Trisomy 21 Placentas: Histopathological and Immunohistochemical Findings using Proliferating Cell Nuclear Antigen

Abstract

Objective: The cause of growth retardation in trisomy 21 and other autosomal trisomies is not known, but may be the result of defective cell proliferation, slowing of the cell cycle, or placental structural abnormalities. Abnormalities of the fetal cell cycle may be reflected in placental growth and can be detected using proliferating cell nuclear antigen (PCNA). Methods: Twelve second-trimester and six third-trimester trisomy 21 placentas were examined histopathologically and stained immunohistochemically using antibodies to PCNA. Normal age-matched placentas were used as controls. Results: The second-trimester trisomy 21 placentas all exhibited many large irregular hypovascular villi. The third-trimester trisomy 21 placentas showed two patterns: (i) many large, irregular hypovascular villi, and (ii) relatively normal-appearing villi with only a few abnormal villi and focal hypervascularity. PCNA staining was significantly greater in second-trimester placentas when compared to third-trimester placentas for both trisomy 21 and controls. There was no significant difference in PCNA staining in trisomy 21 placentas when compared to the normal age-matched controls. Conclusions: PCNA staining indicates no significant differences in proliferation between normal and trisomy 21 placentas. Trisomy 21 placentas show villus abnormalities, including hypovascularity.

Sonographic, Pathologic andKaryotypic Findings in a Rare Case of Placenta fenestrata

“…It has also been argued that the hCG concentrations in triploid pregnancies are often too large to be readily explained by the quantitative differences in placental size or by relative placental immaturity [14]. The second hypothesis suggests that disturbances of villus vascularization might lead to impaired drainage and thus elevation in hCG levels without overt molar or hydropic changes in the placenta [15,16]. Our case with reduced placental vascularization further strengthens this hypothesis.…”

Increased Umbilical Artery Pulsatility Index in Third-Trimester Fetuses with Trisomy 21

“…It was noted that the number of muscular arteries was smaller and the ratio of these arteries to the number of villi was reduced in comparison to the euploid group. Qureshi et al [16 ]examined 6 placentas of trisomy 21 pregnancies. They noted an increased presence of irregular hypovascular villi and focal areas of hypervascularity.…”

Hydrops Fetalis, Thickened Placenta and Other Sonographic Findings in a Low-Level Trisomy 21 Mosaicism: A Case Report

“…So far, it has not been described in pregnancies affected by trisomy 21 mosaicism. The second-trimester trisomy 21 placentas exhibit many large irregular hypovascular villi [9] , which may be related to the defect (or the delay) in the syncytiotrophoblast formation [10] . It has been investigated if there is a tendency for heavy placentas in trisomy 21.…”