Effect Of Maternal Cigarette Smoking On Newborn Iron Stores

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4671-4671 ◽  
Author(s):  
Irina Pateva ◽  
Elisabeth Kerling ◽  
Susan Carlson ◽  
Manju Reddy ◽  
Dan Chen ◽  
...  

Objective Previous small-scale studies suggest that maternal smoking lowers neonatal body iron. Our objective was to study and compare the relationship between maternal and infants’ body iron in smokers and non-smokers in a large matched-pair cohort. Method This was a prospective cohort study involving 144 mothers – 72 smokers and 72 non-smokers and their respective infants. Samples were obtained from maternal blood and infants’ cord blood at delivery for serum transferrin receptor (sTfR) and ferritin levels. Serum TfR and ferritin levels were measured by RAMCO ELISA and RIA assays. The total body iron (TBI) was calculated using the sTfR/ferritin ratio. Results Maternal total body iron and smoking status Women who smoked had lower sTfR, higher ferritin and higher body iron compared to nonsmoking women. Infant’s total body iron, measurements at birth and smoking status In contrast to their respective mothers, we found a small but statistically significant negative correlation between smoking and infants’ total body iron. The number of PPD smoked was negatively correlated with infants’ ferritin and total body iron. The number of days smoked during pregnancy was also negatively correlated with infants’ ferritin and total body iron and positively correlated with infants' sTfR. Birth weight was lower in babies of smokers compared to nonsmokers (mean /- SD =3270 +/-475 vs. 3393 g +/- 475 g, p=0.03). Correlation studies revealed that birth weight in infants of smokers was negatively correlated with PPD smoked and number of days smoked. Birth length in the same infants was also negatively correlated with PPD smoked and number of days smoked. Conclusion Mothers who smoked during pregnancy had higher iron stores but their newborn infants had lower iron stores than those of non-smoking mothers. There may be a negative dose-dependent response between fetal smoke exposure and infant iron stores. Disclosures: No relevant conflicts of interest to declare.

Author(s):  
Iain C. Macdougall

Although erythropoiesis-stimulating agent therapy is the mainstay of renal anaemia management, maintenance of an adequate iron supply to the bone marrow is also pivotal in the process of erythropoiesis. Thus, it is important to be able to detect iron insufficiency, and to treat this appropriately. Iron deficiency may be absolute (when the total body iron stores are exhausted) or functional (when the total body iron stores are normal or increased, but there is an inability to release iron from the stores rapidly enough to provide a ready supply of iron to the bone marrow). Several markers of iron status have been tested, but those of the greatest utility are the serum ferritin, transferrin saturation, and percentage of hypochromic red cells. Measurement of serum hepcidin, which is the master regulator of iron homoeostasis, has to date proved disappointing as a means of detecting iron insufficiency, and none of the available iron markers reliably exclude the need for supplemental iron. Iron may be replaced by either the oral or the intravenous route. In the advanced stages of chronic kidney disease, however, hepcidin is upregulated, and this powerfully inhibits the absorption of iron from the gut. Thus, such patients often require intravenous iron, particularly those on dialysis. Several intravenous (IV) iron preparations are available, and they have in common a core containing an iron salt, surrounded by a carbohydrate shell. The IV iron preparations differ in their kinetics of iron release from the iron–carbohydrate complex. In recent times, several new IV iron preparations have become available, and these allow a greater amount of iron to be given more rapidly as a single administration, without the need for a test dose.


Transfusion ◽  
2016 ◽  
Vol 56 (8) ◽  
pp. 2005-2012 ◽  
Author(s):  
Ritchard G. Cable ◽  
Donald Brambilla ◽  
Simone A. Glynn ◽  
Steven Kleinman ◽  
Alan E. Mast ◽  
...  

Gut ◽  
1978 ◽  
Vol 19 (6) ◽  
pp. 538-542 ◽  
Author(s):  
L W Powell ◽  
J W Halliday ◽  
J L Cowlishaw

2000 ◽  
Vol 343 (5) ◽  
pp. 327-331 ◽  
Author(s):  
Emanuele Angelucci ◽  
Gary M. Brittenham ◽  
Christine E. McLaren ◽  
Marta Ripalti ◽  
Donatella Baronciani ◽  
...  

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3596-3596 ◽  
Author(s):  
Timothy G. St. Pierre ◽  
Gary P. Jeffrey ◽  
Enrico Rossi ◽  
Adam J. Fleming ◽  
Wanida Chua-anusorn ◽  
...  

Abstract Newly diagnosed hereditary hemochromatosis subjects are treated with venesection therapy in order to reduce body iron stores. Liver iron concentration (LIC) is the most reliable indicator of body iron stores. Proton transverse relaxation rate imaging (FerriScan®) enables a highly specific and sensitive measurement of LIC [St. Pierre TG, Clark PR, Chuaanusorn W, Fleming A, Jeffrey GP, Olynyk JK, Pootrakul P, Robins E, Lindeman R. Blood105 (2005) 855–861]. In this study FerriScan® was used to follow the LIC and liver volume in 7 newly diagnosed homozygous C282Y hereditary hemochromatosis patients. Baseline LIC values ranged from 3.4 to 16.7 mg Fe/g dry tissue. The total number of venesected units of blood required to lower the LIC of each subject to the upper end of the normal range was initially estimated from body mass and LIC [Angelucci, E., Brittenham, G.M., McLaren, C.E. et al. (2000) New Eng. J. Med.343, 327–331]. The LIC of each subject was measured again after approximately half the estimated total number of units of blood had been removed, and a third time near completion of the venesection therapy. For each subject, a straight line was fitted to the LIC versus venesected blood volume data. The coefficient of variation of the differences between the measured LIC values and the fitted lines (a measure of the precision of the LIC measurements) was found to be 7 %. Total body iron stores were measured by extrapolating the straight line fit through the LIC vs venesected blood volume to zero LIC and using a value of 0.473 mg Fe/mL for the blood iron concentration. Total liver iron content was determined by simultaneous measurement of LIC and liver volume with MRI. The data indicated that the higher the LIC at diagnosis, the higher was the fraction, α, of the total body iron store located in the liver. Hence a linear model relating α to LIC is proposed, α = β x LIC + α0. Linear regression was used on the 21 measurements of LIC in the study to find the following optimum model parameters α0 = 0.169 and β = 0.0274 g wet liver/mg Fe. Using these parameters the total blood volume (TBV) to be removed from a patient to bring the LIC down from an initial value (LICi) to a target value (LICf) can be calculated using TBV = [(LICi – LICf) x V]/(β x LICi + α0) where V is the liver volume. Using the 21 measurements in this study a straight line relationship between measured and predicted numbers of units of blood to bring LIC to 1 mg Fe/g dry tissue was found to have slope 0.99 and Pearson’s correlation coefficient of 0.97. The data suggest that simultaneous measurement of LIC and liver volume with MRI (data acquisition time less than 30 minutes) can be used to predict venesection requirements in hereditary hemochromatosis. The measurement of baseline LIC also enables an estimate of the possible visceral or metabolic consequences of the iron burden. For example, in the absence of other complicating factors, a measurement of the LIC multiplied by the age of the subject gives a good predictor of iron induced liver damage [Olynyk, J.K, St. Pierre, T.G., Britton, R.S., Brunt, E.M., and Bacon, B.R. (2005) Am. J. Gastro., 100, 837–841].


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1779-1779 ◽  
Author(s):  
Regine Grosse ◽  
Gisela Janssen ◽  
Rainer Engelhardt ◽  
Marketa Groeger ◽  
Oliver Leismann ◽  
...  

Abstract Chelation treatment of patients with iron overload from chronic blood (RBC) transfusion needs continuous monitoring of iron stores, iron influx rates from RBC, chelation dose rates, and compliance. Molar chelator efficacy depicts the combined effect from these variables. Treatment should always aim to maximize the efficacy of a certain chelator in an individual patient in order to reduce organ damage from iron toxicity. In a prospective trial on the oral chelator deferasirox, a total of 12 patients with b-thalassemia major have been followed by SQUID biomagnetic liver susceptometry in intervals of 6 to 12 months over a time period of up to 38 months under deferasirox. Patients were initially on deferoxamine (DFO, Desferal®) and then participated in an international multi-center trial randomized for s.c. DFO and the oral chelator deferasirox (DSX, Exjade®). Liver iron concentration LIC (μg/g-liver wet weight), liver volumes, RBC transfusion rates, chelation dose rates, and compliance from tablet counts were assessed. Total body iron stores were calculated from total liver iron taking into account that 70 – 90 % of the total body storage iron is accumulated in the liver. For each chelation interval, molar efficacies were calculated from the daily iron input rate due to RBC plus the change in total body iron per interval time (= mobilized iron rate), and the molar dose rate of DFO or DSX (Fischer et al: Ann N Y Acad Sci2005; 1054: 350–7), equation 1. \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \[Molar\ efficacy\ [\%]\ =\ mobilized\ iron\ rate/molar\ chelator\ dose\ rate\] \end{document} LIC values were in the range of 836 to 8404 with a median value of 2424 μg/g-liver, while ferritin levels were between 911 and 13609 μg/l with a median ratio of ferritin-to-LIC of 1.0 ((μg/l)/(μg/g)) (range: 0.4 to 3.2). The median molar dose rates for DFO and DSX were 3.2 and 1.6 mmol/d, respectively. For each patient, the molar efficacies for DFO and DSX were averaged. From these averaged values, a mean molar efficacy ± SD of 13.2 ± 3.4 % and 23.6 ± 10.3 % was found for DFO and DSX, respectively. Relative to DFO, in each patient an increase between 5.5 and 27.1 % was found for DSX (mean: 11.7 ± 7.3 %). Patients with a low efficacy on DFO also had a low molar efficacy on DSX and vice versa (e.g., 8.0 and 13.5 % versus 16.0 and 31.9 %). Compliance assessed from tablet count protocols was larger than 90% and did not change these data significantly. On a larger scale in highly compliant thalassemia patients, a molar efficacy of 17.6 ± 4.8 % was observed (Fischer et al: Brit J Haematol2003; 121: 938–48). In comparison to that reference value, the molar efficacy of DFO for this patient group was decreased. The reported molar efficacy of 27.9 ± 13.8 % for DSX obtained from biopsy results (Porter et al: Blood2005; 106(11): 755a) is only insignificantly higher than our value. In summary, we found deferasirox to be two times more efficient than deferoxamine on the same molar dose level, even for patients with a relatively low efficacy under both chelator treatment regimens.


Hepatology ◽  
2003 ◽  
Vol 38 ◽  
pp. 660-660
Author(s):  
S JACQUELINET ◽  
G BRITTENHAM ◽  
E ANGELUCCI ◽  
C MCLAREN ◽  
P BRISSOT

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