Feto-maternal bone remodeling in normal pregnancy and preeclampsia.
OBJECTIVE
To investigate feto-maternal bone turnover in normal pregnancy and preeclampsia and to test the hypothesis whether the reported low bone mass at birth in small-for-gestational age infants is associated with decreased bone formation or increased bone resorption.


METHODS
Thirty-two patients with preeclampsia (17 mild and 15 severe) and 20 normotensive women (controls) with singleton gestations in the third trimester participated in this study. Furthermore, 25 nonpregnant healthy women were chosen as nonpregnant controls. Maternal 24-hour urine specimens and venous blood samples were collected. In addition, fetal cord blood and the first voided neonatal urine were also collected. The freshly separated sera were assayed for osteocalcin (OC) and carboxy-terminal propeptide of type 1 collagen (PICP) by radioimmunoassay. Urine samples were assayed for N-telopeptide of type 1 collagen (NTx) by enzyme-linked immunosorbent assay.


RESULTS
Maternal and cord serum OC and PICP levels were significantly decreased in severe preeclampsia, whereas maternal and first-voided neonatal urinary NTx level were significantly increased compared to the corresponding levels of controls. In both mother and fetus, the coupling index of markers of bone turnover in normal pregnancy or mild preeclampsia was in favor of bone formation, whereas in severe preeclampsia the markers suggested marked bone resorption.


CONCLUSIONS
Increased bone resorption and decreased bone formation occur in preeclampsia in both mother and fetus, being more pronounced in the latter. The increased osteoclastic activity in preeclampsia may be attributed to increased RANKL induced by increased interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor beta2 (TGF-beta2) production.
Shaarawy
Mohamed
M
Department of Obstetrics and Gynecology, Kasr Al-Aini School of Medicine, Cairo University, Cairo, Egypt. Shaarawy@mednet3.camed.eun.eg
Zaki
Sameh
S
Ramzi
Abdel-Megid
AM
Salem
Mahmoud E
ME
El-Minawi
Ahmed M
AM
D000328:Adult; D001862:Bone Resorption / Q000503:physiopathology*; D002352:Carrier Proteins / Q000096:biosynthesis; D016022:Case-Control Studies; D003094:Collagen / Q000097:blood; D024042:Collagen Type I; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D006801:Humans; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age / Q000502:physiology*; D015850:Interleukin-6 / Q000502:physiology; D008431:Maternal-Fetal Exchange; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D015675:Osteocalcin / Q000097:blood; D010010:Osteoclasts; D010455:Peptides / Q000097:blood; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy / Q000502:physiology*; D011263:Pregnancy Trimester, Third; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D016212:Transforming Growth Factor beta / Q000502:physiology; D053781:Transforming Growth Factor beta2; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D002352:Carrier Proteins; D024042:Collagen Type I; D015850:Interleukin-6; D008562:Membrane Glycoproteins; D010455:Peptides; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; C509041:TGFB2 protein, human; C505686:TNFRSF11A protein, human; C505688:TNFSF11 protein, human; D016212:Transforming Growth Factor beta; D053781:Transforming Growth Factor beta2; D014409:Tumor Necrosis Factor-alpha; C052929:collagen type I trimeric cross-linked peptide; D015675:Osteocalcin; D003094:Collagen