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Background: Acute funisitis-the histologic diagnosis of inflammation within the umbilical cord-represents a fetal inflammatory response and has been associated with adverse neonatal outcomes. Little is known regarding the maternal and intrapartum risk factors associated with the development of acute funisitis among term deliveries complicated by intraamniotic infection., Objective: This study aimed to identify the maternal and intrapartum risk factors associated with developing acute funisitis among term deliveries complicated by intraamniotic infection., Study Design: After institutional review board approval, we conducted a retrospective cohort study of term deliveries affected by clinical intraamniotic infection at a single tertiary center between 2013 and 2017, with placental pathology consistent with histologic chorioamnionitis. The exclusion criteria included intrauterine fetal demise, missing delivery information or placental pathology, and documented congenital fetal abnormalities. Maternal sociodemographic, antepartum, and intrapartum factors were compared among patients with acute funisitis on pathology to those without acute funisitis using bivariate statistics. Regression models were developed to estimate the adjusted odds ratios., Results: Of 123 patients meeting the inclusion criteria, 75 (61%) had acute funisitis on placental pathology. Compared with placental specimens without acute funisitis, acute funisitis was observed more frequently among patients with maternal BMI ≥30 kg/m 2 (58.7% vs 39.6%, P=.04) and labor courses with increased rupture of membrane duration (17.3 vs 9.6 hours, P=.001). Use of fetal scalp electrode was observed less frequently in acute funisitis (5.3% vs 16.7%, P=.04) than cases without acute funisitis. In regression models, maternal BMI ≥30 kg/m 2 (adjusted odds ratio, 2.67; 95% confidence interval, 1.21-5.90) and rupture of membrane >18 hours (adjusted odds ratio, 2.48; 95% confidence interval, 1.07-5.75) were significantly associated with acute funisitis. Fetal scalp electrode use (adjusted odds ratio, 0.18; 95% confidence interval, 0.04-0.71) was negatively associated with acute funisitis., Conclusion: In term deliveries with intraamniotic infection and histologic chorioamnionitis, maternal BMI ≥30 kg/m 2 , and rupture of membrane>18 hours were associated with acute funisitis on placental pathology. As insight into the clinical impact of acute funisitis grows, the ability to predict which pregnancies are at the greatest risk for its development may allow for a tailored approach to predicting neonatal risk for sepsis and related comorbidity., (Published by Elsevier Inc.)

Erosive adenomatosis of the nipple (EAN) is a complex benign mammary proliferation that has a variety of histologic appearances. All forms of this lesion are thought to be composed of two apparent cell types: epithelial luminal cells and basal myoepithelial cells. A panel of immunohistochemical reagents was employed to determine whether this divergence of differentiation could be confirmed immunohistochemically. It included antibodies against cytokeratin (CK), vimentin (VIM), glial fibrillary acidic protein (GFAP), and muscle-specific actin (MSA); the latter three markers are associated with myoepithelial differentiation. EAN was also assessed with reagents directed at carcinoembryonic antigen (CEA) and collagen type IV (CIV). Basal glandular cells in EAN homogeneously expressed CK and MSA. They also were positive for VIM in 10 cases, and for GFAP in three. Luminal glandular cells in EAN expressed CK uniformly and CEA focally. Lesional glands were surrounded by a concentric layer of CIV. The authors conclude that two cell types are indeed demonstrable immunohistochemically in EAN, one of which has myoepithelial features. CEA may be expressed by this lesion despite its innocuous biological nature, and constituent glands synthesize basement membrane proteins in a pattern that is characteristic of benign mammary proliferations. Differential diagnosis between EAN and invasive carcinoma of the breast may be facilitated by immunohistologic evaluation, but the latter modality of study is not capable of distinguishing between EAN and other benign proliferative mammary lesions.