a1 Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110029, India
a2 Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas, MD Anderson Cancer Center, Box 301402, Houston, TX 77230, USA
a3 Department of Obstetrics and Gynaecology, Joan C Edwards School of Medicine, 1600 Medical Center Drive, P.O. Box 4500, Huntington, VA 25701, USA
Severe anaemia is associated with increased low birth weight and Barker's hypothesis of ‘fetal origins’ proposes that a nutritional insult during critical periods of development results in adaptations that predispose individuals to adult onset diseases. We hypothesize that endocrine alterations may occur in the maternal–fetal milieu as a consequence of nutritional anaemia during pregnancy. We examined the quantitative variations in hormonal profiles in paired maternal and cord blood samples obtained from mothers and their neonates who were classified based on maternal anaemia status. Our results show that: (1) 74·6 % of the mothers enrolled in the study were anaemic, of which 85·2 % had moderate anaemia and 14·7 % had severe anaemia; (2) anthropometric parameters measured in the mothers indicate that severely anaemic mothers had a significantly low pre- and post-pregnancy weight, a significantly decreased maternal fundal height and abdominal circumference; (3) anthropometric measures in the neonates born to severely anaemic mothers show a significant reduction in ponderal index, birth weight and placental weight; (4) significant increase in both maternal, fetal insulin-like growth factor 1, ferritin levels and increased maternal erythropoietin levels were observed with an increase in severity of anaemia; (5) decreased T3 and increased prolactin levels were observed in the maternal blood of severely anaemic mothers as compared with the control group. An insight into the endocrine modulation to overcome a growth disadvantage due to nutritional anaemia in pregnancy may lead to a better understanding of fetal adaptations invoked when the maternal-placental nutrient supply fails to meet the fetal nutrient demand.
(Received May 21 2007)
(Revised November 16 2007)
(Accepted November 19 2007)
(Online publication February 13 2008)
p1 Present address: Department of Medicine, Div of Allergy, Immunology, and Rheumatology, 310 Multi Research Bldg, Buffalo General Hospital, 100 High Street, Buffalo, NY 14 203, USA.
Abbreviations: EGF, epidermal growth factor; GH, growth hormone; hPL, placental lactogen; IDA, Fe-deficiency anaemia; IGF, insulin-like growth factor; PRL, prolactin; TSH, thyroid-stimulating hormone