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      Acute Chorioamnionitis and Funisitis: Definition, Pathologic Features, and Clinical Significance


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          Acute inflammatory lesions of the placenta consist of diffuse infiltration of neutrophils at different sites in the organ. These lesions include acute chorioamnionitis, funisitis, and chorionic vasculitis, and represent a host response (maternal or fetal) to a chemotactic gradient in the amniotic cavity. While acute chorioamnionitis is evidence of a maternal host response, funisitis and chorionic vasculitis represent fetal inflammatory responses. Intra-amniotic infection has been generally considered to be the cause of acute histologic chorioamnionitis and funisitis; however, recent evidence indicates that “sterile” intra-amniotic inflammation, which occurs in the absence of demonstrable microorganisms but can be induced by “danger signals”, is frequently associated with these lesions. In the context of intra-amniotic infection, chemokines (such as interleukin-8 and granulocyte chemotactic protein) establish a gradient favoring the migration of neutrophils from maternal or fetal circulation into the chorioamniotic membranes or umbilical cord, respectively. Danger signals released during the course of cellular stress or cell death can also induce the release of neutrophil chemokines. The prevalence of chorioamnionitis is a function of gestational age at birth, and is present in 3-5% of placentas delivered at term, but in 94% of placentas delivered between 21-24 weeks of gestation. The frequency is higher in patients with spontaneous labor, preterm labor, clinical chorioamnionitis (preterm or term), or ruptured membranes. Funisitis and chorionic vasculitis are the hallmarks for the fetal inflammatory response syndrome, a condition characterized by an elevation in fetal plasma concentrations of interleukin-6, associated with the impending onset of preterm labor, a higher rate of neonatal morbidity (after adjustment for gestational age), and multi-organ fetal involvement. This syndrome is the counterpart of the systemic inflammatory response syndrome in adults; however, in fetuses, it is a risk factor for short- and long-term complications (i.e. neonatal sepsis, bronchopulmonary dysplasia, periventricular leukomalacia, and cerebral palsy). This article reviews the definition, pathogenesis, grading and staging, and clinical significance of the most common lesions in placental pathology. Illustrations of the lesions and diagrams of the mechanisms of disease are provided.

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          Author and article information

          Am J Obstet Gynecol
          Am. J. Obstet. Gynecol.
          American journal of obstetrics and gynecology
          26 October 2015
          October 2015
          01 October 2016
          : 213
          : 4 0
          : S29-S52
          [1 ] Department of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea
          [2 ] Perinatology Research Branch, Program for Perinatal Research and Obstetrics, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD and Detroit, MI, USA
          [3 ]Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI, USA
          [4 ]Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI, USA
          [5 ]Department of Molecular Obstetrics and Genetics, Wayne State University, Detroit, MI, USA
          [6 ]Department of Obstetrics and Gynecology, Wayne State University, Detroit, Michigan, USA
          [7 ]Department of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Korea
          [8 ]Department of Pathology, Haeundae Paik Hospital, Inje University College of Medicine, Busan Korea
          Author notes
          Address correspondence to: Roberto Romero, MD, D. Med. Sci, Perinatology Research Branch, NICHD/NIH/DHHS, Wayne State University/Hutzel Women's Hospital, 3990 John R, Box 4, Detroit, MI 48201, USA, Telephone: (313) 993-2700, Fax: (313) 993-2694, romeror@ 123456mail.nih.gov
          PMC4774647 PMC4774647 4774647 nihpa719305

          clinical chorioamnionitis,chorionic vasculitis,ascending intra-amniotic infection,acute villitis,sterile inflammation,staging,prematurity,pregnancy,placental pathology,pathologic grading,nosology,microbial invasion of the amniotic cavity,interleukin (IL)-8,granulocyte chemotactic protein,fetal inflammatory response syndrome,CXCL6


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