Maternal diabetes mellitus is associated with altered deposition of fibrin-type fibrinoid at the villous surface in term placentae.
Placentae from control and diabetic patients were used to test three null hypothesis: (1) there are no significant group differences in the volumes of villous syncytiotrophoblast compartments or intervillous fibrin-type fibrinoid, (2) perivillous fibrin-type fibrinoid is deposited randomly at the surface of trophoblast, and (3) amounts and deposition patterns of perivillous fibrin-type fibrinoid do not vary between groups. Term placentae were collected from non-diabetic subjects and five groups of diabetic women classified according to duration, severity and insulin dependence. Tissue specimens and sections were obtained by uniform random sampling. Volumes and surface areas of fibrin-type fibrinoid and trophoblast compartments (thin, syncytial knot, syncytial bridge and denuded regions) were estimated stereologically and compared using variance, chi-squared and contingency table analyses. As to null hypothesis (1), no group differences in volumes of trophoblast compartments were found but volumes of intervillous fibrin-type fibrinoid were greater in the non-insulin-dependent diabetic group. As to null hypothesis (2), regardless of group, fibrin-type fibrinoid was deposited preferentially at sites of denudation in every placenta examined. As to null hypothesis (3), villous surface areas occupied by perivillous fibrin-type fibrinoid were greater in type 1 (insulin-dependent) diabetics with complications (diabetic nephropathy or retinopathy). The surfaces of trophoblast occupied by fibrin-type fibrinoid were also notably larger in non-insulin-dependent diabetics and type 1 diabetics with complications. Except for the surface of denudation sites (which also increased in diabetes), there were no differences in the surfaces of trophoblast regions. These results confirm that the haemostatic steady state is perturbed in the diabetic placenta, that perivillous fibrin-type fibrinoid is deposited preferentially at sites of epithelial loss/damage, and that some diabetic groups are affected differentially.
Mayhew
T M
TM
Centre for Integrated Systems Biology and Medicine, School of Biomedical Sciences, Queen's Medical Centre, University of Nottingham, UK. terry.mayhew@nottingham.ac.uk
Sampson
C
C
D000328:Adult; D002824:Chorionic Villi / Q000378:metabolism* / Q000473:pathology; D016640:Diabetes, Gestational / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005337:Fibrin / Q000378:metabolism*; D006801:Humans; D007231:Infant, Newborn; D007743:Labor, Obstetric; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000378:metabolism* / Q000473:pathology; D014327:Trophoblasts / Q000378:metabolism / Q000473:pathology
D005337:Fibrin