الفهرس 
Iron HomeostasisOnly 14 pages are availabe for public view
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Abstract
Background: iron is essential element involved in a broad range of biologically important reactions critical for cellular function and also plays a role in oxygen transferring and despite its low daily requirements iron deficiency is the most common nutritional disorder in the world. Maternal diabetes mellitus was thought to be associated with depletion of fetal iron stores in proportion to the degree of maternal control and presence or absence of complications of diabetes, but not maternal iron status. Infants of diabetic mothers were found to have higher fetal iron demands at least partly explained by increased erythropoiesis secondary to intra-uterine hypoxia. Diagnosis of ID is based on a panel of laboratory measurements that show the state of storage, transport, and functional iron compartments .Most of these parameters can be altered by infection or inflammation, which affects their sensitivity and specificity. The diagnosis of ID in children may be improved by the use of 2 recently proposed biomarkers, serum transferrin receptor (sTfR) and sTfR/log ferritin (sTfR-F index)
Aim of the work: in this study we aimed to assess the effect of maternal diabetes on neonatal cord blood iron stores.
Patient and Method: this case-control study was conducted on 100 maternal/cord blood pairs who were included in the study from Obstetrics and Gynecology Department at El- Nile Insurance Hospital, Shubra El Khema, during the period from November 2015 to July 2016.
Results The infants of the diabetic mothers had significantly lower levels of ferritin (27.52 vs 91.87 ng/ml; p,0.001)
and higher STfR (28.53 vs 26.66 mg/l; p,0.038) and TfR-F index (3.91 vs 1.21; p,0.001) than controls. They
, were born at an earlier gestation (37.86vs 38.54weeks; p,0.01) and had higher birth weight (3.87 vs 3.34 kg; p = 0.001) and had higher hemoglobin level( 15.75 vs14.17 g/dl ;p=0.001).
.Conclusion: this study confirmed that iron stores are lower at birth in infants of diabetic mothers. This appeared to be due to the effects of increased erythropoiesis secondary to chronic intrauterine hypoxia. Fetal iron stores were affected by maternal glycemic control and not related to maternal iron supplement.