Chorionic Histiocytic Hyperplasia is Associated With Chronic Inflammatory Lesions in the Placenta

Background Chorionic histiocytic hyperplasia (CHH) is a cellular proliferation at the base of the chorion that was identified by the authors in examining placentas for chronic chorioamnionitis (CC). This study is a retrospective review of cases diagnosed with CHH, describing its incidence alone and...

Full description

Saved in:
Bibliographic Details
Published inPediatric and developmental pathology Vol. 20; no. 3; p. 197
Main Authors Katzman, Philip J, Metlay, Leon A, McMahon, Loralee A, LiQiong, Li, Zhang, Bin
Format Journal Article
LanguageEnglish
Published United States 01.06.2017
Subjects
Online AccessGet more information

Cover

Loading…
More Information
Summary:Background Chorionic histiocytic hyperplasia (CHH) is a cellular proliferation at the base of the chorion that was identified by the authors in examining placentas for chronic chorioamnionitis (CC). This study is a retrospective review of cases diagnosed with CHH, describing its incidence alone and with associated lesions, and the immunophenotype of lesional cells. Design In this retrospective study, a laboratory information system search over a 34-month period using the key phrase "chorionic stromal" was performed. Cases identified were reviewed for presence of the following: CC, chronic villitis (CV), chronic deciduitis (CD), maternal (MIR), and fetal (FIR) acute inflammatory responses, meconium deposition; and whether CD3 immunostaining was performed. Incidences were tabulated and compared with known prevalences in our population. Select cases were stained with various immunostains to identify cell lineage and X and Y fluorescent probes to identify fetal or maternal cell origin in cases with male infants. Results Eighty cases of CHH were identified during the study period. Incidences of inflammatory lesions associated with CHH were: CV (54/80, 68%), CD (32/80, 40%), CC (25/80, 31%), MIR (39/80, 49%), and FIR (9/80, 11%). Only chronic inflammatory lesions had a significant correlation with the co-incidence of CHH. CC was identified alongside CHH in 12 of 22 cases in which a CD3 immunostain was performed. The cell population in CHH was vimentin+, CD68+, CD3-, CD45-, CD56-, hPL-, SMA-, OCT 3/4- and, in some cases, variably mixed with CD3+ lymphocytes. The cells had a male genotype by fluorescent in situ hybridization analysis. Conclusion The association of CHH with acute and chronic inflammatory conditions and its immunophenotype suggest that it may be a reactive process. CD3 immunostaining is helpful to identify concurrent CC.
ISSN:1093-5266
DOI:10.1177/1093526616689186