The Relationship between Decreased Iron Stores, Serum Iron and Neonatal Hypoglycemia in Large-for-Date Newborn Infants

ABSTRACT. We assessed the relationship between neonatal hypoglycemia and newborn iron status in 15 hypoglycemic, large-for-date newborn infants, 12 of whom were infants of diabetic mothers. These infants had significantly lower mean serum iron concentrations, ferritin concentrations, percent iron-binding saturation and calculated iron stores, and significantly higher mean transferrin concentrations, total iron-binding capacity concentrations and mid-arm circumference: head circumference ratios when compared with either 15 euglycemic large-for-date or 15 euglycemic appropriate-for-date control infants ( p < 0.001 for all comparisons). All hypoglycemic infants had ferritin concentrations below the 5th percentile as compared to 3 % of controls ( p < 0.001), and 67 % had transferrin concentrations above the 95th percentile (controls: 0 %; p < 0.001). Only the hypoglycemic infants demonstrated a significant negative linear correlation between ferritin and transferrin concentrations ( r =−0.83; p < 0.001). Decreased serum iron concentrations were associated with size at birth ( r =−0.60; p = 0.01) and with increased red cell iron ( r =−0.60; p = 0.01), implying a redistribution of iron dependent on the degree of fetal hyperglycemia and hyperinsulinemia. Infants with increased red cell iron had more profound neonatal hypoglycemia. These results show a significant association between decreased iron stores and neonatal hypoglycemia in macrosomic newborn infants associated with a significant shift of iron into red blood cells.     

Cord transferrin and ferritin values in newborn infants at risk for prenatal uteroplacental insufficiency and chronic hypoxia

We measured cord transferrin and ferritin levels in 50 newborn infants with fetal conditions associated with either uteroplacental vascular insufficiency or chronic hypoxia. Sixteen small for gestational age infants, 21 infants of mothers with preeclampsia, and 13 symptomatic infants of diabetic mothers had significantly higher transferrin levels and lower ferritin levels and calculated iron stores than did asymptomatic gestational age-matched control infants without these conditions. Cord ferritin levels and calculated iron stores were significantly lower in the infants of diabetic mothers than in any other group of infants. Cord transferrin levels were inversely correlated with ferritin levels (r = -0.59, P less than 0.001) and were unrelated to transthyretin levels and birth weight in the high-risk infants, but were positively correlated with ferritin levels (r = 0.50, P less than 0.001), transthyretin levels (r = 0.65, P less than 0.001), and birth weight (r = 0.75, P less than 0.001) in the control infants. We conclude that cord transferrin levels do not reflect protein-energy status in newborn infants with prenatal histories suggesting uteroplacental insufficiency or chronic hypoxia, and that when associated with decreased cord ferritin levels, indicate possible impaired iron stores in these infants.     

Abnormal iron distribution in infants of diabetic mothers: spectrum and maternal antecedents

Because chronic hypoxemia causes a redistribution of iron from serum and storage pools into an expanding erythrocyte mass, and because infants of diabetic mothers are often hypoxemic in utero and have a high prevalence of polycythemia at birth, we studied iron distribution in 43 term infants of diabetic mothers. Twenty-four infants were at an appropriate size for gestational age; 19 were large for gestational age. At birth, 28 infants (65%) had abnormal serum iron profiles; eight had decreased ferritin concentrations only (stage 1), nine had decreased ferritin and increased total iron-binding capacity values (stage 2), and 11 had these serum findings plus elevated free erythrocyte protoporphyrin concentrations (stage 3). The hypoglycemic infants who were large for gestational age (n = 14) had a higher prevalence of abnormal iron profiles than euglycemic infants who were appropriate in size for gestational age (n = 20; 93% vs 50%; p = 0.009). Progressively abnormal iron profiles were associated with higher glycosylated fetal hemoglobin values, greater degrees of macrosomia, increased hemoglobin and erythropoietin concentrations, and increased erythrocyte/storage iron ratios. Erythropoietin concentrations were inversely linearly correlated with serum iron values (n = 32, r = -0.54; p = 0.003). The combined erythrocyte and storage iron pools were significantly lower in infants with abnormal iron values whose mothers were diabetic, particularly in infants of women with confirmed diabetic vasculopathy. We speculate that these findings are likely due to (1) increased fetal iron utilization during compensatory hemoglobin synthesis in response to chronic hypoxemia and (2) reduced iron transfer during late gestation complicated by diabetes.     

Perinatal aspects of iron metabolism

Iron sufficiency is critical for rapidly developing fetal and neonatal organ systems. The majority of iron in the third trimester fetus and the neonate is found in the red cell mass (as hemoglobin), with lesser amounts in the tissues as storage iron (e.g. ferritin) or functional iron (e.g. myoglobin, cytochromes). Iron is prioritized to hemoglobin synthesis in red cells when iron supply does not meet iron demand. Thus, non-heme tissues such as the skeletal muscle, heart and brain will become iron deficient before signs of iron-deficiency anemia. Gestational conditions that result in lower newborn iron stores include severe maternal iron deficiency, maternal hypertension with intrauterine growth retardation and maternal diabetes mellitus. Stable, very low birthweight premature infants are also at risk for early postnatal iron deficiency because they accrete less iron during gestation, grow more rapidly postnatally, are typically undertreated with enteral iron and receive fewer red cell transfusions. Conversely, iron overload remains a significant concern in multiply transfused sick preterm infants because they have low levels of iron-binding proteins and immature antioxidant systems. CONCLUSION: The highly variable iron status of preterm infants combined with their risk for iron deficiency and toxicity warrants careful monitoring and support in the newborn and postdischarge periods.     

The effect of prolonged intrauterine hyperinsulinemia on iron utilization in fetal sheep

Newborn infants of poorly controlled insulin-dependent diabetic mothers demonstrate a redistribution of iron from serum and tissue stores into red blood cells. These changes may be due to increases in iron utilization during augmented Hb synthesis, which compensates for chronic intrauterine hypoxemia induced by prolonged fetal hyperinsulinemia. We tested this hypothesis by measuring plasma iron, total iron-binding capacity, percent iron-binding capacity saturation (total iron-binding capacity saturation), Hb concentration, total red cell Hb, and total red cell iron in the arterial blood of 11 chronically instrumented fetal sheep after 7-12 d of infusion with 15 U/day of insulin (n = 5) or placebo (n = 6). The insulin-infused fetal sheep had higher mean +/- SD plasma insulin concentrations (448 +/- 507 versus 11 +/- 8 mU/L; p less than 0.001) and lower arterial oxygen saturations (38 +/- 7 versus 54 +/- 9%; p less than 0.02). The insulin-infused group had a lower mean plasma iron concentration (20.8 +/- 10.9 versus 42.1 +/- 14.7 microM/L; p less than 0.02) and total iron-binding capacity saturation (36 +/- 20 versus 64 +/- 22%; p less than 0.02) and a higher total red cell Hb (45.4 +/- 8.7 versus 32.6 +/- 8.8 g; p less than 0.02) and total red cell iron content (154 +/- 29 versus 111 +/- 29 mg; p less than 0.02) when compared with the placebo group. Seven to 12 d of intrauterine hyperinsulinemia decreases serum iron and increases total red cell iron, most likely by stimulating increased Hb synthesis in response to low arterial oxygen saturation.(ABSTRACT TRUNCATED AT 250 WORDS)     

The influence of gestational age, size for dates, and prenatal steroids on cord transferrin levels in newborn infants

Serum transferrin levels assess protein status in older children and adults. To generate standards for its use in newborn infants, we measured umbilical cord serum transferrin levels in 161 appropriate (AGA), 25 large (LGA) and 16 small (SGA) for gestational age infants between 25 and 43 weeks' gestation. We also assessed the effects of intrauterine growth, exposure to prenatal steroids, and presence of pulmonary maturity on neonatal transferrin levels. Cord transferrin levels in AGA infants were significantly correlated with increasing gestational age (r = 0.60; p less than 0.001). Infants born before 37 weeks' gestation had significantly lower transferrin levels, when compared with those born at term (p less than 0.001). LGA infants had significantly higher levels than age-matched AGA infants (253 +/- 75 vs. 214 +/- 53 mg/dl; p less than 0.025). Despite significantly lower mean birth weights (p less than 0.001), SGA infants also had significantly higher levels than gestational age-matched AGA controls (227 +/- 63 vs. 167 +/- 40 mg/dl; p less than 0.005). For infants less than 35 weeks' gestation, neither the 20 preterm infants with exposure to prenatal steroids (maternal betamethasone), nor the 26 infants with pulmonary maturity had significantly elevated transferrin levels, when compared with gestational age-matched control infants. Newborn transferrin levels correlate well with gestational age and are significantly affected by size for dates, but not by a brief course of prenatal steroids or by pulmonary maturity.     

Novel red cell indices indicating reduced availability of iron are associated with high erythropoietin concentration and low ph level in the venous cord blood of newborns

There is evidence that an elevated erythropoietin (EPO) concentration is associated with signs of iron deficient erythropoiesis. The aim of this study was to evaluate the iron status by means of novel cellular indices and serum iron markers and to determine whether these are associated with EPO and pH in the venous cord blood of 193 full-term newborns. There were positive correlations between EPO and the percentage of hypochromic red blood cells (%HYPOm) and reticulocytes (%HYPOr) [r = 0.45 (p < 0.001) and r = 0.56 (p < 0.001), respectively]. %HYPOm and %HYPOr also had negative correlations with pH [r = -0.53 (p = 0.001) and r = -0.46 (p = 0.001), respectively]. Newborns who had low pH (pH < or =7.15, n = 16) had significantly higher %HYPOm, %HYPOr, and serum transferrin receptor and transferrin concentrations in their cord blood than newborns with normal pH. Thus, in newborn cord blood, the higher number of red cells and reticulocytes with lower Hb content may have impaired the oxygen carrying capacity that has been a trigger for EPO production. Furthermore, signs of lower hemoglobinization of red cells are associated with low umbilical vein pH in the newborns, indicating an increased risk of birth asphyxia.     

Serum transferrin levels in the longitudinal assessment of protein-energy status in preterm infants

We prospectively measured serum transferrin levels weekly from birth until discharge in 33 preterm newborn infants hospitalized on the newborn intensive care unit (n = 130 weeks) to study whether transferrin levels accurately reflect recent nutritional intakes and predict subsequent changes in anthropometric measurements and serum protein levels. Mean daily protein and caloric intakes were no greater during weeks when transferrin levels increased than when levels decreased. There were weak but statistically significant linear relationships between protein intake and transferrin levels (r = 0.24, p less than 0.01), caloric intake and transferrin levels (r = 0.27, p less than 0.01), and magnitudes of weekly changes in protein intake and transferrin levels (r = 0.31, p less than 0.001), and magnitudes of weekly changes in caloric intake and transferrin levels (r = 0.27, p less than 0.01). Transferrin levels did not reflect same-week weight or midarm circumference (MAC) gains, nor did they predict the following week's gains. Mean anthropometric measurement gains were similar following weeks when transferrin levels increased or decreased. There were no positive linear relationships between the magnitudes of changes in transferrin levels and same-week weight gain (r = -0.35), same-week MAC gain (r = -0.27), or following-week MAC gain (r = 0.01). Weak correlations were found with following-week albumin levels (r = 0.32, p less than 0.001) and with same-week transthyretin levels (r = 0.44, p less than 0.001). Weekly serum transferrin levels are not useful for longitudinal surveillance of protein-energy status in preterm infants.     

Iron status at 9 months of infants with low iron stores at birth

OBJECTIVE: To determine the 9-month follow-up iron status of infants born with abnormally low serum ferritin concentrations.Study design: Ten infants of >34 weeks' gestation with cord serum ferritin concentrations <5th percentile at birth (<70 microg/L) and 12 control infants with cord serum ferritin concentrations >80 microg/L had follow-up serum ferritin concentrations measured at 9 +/- 1 month of age. The mean follow-up ferritins, incidences of iron deficiency and iron-deficiency anemia, and growth rates from 0 to 12 months were compared between the two groups. RESULTS: At follow-up, the low birth ferritin group had a lower mean ferritin than the control group (30 +/- 17 vs 57 +/- 33 microg/L; P =.03), but no infant in either group had iron deficiency (serum ferritin <10 microg/L) or iron-deficiency anemia. Both groups grew equally well, but more rapid growth rates were associated with lower follow-up ferritin concentrations only in the low birth ferritin group (r = -0.52; P =.05). Both groups were predominantly breast-fed without iron supplementation before 6 months. CONCLUSIONS: Infants born with serum ferritin concentrations <5th percentile continue to have significantly lower ferritin concentrations at 9 months of age compared with infants born with normal iron status, potentially conferring a greater risk of later onset iron deficiency in the second postnatal year.     

Hepatic iron storage in very low birthweight infants after multiple blood transfusions

OBJECTIVE: To investigate the effect of multiple blood transfusions on hepatic iron storage in preterm, very low birthweight (VLBW) infants. METHODS: Seventeen VLBW infants who died within the first six months of life and underwent postmortem examination were studied. Serum ferritin, iron, and total iron binding capacity were measured within the week before the infants' death. Liver iron concentration was quantitatively determined by atomic absorption spectrophotometry and semiquantitatively assessed by histochemical liver iron grading. The clinical characteristics and the iron results were compared between infants receiving < 100 ml of blood (group A) and those receiving >/= 100 ml (group B). Spearman's correlation coefficient was used to evaluate the relation between the volume of blood transfused and serum/liver iron concentrations. Statistically significant variables associated with liver iron concentration were further subjected to multivariate stepwise regression analysis. RESULTS: Infants in group B had significantly higher serum iron (p < 0.01), serum ferritin (p < 0.01), and liver iron concentration (p < 0.01) than those in group A. The total and net volume of blood transfused were significantly associated with liver iron concentration (p < 0.001, r = 0.86; p < 0.001, r = 0.71 respectively), semiquantitative histochemical liver iron grading (p < 0.001, r = 0.80; p < 0.005, r = 0.71 respectively), and serum ferritin (p < 0.001, r = 0.84; p < 0.01, r = 0.69 respectively). In addition, both liver iron concentration and liver iron grading were found to be significantly associated with serum ferritin (p < 0.001, r = 0.76; p < 0.005, r = 0.68 respectively). Multivariate stepwise regression analysis indicated that the (log) liver iron concentration was significantly associated with the (log) volume of blood transfusion (p < 0.001; regression coefficient 0.39, SE 0.09), after adjustment for gestational age (R(2) = 0.84). CONCLUSIONS: This study showed a significant positive relation between the volume of blood transfused and the liver iron concentration in preterm VLBW infants. Although the transfusional blood volume correlated closely with the amount of iron deposited in hepatic tissues, clinical manifestations of iron overload were not observed. Carers should be aware of this potential harmful effect before prescribing blood or routine iron supplement to vulnerable preterm infants.     

Evaluation of soluble transferring receptor levels in children with iron deficiency and beta thalassemia trait,and in newborns and their mothers

In this study we first aimed to investigate the value of soluble transferrin receptor levels (sTfR) in healthy, iron deficient and beta thalassemia trait children and to determine whether sTfR is a useful indicator of iron deficiency. Secondly, we investigated the effects of iron supplementation of sTfR levels in a group of iron deficient children. Third was to describe sTfR in newborn infants and determine whether or not maternal iron deficiency is an important predictor of infant sTfR. Six groups were formed: Children with iron deficiency (n=22), post-iron therapy (n=16), beta thalassemia traits (n=19), healthy children (n=19), full-term newborns (n=20), and their mothers (n=19), Complete blood count (CBC), serum iron, iron-binding capacity, ferritin and sTfR levels were measured. sTfR/log ferritin indexes were calculated. sTfR levels of children with iron deficiency and with beta thalassemia trait were found to be significantly higher than those of healthy children (p<0.0001 and p<0.001). Children with iron deficiency showed a greater increase in the levels of sTfR than those with beta thalassemia traits (p=0.008). Although sTfR levels of subjects having iron therapy decreased, the levels still remained high compared to controls (p=0.002). Newborns had significantly higher levels of sTfR than controls (p<0.0001). Although sTfR levels of mothers with iron deficiency were higher than those of mothers having no iron deficiency (p=0.009), there was no difference in the levels of sTfR between newborns of both groups of mothers (p=0.790). sTfR is a useful parameter which shows body iron status as well as erythropoietic activity in children. It is independent of mother's iron status, and is due to erythropoietic activity in newborns.     

Smoking during pregnancy--hematological observations in the newborn

Hematological values were measured in 28 newborn infants of mothers smoking 10-20 cigarettes daily during pregnancy, and in 25 infants of non-smokers. Higher hematocrit levels were found on the 1st day of life in infants of smoking mothers (60.8 +/- 5.0%, mean +/- S.D.) compared to controls (57.5 +/- 4.8%) (p less than 0.05). The hematocrit levels correlated positively with the maternal smoking level (r = 0.318, p less than 0.05) and the maternal serum thiocyanate concentrations at delivery (r = 0.389, p less than 0.01). Cord serum values for erythropoietin, serum-iron, transferrin and ferritin showed no statistically significant difference between the two groups. A significant inverse correlation was found between the hematocrit value on the 1st day of life and the cord serum ferritin concentration (r = -0.495, p less than 0.005). The present results suggest that maternal smoking stimulates fetal erythropoiesis, probably through a hypoxic effect on the fetus, dose related to the maternal smoking level. Increased erythropoiesis may cause increased iron incorporation into erythrocytes at expense of iron storage in the bone marrow and reticuloendothelial system.     

Metabolic events in infants of diabetic mothers during first 24 hours after birth. I. Changes in plasma glucose, insulin and glucagon

Changes in plasma glucose, nonantibody-bound insulin and glucagon concentrations were studied in 32 newborn infants of diabetic mothers (IDM) during the first 24 hours after birth. Ten infants were born to White class A mothers and 22 to class B-F mothers. The infants were kept fasting during the investigative period and blood was sampled from an umbilical artery catheter. At birth, plasma glucose and glucagon levels were similar in the class A and B-F infants, whereas nonantibody-bound insulin levels were approximately 15-fold higher in the class B-F infants than in the class A infants (p less than 0.001). After birth, plasma glucose fell in all infants, the nadir being reached at two hours (p less than 0.01). Plasma glucose fell by approximately 35% in the class A infants and 63% in the class B-F infants (p less than 0.01). Eight IDM had asymptomatic hypoglycemia (plasma glucose less than 1.9 mmol/l) and four of these infants had glucose levels below 1.7 mmol/l and were withdrawn from further study. In the remaining four hypoglycemic IDM, plasma glucose was about 1.6-fold higher (p less than 0.01) and insulin about 11-fold higher (p less than 0.001) at birth compared to the 24 normoglycemic IDM. The hypoglycemia was attended by unchanged insulin levels in the class A infants, whereas insulin fell in the class B-F infants (p less than 0.01). However, during the whole investigative period, plasma insulin of the class B-F infants was higher than that of the class A infants (p less than 0.01). After birth, plasma glucagon increased slowly in all IDM and peak values were reached after 12 hours in the class A infants (p less than 0.05) and 24 hours in the class B-F infants (p less than 0.01). Only those infants who became hypoglycemic after birth exhibited a significant increment in plasma glucagon from 0.2 hours (p less than 0.05). These results suggest that neonatal hypoglycemia of IDM results from high plasma levels of nonantibody-bound insulin together with a very retarded increment in plasma glucagon levels. The degree of neonatal hypoglycemia and hyperinsulinemia of an individual IDM seems to be positively correlated to the severity of the diabetes of the mother.     

Comparison of 2 iron doses in infants receiving recombinant human erythropoietin therapy

OBJECTIVE: To compare iron sufficiency in premature infants receiving high-dose recombinant human erythropoietin (r-HuEPO), 1200 IU/kg per week, supplemented with 6 or 12 mg/kg per day of enteral iron. DESIGN: We conducted a prospective, double-blind, controlled study of premature infants receiving r-HuEPO therapy, randomly assigned to receive 2 different doses of iron. Measurements of ferritin, iron, total iron-binding capacity, reticulocyte count, hemoglobin level, and hematocrit were obtained at baseline, 4, and 6 weeks. Transferrin saturation was calculated; the number of blood transfusions and the incidences of sepsis were recorded. SETTING: This study was performed in the neonatal intensive care unit at Loma Linda University Children's Hospital, Loma Linda, Calif. SUBJECTS: Infants with a gestational age of 32 weeks or younger, older than 7 days, and receiving r-HuEPO therapy from March 1, 1997, to June 30, 1998, were eligible for the study. Infants were randomly assigned to receive 6 mg/kg per day or 12 mg/kg per day of enteral iron during a course of r-HuEPO therapy for 4 to 6 weeks. RESULTS: Sixty-four infants were enrolled in the study. Twelve infants did not complete the study; 52 completed 4 weeks and 41 completed 6 weeks of the study. While ferritin levels and transferrin saturation decreased in both groups over the study period, there were no differences between the 2 study groups. CONCLUSIONS: Infants receiving high-dose r-HuEPO therapy (1200 IU/kg per week) decrease their ferritin levels (measure of iron stores) even when receiving high enteral iron supplementation. Given that the ferritin levels were similar between the 2 groups, we speculate that the additional iron either was not absorbed or was not stored.     

Profile of bone marrow iron stores in childhood iron deficiency anemia

To demonstrate the importance of bone marrow iron stores, we examined the complete hemogram, serum iron (SI), serum iron-binding capacity (SIBC), transferrin saturation (TS), serum ferritin and bone-marrow-stored iron in 31 children with iron deficiency (ID). The ages of the patients ranged from one to 14 years (mean 3.7 +/- 3.9). Laboratory findings of the 31 patients were as follows: hemoglobin (Hb) 8.5 +/- 2.4 g/dl, hematocrit (Hct) 27.8 +/- 6.3 percent, mean corpuscular volume (MCV) 58.6 +/- 8.6 fl, red blood cell count (RBC) 4 +/- 0.8 10(12)/L, red cell distribution width (RDW) 19.3 +/- 4.9, SI 17.2 +/- 9.3 microg/dl, SIBC 311 +/- 50.5 microg/dl, TS 5.5 +/- 2.8 percent and ferritin 6.7 +/- 7.3 ng/dl. In the bone marrow smears with iron stains, all patients' scores were zero for iron stores, which shows that bone-marrow-stored iron in childhood is easily affected. Because of the traumatic effect of bone marrow aspiration, it is recommended that it not be done routinely. The diagnosis of ID could be especially difficult in patients with low SI levels but normal SIBC levels and in patients with chronic inflammatory diseases. In those conditions, illustration of bone marrow stores could be of particular assistance for diagnosis of iron deficiency.     

Impact on iron status of introducing cow's milk in the second six months of life

To determine the impact on iron status of introducing cow's milk (CM) into the diet during the second 6 months of life, nutrient intake was assessed and iron status measured in 100 infants. Nutrient intake for 40 of the 45 infants, age 8 to 13 months, fed CM as the primary beverage for at least 3 months prior to the study and for 45 of 55 infants the same age fed a milk-based infant formula (FF) as the primary beverage for at least 3 months were assessed. All infants in the study were healthy, and the majority were taking no medications or supplements other than vitamins or fluoride for 3 weeks prior to the assessment. Blood drawn by peripheral venipuncture was analyzed by Coulter Counter for complete blood count; plasma albumin, iron, ferritin, transferrin saturation, and total iron-binding capacity were measured in all infants. CM-fed infants had significantly lower mean iron and vitamin C intakes, plasma albumin, transferrin saturation, and ferritin than did FF infants. The frequency of low plasma iron, low transferrin saturation, and low plasma ferritin was significantly greater in CM-fed than in FF infants. The percentage of subjects with three or more abnormal iron indices was more than twice as great in CM-fed infants (58%) as in FF infants (23%). Feeding infants iron-fortified formula to 12 months of age appears to deter iron deficiency.     

Gender difference in cord serum ferritin concentrations.

We measured cord serum ferritin concentrations in a total of 255 infants (116 females and 139 males), and evaluated the association between these values and various neonatal as well as maternal characteristics. The mean ferritin concentration in females (166 +/- 110 microg/l) was significantly higher than that in male infants (123 +/- 77 microg/l). The gender differences in ferritin were significant within groups of infants with fetal growth restriction, those who weighed <3,000 g, those whose mothers were African Americans or <25 years old. Maternal serum ferritin concentrations at 36 weeks of gestation significantly correlated with cord serum ferritin of male infants (r = 0.32, p < 0.001), whereas the association was not significant for females (r = 0.09, p > 0.41). Although the mechanism of the gender difference is unknown, it may be important to consider the sex of neonates when evaluating their iron nutriture immediately after birth.     

Evaluation of iron status in women with pregnancy complicated by tobacco smoking

Relatively common iron deficiency in pregnant women is assumed to be enhanced by cigarette smoking. In the presented studies we determined cotinine in serum and urine of 75 pregnant women in order to select groups of smoking women and tobacco abstinence. In the smoking group, a mean concentration of cotinine 1039 +/- 560 mg/L in serum and 1025 +/- 540 mg/L in urine were observed. For assessment of iron status we determined in serum: iron, iron-binding capacity (TIBC), transferrin, transferrin saturation, soluble transferrin receptor and ferritin. In serum of smoking woman in comparison to non smoking, the level of ferritin and transferrin was higher but non significantly. Significant increase of TIBC (p < 0.05) and decrease of transferrin saturation (p < 0.05) was observed. Therefore iron deficiency in transport compartment can not be excluded. The concentration of soluble transferrin receptor was the same in both groups studied. However, in late pregnancy (above 27 week of gestation) ferritin concentration less than 20 mg/L of serum was observed in 70% of smoking and only in 39% of non smoking women (p < 0.05). We concluded that cigarette smoking during pregnancy did not have any effect on the entry of iron-bearing transferrin to cells mediated by soluble transferrin receptor, but affected the level of iron-storage ferritin, which leads to iron deficiency in the storage compartment (ID I).     

Iron-deficiency anaemia and its response to oral iron: report of a study in rural Gambian children treated at home by their mothers

Haematological and iron parameters, measured in 907 children aged from 6 months to 5 years in rural Gambia at the start of the rainy season, differed from those in American reference populations as follows: mean haemoglobin levels were much lower at ages 1 and 2 years and mean levels of mean corpuscular volume (MCV) were lower at all ages (at age 1 year mean haemoglobin was 11.2 g/dl and mean MCV 68.2 fl); in a sample of 249 children randomly selected from the whole study population, mean serum iron levels were similar but mean transferrin saturation and mean serum ferritin levels were lower, especially at ages 1-3 years (at age 1 year mean serum iron was 11.1 mumol/l, mean transferrin saturation 16.9%, and geometric mean serum ferritin 8.8 ng/ml. A total of 213 children (23%) whose haemoglobin and mean corpuscular volume were both less than the 3rd percentile of the reference population received oral iron or placebo from their mothers during the rainy season when malaria transmission is maximal. Mean levels of haemoglobin, mean corpuscular volume, serum iron, transferrin saturation and serum ferritin rose in the iron-treated group and fell in the placebo group at all ages, except under 1 year for serum ferritin, to produce significant differences between the groups by the end of the study. Total iron-binding capacity showed no significant changes during the study. We concluded that oral iron given by the mother during the rainy season can be used to treat iron-deficiency anaemia in Gambian children who would otherwise become more anaemic.     

Soluble transferrin receptor as an indicator of iron deficiency in HIV-infected infants

BACKGROUND: Iron deficiency is common in human immunodeficiency virus (HIV)-infected infants in sub-Saharan Africa. It is not known whether soluble transferrin receptor (sTfR) is a good indicator of iron deficiency in infants with HIV. METHODS: We evaluated sTfR as an indicator of iron deficiency in 134 HIV-infected 9-month-old infants in Kampala, Uganda. Ferritin <12 microg/L and microcytic, hypochromic anaemia were used as indicators of iron deficiency, respectively. The presence of inflammation was indicated by C-reactive protein >5 mg/L or alpha1-acid glycoprotein >1 g/L. RESULTS: Receiver operator characteristic curves showed that the area under the curve was 0.67 when sTfR receptor was compared with low ferritin and 0.71 when sTfR was compared with microcytic, hypochromic anaemia. The appropriate calculated cut-offs of sTfR >3.74 microg/mL (43.98 nmol/L) and >3.53 microg/mL (41.55 nmol/L) show adequate specificities of 60% and sensitivities of 63% and 69% for low ferritin and microcytic, hypochromic anaemia, respectively. C-reactive protein and alpha 1-acid glycoprotein were strongly correlated with serum ferritin (r=0.371 and r=0.458, respectively, both p<0.0001) but were not correlated with sTfR (r=0.009 and r= -0.003, respectively, both p=0.9). In all, 78.6% of infants had alpha l-acid glycoprotein >1 g/L and 54.7% had C-reactive protein >5 g/L. CONCLUSIONS: Soluble TfR appears to be an adequate indicator of iron deficiency in HIV-infected infants.