CELIAC DISEASE, PREGNANCY, SMALL FOR GESTATIONAL AGE: ROLE OF EXTRAVILLOUS TROPHOBLAST

Abstract

It is questionable whether development of the intrauterine growth retardation or small for gestational age (SGA) children is related directly to inflammation associated with celiac disease. Localization and the amount of gliadin, Fas-L, as well as the incidence of apoptosis in 32-term placentas, was analyzed immunohistochemically and with in situ hybridization in a blinded fashion; these were correlated with the weight of their newborns. Extravillous trophoblasts (EVTs) from the noncompliant women were overloaded with gliadin; there was a moderate amount or no gliadin present in the controls. The weight of newborns was lower if extravillous trophoblasts were loaded with gliadin (−2.24SD) (p = 0.004). Increased apoptosis of EVT in placentas of noncompliant women was consistent with abundant expression of Fas-L in those cells and was linked to the low birth weight of newborns. Exposure to gliadin alters extravillous trophoblast dynamics by causing an increase in apoptotic shedding. In genetically predisposed individuals, gliadin affects fetal part of the placenta causing children to be small for their age. A gluten-free diet during pregnancy prevents SGA children and, thus, the fetal origin of serious adult diseases.

Keywords:

• apoptosis
• celiac disease
• extravillous trophoblast
• Fas-L
• gliadin
• SGA