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Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome

Anatomopathologic studies have failed to define the fetal inflammatory response syndrome (FIRS) as a cause of fetal death. Here, liver fragments of perinatal autopsies were collected at a university hospital from 1990 to 2009 and classified according to the cause of death, perinatal stress, and gest...

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Autores principales: Pereira, Lívia Helena M., Machado, Juliana R., Olegário, Janaínna G. P., Rocha, Laura P., Silva, Marcos V., Guimarães, Camila S. O., Reis, Marlene A., Castellano, Lúcio Roberto, Ramalho, Fernando S., Corrêa, Rosana R. M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3934536/
https://www.ncbi.nlm.nih.gov/pubmed/24659848
http://dx.doi.org/10.1155/2014/252780
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author Pereira, Lívia Helena M.
Machado, Juliana R.
Olegário, Janaínna G. P.
Rocha, Laura P.
Silva, Marcos V.
Guimarães, Camila S. O.
Reis, Marlene A.
Castellano, Lúcio Roberto
Ramalho, Fernando S.
Corrêa, Rosana R. M.
author_facet Pereira, Lívia Helena M.
Machado, Juliana R.
Olegário, Janaínna G. P.
Rocha, Laura P.
Silva, Marcos V.
Guimarães, Camila S. O.
Reis, Marlene A.
Castellano, Lúcio Roberto
Ramalho, Fernando S.
Corrêa, Rosana R. M.
author_sort Pereira, Lívia Helena M.
collection PubMed
description Anatomopathologic studies have failed to define the fetal inflammatory response syndrome (FIRS) as a cause of fetal death. Here, liver fragments of perinatal autopsies were collected at a university hospital from 1990 to 2009 and classified according to the cause of death, perinatal stress, and gestational age (GA) of the fetus. IL-6, TNF-α, and C-reactive protein (CRP) expression were immunostained, respectively, with primary antibody. Cases with congenital malformation, ascending infection, and perinatal anoxia showed increased IL-6, CRP, and TNF-α, respectively. Prematures presented higher expression of IL-6 whereas term births showed higher expression of CRP. Cases classified as acute stress presented higher expression of IL-6 and TNF-α and cases with chronic stress presented higher expression of CRP. GA correlated negatively with IL-6 and positively with CRP and TNF-α. Body weight correlated negatively with IL-6 and positively with CRP and TNF-α. Despite the diagnosis of FIRS being clinical and based on serum parameters, the findings in the current study allow the inference of FIRS diagnosis in the autopsied infants, based on an in situ liver analysis of these markers.
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spelling pubmed-39345362014-03-23 Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome Pereira, Lívia Helena M. Machado, Juliana R. Olegário, Janaínna G. P. Rocha, Laura P. Silva, Marcos V. Guimarães, Camila S. O. Reis, Marlene A. Castellano, Lúcio Roberto Ramalho, Fernando S. Corrêa, Rosana R. M. Dis Markers Research Article Anatomopathologic studies have failed to define the fetal inflammatory response syndrome (FIRS) as a cause of fetal death. Here, liver fragments of perinatal autopsies were collected at a university hospital from 1990 to 2009 and classified according to the cause of death, perinatal stress, and gestational age (GA) of the fetus. IL-6, TNF-α, and C-reactive protein (CRP) expression were immunostained, respectively, with primary antibody. Cases with congenital malformation, ascending infection, and perinatal anoxia showed increased IL-6, CRP, and TNF-α, respectively. Prematures presented higher expression of IL-6 whereas term births showed higher expression of CRP. Cases classified as acute stress presented higher expression of IL-6 and TNF-α and cases with chronic stress presented higher expression of CRP. GA correlated negatively with IL-6 and positively with CRP and TNF-α. Body weight correlated negatively with IL-6 and positively with CRP and TNF-α. Despite the diagnosis of FIRS being clinical and based on serum parameters, the findings in the current study allow the inference of FIRS diagnosis in the autopsied infants, based on an in situ liver analysis of these markers. Hindawi Publishing Corporation 2014 2014-02-10 /pmc/articles/PMC3934536/ /pubmed/24659848 http://dx.doi.org/10.1155/2014/252780 Text en Copyright © 2014 Lívia Helena M. Pereira et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Pereira, Lívia Helena M.
Machado, Juliana R.
Olegário, Janaínna G. P.
Rocha, Laura P.
Silva, Marcos V.
Guimarães, Camila S. O.
Reis, Marlene A.
Castellano, Lúcio Roberto
Ramalho, Fernando S.
Corrêa, Rosana R. M.
Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome
title Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome
title_full Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome
title_fullStr Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome
title_full_unstemmed Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome
title_short Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome
title_sort interleukin-6 and c-reactive protein are overexpressed in the liver of perinatal deaths diagnosed with fetal inflammatory response syndrome
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3934536/
https://www.ncbi.nlm.nih.gov/pubmed/24659848
http://dx.doi.org/10.1155/2014/252780
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