³⁺) microencapsulated iron for 6 wk. The last week of experiments trinitrobenzene sulfonic acid (TNBS) colitis was induced. In the second set, juvenile rats received the microencapsulated ferric iron for 6 wk and were also submitted to TNBS colitis during the last week of experiments. In both sets of experiments, animals were sacrificed 7 d after TNBS instillation. Severity of the inflammation was assessed by scoring macroscopic lesions and quantifying colonic myeloperoxidase (MPO) activity. Alteration of the microflora profile was estimated using quantitative polymerase chain reaction (qPCR) by measuring the evolution of total caecal microflora, Bacteroidetes, Firmicutes and enterobacteria. Neither ferrous nor ferric iron daily exposures at the juvenile period result in any effect in control animals at adulthood although ferrous iron repeated administration in infancy limited weight gain. Ferrous iron was unable to limit the experimental colitis (1.71 ± 0.27 MPO U/mg protein vs 2.47 ± 0.22 MPO U/mg protein in colitic mice). In contrast, ferric iron significantly prevented the increase of MPO activity (1.64 ± 0.14 MPO U/mg protein) in TNBS-induced colitis. Moreover, this positive effect was observed at both the doses of ferric iron used (75 and 150 mg/kg per day po--6 wk). In the study we also compared, in both rats and mice, the consequences of chronic repeated low level exposure to ferric iron (75 mg/kg per day po--6 wk) on TNBS-induced colitis and its related dysbiosis. We confirmed that ferric iron limited the TNBS-induced increase of MPO activity in both the rodent species. Furthermore, we assessed the ferric iron incidence on TNBS-induced intestinal microbiota dysbiosis. At first, we needed to optimize the isolation and quantify DNA copy numbers using standard curves to perform by qPCR this interspecies comparison. Using this approach, we determined that total microflora was similar in control rats and mice and was mainly composed of Firmicutes and Bacteroidetes at a ratio of 10/1. Ferric juvenile administration did not modify the microflora profile in control animals. Total microflora numbers remained unchanged whichever experimental conditions studied. Following TNBS-induced colitis, the Firmicutes/Bacteroidetes ratio was altered resulting in a decrease of the Firmicutes numbers and an increase of the Bacteroidetes numbers typical of a gut inflammatory reaction. In parallel, the subdominant population, the enterobacteria was also increased. However, ferric iron supplementation for the juvenile period prevented the increase of Bacteroidetes and of enterobacteria numbers consecutive to the colitis in both the studied species at adulthood. Rats and mice juvenile chronic ferric iron ingestion prevents colitis and dysbiosis at adulthood as assessed by the first interspecies comparison.

Interactions Between Ferroportin and Hephaestin in Rat Enterocytes Are Reduced After Iron Ingestion

Ferroportin (Fpn) is a multiple transmembrane protein required for iron export into the systemic circulation, in cooperation with hephaestin (Heph). Despite the importance of Fpn in iron transport, there is controversy about its topology and functional state upon interaction with Heph. The topology of Fpn was determined using monospecific antisera against its different epitopes, in sheets of cells from duodenum that were or were not permeabilized with detergent. Immunoprecipitation and blue native polyacrylamide gel electrophoresis, followed by immunoblot analysis, were used to determine the extent of interactions between Fpn and Heph. Antisera against the intracellular, C-termini of divalent metal transporter (Dmt1) and Heph served as controls. Immunofluorescence analysis with antisera against amino acids 172-193 of Fpn (anti-Fpn 172) detected Fpn only in permeabilized cells, whereas anti-Fpn 232 (amino acids 232-249), anti-Fpn 370 (amino acids 370-420), and anti-Fpn C (the C-terminus) detected Fpn in nonpermeabilized and permeabilized cells. Immunoprecipitation studies showed that Fpn and Heph coprecipitated with either anti-Fpn or anti-Heph. Blue native polyacrylamide gel electrophoresis studies revealed that a fraction of Fpn comigrates with Heph; the apparent interaction decreases after iron ingestion. Studies with antisera to different epitopes of Fpn indicate that the topology of Fpn is consistent with an 11-transmembrane model, with the C-terminus exposed on the cell surface. Reduced interactions between Fpn and Heph after iron ingestion indicate that this is a regulatory mechanism for limiting further iron absorption.

Effect of Deferasirox on Iron Absorption in a Randomized, Placebo-Controlled, Crossover Study in a Human Model of Acute Supratherapeutic Iron Ingestion

In 2005, the Food and Drug Administration approved deferasirox as an oral iron chelating agent for chronic iron overload. To determine usefulness in management of acute iron ingestion, we study the effect of orally administered deferasirox in healthy human adults. A double-blinded, placebo-controlled, randomized, crossover study of 8 healthy human volunteers was conducted. Subjects ingested 5 mg/kg of elemental iron in the form of ferrous sulfate. One hour after iron ingestion, subjects were randomized to receive 20 mg/kg of deferasirox or placebo. Serial iron levels were then obtained. A 2-week washout was used between study arms. The paired t test was used to compare area under time-concentration curves from baseline to both 12- and 24-hour iron levels between groups. Baseline serum iron levels were similar in the 2 groups. Deferasirox significantly reduced serum iron area under concentration-time curves compared with placebo during both 1 to 12 hours and 1 to 24 hours (12 hour=577 μmol-hour/L and 392 μmol-hour/L, 95% confidence interval for the difference 15.8 to 353.0 μmol-hour/L; 24 hour=808 μmol-hour/L and 598 μmol-hour/L, 95% confidence interval for difference 54.4 to 366.7 μmol-hour/L). Orally administered deferasirox significantly reduced serum iron levels when administered 1 hour after iron ingestion during the 12- and 24-hour periods after acute ingestion of 5 mg/kg of elemental iron in healthy human volunteers. Further study is required to determine optimal dosing, but deferasirox may be an important addition to current therapy for acute iron poisoning.

Iron Pill-induced Tumefactive Mucosal Injury of the Hypopharynx

Iron pill-induced mucosal injury of the airways with massive necrosis and stricture of the lower airways is known to occur, but symptomatic injury of the hypopharyngeal mucosa secondary to therapeutic oral iron ingestion has not been described. We report iron-sulfate-induced mucosal injury of the hypopharynx in a patient receiving therapeutic oral iron supplementation. The patient presented with dysphagia when swallowing pills, but not when eating or drinking. Imaging studies and clinical examination revealed an ulcerated and protuberant hypopharyngeal mass. Histology showed mucosal ulceration with deposits of extracellular crystalline iron particles. The histologic changes were identical to those seen in patients with "iron pill" gastritis.

Fulminant hepatic failure in woman with iron and non-steroidal anti-inflammatory drug intoxication

A 17-year-old, previously healthy female ingested 16,000 mg iron sulphate (96.15 mg of iron ions per kg of b.wt.) with a suicidal intent. The patient was admitted to a toxicology unit 10 hours after the drug ingestion. Serum iron concentration at admission was 2351 μg% (421.0 μmol/L). In the course of the intoxication, hemorrhagic gastritis, renal insufficiency and increasing signs of fulminant hepatic failure complicated with coagulopathy and encephalopathy were observed. Treatment with deferoxamine was started immediately after admission to the hospital and continued for 15 hours until the serum concentration of iron decreased to 145 μg% (25.9 μmol/L). Patient was qualified for liver transplant, therefore albumin dialysis as a bridge to liver transplantation was performed. In spite of two procedures of albumin dialysis using the Prometheus system, deep coma, shock and respiratory insufficiency developed. The patient died 80 hours after iron ingestion. In the presented case, the ingestion of a very high dose of iron and late introduction of deferoxamine treatment contributed to fulminant liver failure and fatal outcome of the intoxication.

Estimativa da ingestão de ferro e vitamina C em adolescentes no ciclo menstrual

The vitamin C and iron ingestion level was evaluated in adolescents during the three phases of the menstrual cycle. The food intake of 30 adolescents was analyzed during the premenstrual, menstrual, and postmenstrual phases, by the registration technique, with the analysis of two registrations per individual, in each phase. The prevalence estimate was done considering six dietary registrations for each adolescent. The patterns used as reference were the Dietary Reference Intakes (DRI) - Estimated Average Requirement (EAR) from Institute of Medicine - IOM (2001), using the probability approaches and the cut - point method for the iron and vitamin C respectively, in addition to the values from the Recommended Dietary Allowances (National Research Council). The adolescents were aged 15.5 +/- 1.7; the age of the menarche was 11.8 +/- 1,1; and gynecological age 3.6 +/- 1.9. The medial consumption of iron was 10.6 mg/day and of vitamin C 77.6 mg/day. It was observed by DRIs-EAR an estimate of inadequacy for iron of 22.6% and for vitamin C of 34% and by National Research Council, 63.3% and 20%, respectively. Despite the divergence among the patterns, both results shows a nutritional risk for the studied population. The accomplishment of wider dietary studies, using DRI-EAR is suggested, favoring nutritional diagnoses with subsequent evaluation of intervention measures.

Contribution of Drinking Water to Dietary Requirements of Essential Metals

Drinking water can be a source of essential metals, but only one study published thus far has compared the intake of essential metals in drinking water to dietary reference intakes. This assessment compares the ingestion of chromium (Cr), copper (Cu), iron (Fe), manganese (Mn), selenium (Se), and zinc (Zn) from drinking water at the maximum concentrations that should be found in water, or at concentrations that are potentially more likely to be found in Canadian water, to the recommended dietary allowance or adequate intake values established by the Institute of Medicine. At guideline limits, water provides sufficient Cr and Cu to meet nutritional requirements, and Mn and Zn levels are sufficient for some age categories to meet nutritional requirements. At concentrations that are more likely to be found in Canadian water, adequate intakes for Cr and Mn may be met by water alone for bottle-fed infants, and water was estimated to provide 23–66% of daily Cu requirements. Drinking water might become a significant source of some essential metals in individuals whose diets are low in these metals, especially in the case of Cu.

Melanosis Ilei Associated with Chronic Ingestion of Oral Iron

Melanosis can affect various parts of the gastrointestinal tract. Melanosis of the colon is not uncommon, while melanosis of the ileum is extremely rare. We report a case of melanosis ilei associated with chronic ingestion of oral iron (256 mg of ferrous sulfate once or twice daily for approximately 5 years) in a 32-year-old woman with end-stage renal disease. The findings of a colonoscopy, which was performed as a part of her medical checkup, were normal up to the cecum; however, numerous brownish-black punctuate pigmentations of the ileal mucosa were observed. Microscopic examination revealed hemosiderosis in the lamina propria of the ileal mucosa, particularly at the tips of villi. The diagnosis of melanosis (hemosiderosis) ilei was made based on the endoscopic and histological findings.

Iron and Parenteral Nutrition

There is ample evidence that iron is an essential trace element, but assessment of iron status and decisions on the amounts needed and the means of delivery in patients on parenteral nutrition (PN) have been unclear. Although iron requirements may diminish during acute illness, the frequent concurrence of blood loss and iron deficiency argue strongly for maintenance of levels of delivery in line with basal requirements. Maintenance of iron delivery has not been thought likely to present risk, but new data are questioning this. The needs of menstruating, pregnant, and lactating women are greater than those of adult men. The evidence favors an intravenous dose of around 1 mg of elemental iron per day in adult men and postmenopausal women. Doses of 1.5 mg/d [DOSAGE ERROR CORRECTED] in menstruating women and 2.0 mg/d [DOSAGE ERROR CORRECTED] for those in the later stages of pregnancy or lactating can be supported. A calibrated response is required in the growing child. Continued monitoring of iron status is recommended. Iron is an essential component for most PN regimens. The quantity of iron to be included should take account of predicted requirements.

A Proposed Unified Theory for Pseudomelanosis Duodeni: Mucosal Iron Overload from Iron Containing Medications and GI Bleeding or Abnormal Iron Metabolism from Excessive Hepcidin

Purpose: To further describe pseudomelanosis of the GI tract, a poorly understood clinicopathologic entity characterized by the endoscopic finding of punctate darkly pigmented mucosa. Case 1: A 60-year-old man with chronic renal insufficiency presented with dysphagia. He was taking hydralazine, metoprolol and hydrochlorothiazide for hypertension and ferrous sulfate for anemia. Esophagogastroduodenoscopy (EGD) revealed punctate, darkly brown-black pigmentation in the descending duodenum. Pathological examination of biopsies revealed - at the tips of numerous uninflamed villi - clumps of dark brown-black pigmentation which contained iron, as demonstrated by iron stains. Electron microscopy demonstrated densely osmophilic, coarsely granular and focally confluent granules within the cytoplasm of macrophages in the lamina propria of duodenal villi. Case 2: A 61-year-old man with end-stage renal disease on dialysis, multiple myeloma and hypertension underwent EGD for anemia. Medications included hydralazine and metoprolol. EGD revealed darkly brown-black pigmentation in the stomach and descending duodenum. Pathological examination of biopsies revealed prominent clumps of darkly brown-black pigmentation, which contained iron as demonstrated by iron stains. Discussion: Review of 55 cases, including the current 2 cases, showed significant association of pseudomelanosis with iron ingestion, GI bleeding and chronic inflammatory conditions like chronic renal insufficiency. The common denominator of all three associations is excess iron accumulation in GI mucosa whether from excessive ingestion, intraluminal blood, or interference with iron absorption. We hypothesize that excessive hepcidin from systemic inflammation interferes with iron absorption from mucosa leading to local accumulation.Figure: Endoscopic videophotograph in Case 1 reveals darkly brown-black, punctate pigmentation in the descending duodenum.

Eating practices, nutritional status and constipation in patients with Rett syndrome

Disturbance in chewing, swallowing and digestive motility may predispose to feeding and nutritional abnormalities in patients with Rett syndrome. To evaluate the dietary habits, nutritional status and the prevalence of constipation in patients with classical Rett syndrome. Twenty seven female patients between the ages of 2.6 and 21.8 years were studied. The following parameters were evaluated: food register, weight, height and intestinal movement characteristics. Weight and height were compared with the National Center for Health Statistics standards. The inability to ingest solid foods was observed in 80.8% of the patients. A height-to-age deficit was observed in 13 (48.1%) of the girls, being more intense in patients at stage IV. Weight-for-height deficit was found in 10 (37.0%) patients, 15 (55.6%) showed normal weight and 2 (7.4%) were overweight for their height. The median ingestion of energy, according to weight-for-height, was equal to 106.6%. Insufficient iron ingestion was observed in 63.0% and insufficient calcium in 55.6% of the patients. Constipation was verified in 74.1% of the patients and did not show a relationship with the quantity of fiber in the diet. Various nutritional problems, as well as, intestinal constipation were observed in these patients with Rett syndrome, and they must be considered in the multidisciplinary therapeutic planning of these individuals.

Immunoassay for Human Hepcidin in Blood

We developed and validated the first ELISA for hepcidin, the principal iron-regulatory hormone that has been very difficult to measure. The competitive ELISA uses a biotin-tagged hepcidin as a tracer to quantify hepcidin in serum, plasma or urine. In healthy volunteers, the 5–95% range of serum hepcidin concentrations was 29–254 ng/ml in men (n=65) and 17–286 ng/ml in women (n=49), with median concentrations 112 vs. 65, p<0.001. The lower limit of detection was 5 ng/ml. Serum, EDTA plasma and heparin plasma hepcidin measurements were in agreement (r> 0.98). Serum and urinary hepcidin concentrations in 24 healthy subjects correlated well (r=0.82). Serum hepcidin appropriately correlated with serum ferritin (r=0.63) reflecting the regulation of both proteins by iron stores. Healthy volunteers showed a diurnal increase of serum hepcidin at noon and 8pm compared to 8am, and a transient rise of serum hepcidin in response to iron ingestion. In 18 young healthy women, serum hepcidin correlated well (p<0.05) with intestinal iron absorption both from a food (r=0.49) and supplemental iron source (r=0.51), as determined by a stable iron isotope technique. In a variety of clinical conditions associated with iron disturbances we observed the appropriate changes in hepcidin concentrations: undetectable or low in patients with iron deficiency anemia (ferritin<10 ng/ml), treated HFE hemochromatosis, and juvenile hemochromatosis, and abnormally high in patients with inflammation (CRP>10 mg/dl), multiple myeloma, or chronic kidney disease. The new blood hepcidin ELISA yields accurate and reproducible measurements that appropriately reflect physiologic, pathologic and genetic influences, and is informative about the etiology of iron disorders.

Immunoassay for human serum hepcidin

AbstractWe developed and validated the first serum enzyme-linked immunosorbent assay for hepcidin, the principal iron-regulatory hormone that has been very difficult to measure. In healthy volunteers, the 5% to 95% range of hepcidin concentrations was 29 to 254 ng/mL in men (n = 65) and 17 to 286 ng/mL in women (n = 49), with median concentrations 112 versus 65 (P < .001). The lower limit of detection was 5 ng/mL. Serum hepcidin concentrations in 24 healthy subjects correlated well with their urinary hepcidin (r = 0.82). Serum hepcidin appropriately correlated with serum ferritin (r = 0.63), reflecting the regulation of both proteins by iron stores. Healthy volunteers showed a diurnal increase of serum hepcidin at noon and 8 pm compared with 8 am, and a transient rise of serum hepcidin in response to iron ingestion. Expected alterations in hepcidin levels were observed in a variety of clinical conditions associated with iron disturbances. Serum hepcidin concentrations were undetectable or low in patients with iron deficiency anemia (ferritin < 10 ng/mL), iron-depleted HFE hemochromatosis, and juvenile hemochromatosis. Serum hepcidin concentrations were high in patients with inflammation (C-reactive protein > 10 mg/dL), multiple myeloma, or chronic kidney disease. The new serum hepcidin enzyme-linked immunosorbent assay yields accurate and reproducible measurements that appropriately reflect physiologic, pathologic, and genetic influences, and is informative about the etiology of iron disorders.

Emergency Laparoscopic-Assisted Gastrotomy for the Treatment of an Iron Bezoar

Iron ingestion accounts for approximately 3% of calls to poison control centers. The profound local and systemic effects of an iron overdose have an associated mortality rate of 5%. Laparotomy and gastrotomy has been reported as a life-saving maneuver to extract the retained iron aggregates that are notoriously resistant to, removal by conventional emesis or lavage techniques. In this paper, we describe, for the first time, the use of laparoscopic-assisted gastrotomy in the treatment of an iron overdose. A 14-year-old girl attempted suicide by means of a polydrug drug overdose, which included ferrous fumarate, at a calculated potentially lethal dose of 70 mg/kg. A gastric iron bezoar was seen on plain radiograph. The regional poison control center recommended surgical removal of the retained iron tablets. Upper endoscopy confirmed the retention of iron and showed its dense adherence to the gastric mucosa. A 5-mm laparoscope was introduced at the umbilicus, and the stomach was grasped by an instrument introduced through a left-upper quadrant incision. The incision was then enlarged to allow the formation of a gastrotomy. The iron bezoar was removed with the aid of digital disimpaction and copious saline irrigation. The patient made a rapid postoperative recovery prior to undergoing psychiatric treatment. We conclude that laparoscopic-assisted gastrotomy is a simple and safe option in the acute management of a retained iron bezoar.

Iron feeding induces ferroportin 1 and hephaestin migration and interaction in rat duodenal epithelium

Intestinal iron absorption involves proteins located in the brush border membrane (BBM), cytoplasm, and basolateral membrane (BLM) of duodenal enterocytes. Ferroportin 1 (FPN1) and hephaestin (Heph) are necessary for transport of iron out of enterocytes, but it is not known whether these two proteins interact during iron absorption. We first examined colocalization of the proteins by cotransfection of HEK293 cells with pDsRed-FPN1 with pEmGFP-Heph or with the COOH-terminal truncated pEmGFP-HephDelta43 or -HephDelta685 and found that FPN1 and Heph with or without the COOH terminus colocalized. In rat duodenal enterocytes, within 1 h of iron feeding prominent migration of FPN1 from the apical subterminal zone to the basal subnuclear zone of the BLM occurred and increased to at least 4 h after feeding. Heph exhibited a similar though less prominent migration after iron ingestion. Analysis using rat duodenal epithelial cell sheets demonstrated that 1) by velocity sedimentation ultracentrifugation, FPN1 and Heph occupied vesicles of different sizes prior to iron feeding and migrated to similar fractions 1 h after iron feeding; 2) by blue native/SDS-PAGE, FPN1, and Heph interacted to form two complexes, one containing dimeric FPN1 and intact Heph and the other consisting of monomeric FPN1 and a Heph fragment; and 3) by immunoprecipitation, anti-Heph or anti-FPN1 antiserum coimmunoprecipitated FPN1 and Heph. Thus the data indicate that FPN1 and Heph migrate and interact during iron feeding and suggest that dimeric FPN1 is associated with intact Heph.

A Single High Dose of Ascorbic Acid and Iron Is Not Correlated with Oxidative Stress in Healthy Volunteers

Fe (II) is a potential prooxidant in vivo and can induce cellular oxidative stress. Ascorbic acid (AA) is a powerful physiological antioxidant and, in the presence of free Fe (II), can exhibit prooxidant effects in vitro. However, in vivo prooxidant effects of Fe (II) and AA have not yet been indisputably demonstrated. Here we evaluate the potential toxic effect of supplementation of Fe (II) associated with AA. Nine healthy, nonsmoking male volunteers (20–31 years old) participated in the crossover study design. The volunteers were supplemented with either a dose of 2 g of AA, 150 mg of iron carbonyl or 2 g of AA plus 150 mg of iron carbonyl with a washout period of 15 days between each treatment. AA, iron, ferritin, thiobarbituric acid-reactive substances, catalase, δ-aminolevulinic dehydratase and SH thiol groups were measured in the blood of the volunteers. Plasma AA levels were increased at 2, 5 and 24 h after AA or AA plus iron ingestion. Plasma Fe levels were increased at 2 and 5 h in the AA plus iron group. Erythrocyte malondialdehyde levels decreased at 5 and 24 h after AA and 5 h after AA plus iron ingestion. Catalase activity from erythrocytes was increased 5 h after supplementation with AA plus iron. There was no significant difference between groups in the other biochemical parameters evaluated. Thus, the present study does not support the hypothesis that the combination of high plasma concentrations of AA and iron, or iron alone, could cause in vivo oxidative damage after a single supplementation dose.

Synergistic interaction between excess hepatic iron and alcohol ingestion in hepatic mutagenesis

Background/aim Hereditary hemochromatosis (HH) and dietary iron overload are the main iron-loading diseases. Fibrosis, cirrhosis and hepatocellular carcinoma (HCC) are complications to HH and dietary iron overload possibly influenced by co-factors. Alcohol may be one such factor. The aim therefore was to determine the extent of synergistic interaction between free hepatic iron and alcohol, complicating dietary iron overload in HCC pathogenesis. Methods Four groups of 20 Wistar albino rats were used: group 1 (C) was fed the chow diet; group 2 (Fe) was supplemented with 0.75% ferrocene iron; group 3 (Fe + Al), 0.75% iron and 7% ethanol; and group 4, 7% ethanol (Al) for 12 months. Iron profile, superoxide/nitrite free radicals, lipid peroxidation (LPO)/8-isoprostane (8-IP), 8-hydroxydeoxyguanosine (8-OHdG), oxidative lipid/DNA damage immunohistochemistry, transaminases (AST/ALT) and Ames mutagenesis tests were performed. Results Significant differences were observed in the Fe + Al group for LPO, 8-IP, AST and ALT ( p < 0.001, 0.001, 0.001 and 0.001, respectively) compared to other groups. A three-fold synergistic interaction was observed for the same parameters. Furthermore, significant differences of p < 0.05 and 0.001 were observed for 8-OHdG and mutagenesis, respectively, with an additive synergy in the Fe + Al group. ALT/8-OHdG and ALT/mutagenesis correlated positively ( p < 0.04 and 0.008, respectively). The immunohistochemistry revealed iron/alcohol multiplicative synergism with hydroxyl radical involvement. Conclusion Mutagenic effects of iron and alcohol are synergistically multiplicative implicating hydroxyl free radicals in hepatocarcingenesis.

Dissolution of copper, tin, and iron from sintered tungsten–bronze spheres in a simulated avian gizzard, and an assessment of their potential toxicity to birds

The rates of dissolution of copper, tin, and iron from sintered tungsten–bronze spheres (51.1%W, 44.4%Cu, 3.9%Sn, 0.6%Fe, by mass) were measured in an in vitro simulated avian gizzard at pH 2.0, and 42C. Most of the spheres had disintegrated completely to a fine powder by day 14. Dissolution of copper, tin, and iron from the spheres was linear over time; all r > 0.974; all P < 0.001. The mean rate of release of copper, tin, and iron was 30.4 mg, 2.74 mg, and 0.38 mg per g tungsten–bronze per day, respectively. These rates of metal release were compared to those in published studies to determine whether the simultaneous ingestion of eight spheres of 3.48 mm diameter would pose a toxic risk to birds. The potential absorption rates of iron and tin (0.54 mg Fe/day, and 3.89 mg Sn/day) from eight tungsten–bronze spheres of total mass 1.42 g would not prove toxic, based on empirical studies of tin and iron ingestion in waterfowl. The release of 43.17 mg copper/day from eight tungsten–bronze spheres, while exceeding the daily copper requirements of domesticated birds, is far below the levels of copper known to cause copper toxicosis in birds. We conclude that sintered tungsten–bronze material made into gunshot, fishing weights, or wheel balance weights, would not pose a toxic risk to wild birds when ingested.

Variáveis maternas e infantis associadas à ocorrência de anemia em crianças nos serviços de atenção básica em São Paulo

OBJETIVO: Analisar variáveis maternas e infantis associadas à ocorrência de anemia em crianças atendidas por serviços de atenção básica à saúde do município de São Paulo. MÉTODOS: Participaram do estudo 357 crianças, de quatro a 24 meses, de três serviços de atenção básica à saúde da região sul da cidade. As variáveis foram separadas em categorias relacionadas à mãe e à criança. A dosagem de hemoglobina foi realizada por punção digital, com ponto de corte de 11g/dL para o diagnóstico de anemia. O teste t de Student foi aplicado para comparar as médias de hemoglobina de dois grupos independentes; a ANOVA, para três ou mais grupos; e o teste de Mann-Whitney para comparar a velocidade de crescimento e o grupo etário. RESULTADOS: A prevalência de hemoglobina abaixo de 11g/dL foi de 60%. Entre as variáveis maternas, não se constatou associação com a ocorrência de anemia. Houve associação entre anemia, gênero da criança e velocidade de ganho de peso. Quanto à alimentação, não foi encontrada associação entre tempo de aleitamento materno e anemia, mas houve associação com a ingestão quantitativa e qualitativamente pobre em ferro. CONCLUSÕES: A alta prevalência de anemia relacionou-se ao gênero masculino, no qual a velocidade de crescimento em menores de seis meses e naqueles com 18 a 24 meses foi maior, além de se associar à baixa ingestão de ferro na dieta.

Universal versus Selective Iron Supplementation for Infants and the Risk of Unintentional Poisoning in Young Children: A Comparative Study of Two Populations

Iron continues to be a common cause of poisoning in young children, in part due to its widespread use and easy accessibility. To determine differences in the epidemiology and outcome of unintentional iron ingestion by young children in populations practicing selective (eg, US) versus universal (eg, Israel) iron supplementation to infants. All cases of unintentional iron ingestion in children younger than 7 years in a one year period were identified through the poison control center databases of 2 sites (Illinois and Israel). Parameters compared include patient sex and age; type, form, and dose of iron preparation; circumstances and clinical manifestations; management; and outcome. A total of 602 children were identified: 459 in Illinois and 143 in Israel. The majority of Illinois children ingested multivitamin preparations (94%), whereas Israeli children ingested single-ingredient iron preparations (78%) (p < 0.001). Iron doses ingested were higher in Israel (median 14.5 vs 6.6 mg/kg; p < 0.001) but remained within the nontoxic range for most children. No deaths or severe poisonings were reported, and 93% of children in both groups were asymptomatic. The majority of ingestions in both locations were due to unintentional self-ingestion. However, parental miscalculation occurred more frequently in Israel (16%) than in Illinois (1%). Universal iron supplementation to infants was not associated with a negative impact on the outcome of pediatric unintentional ingestions. Low-dose exposures were safely managed by on-site observation.