Inflammatory markers in women with reported benign gynecologic pathology: an analysis of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.


Journal

Annals of epidemiology
ISSN: 1873-2585
Titre abrégé: Ann Epidemiol
Pays: United States
ID NLM: 9100013

Informations de publication

Date de publication:
04 2022
Historique:
received: 18 05 2021
revised: 14 11 2021
accepted: 01 12 2021
pubmed: 16 12 2021
medline: 6 4 2022
entrez: 15 12 2021
Statut: ppublish

Résumé

Associations between benign gynecologic pathologies and circulating inflammatory markers are unknown. Our goal was to evaluate self-reported history of benign gynecologic pathology and subsequent alterations in systemic inflammation. Using nested case-control studies from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, study-specific associations between self-reported history of benign ovarian cysts, uterine fibroids, and endometriosis with inflammatory marker concentrations were evaluated using logistic regression and combined using meta-analysis. Inflammatory markers associated with individual benign pathologies were mutually adjusted for one another to evaluate independent associations. Compared to women without a self-reported history of the pathology evaluated, benign ovarian cysts were associated with increased PAI-1 (OR [95% CI] 6.24 [2.53-15.39], P <.001) and TGF-β1 (3.79 [1.62-8.86], P =.002) and decreased BCA-1 (0.38 [0.19-0.73], P =.004). Uterine fibroids were associated with decreased CXCL11 (0.37 [0.22-0.63], P <.001) and VEGFR3 (0.40 [0.24-0.65], P <.001). Endometriosis was associated with increased SIL-4R (4.75 [1.84-12.26], P =.001). Self-reported history of benign gynecologic pathologies were associated with alterations in inflammatory markers that have been previously linked to cancer risk. Understanding interactions between benign gynecologic pathologies and the systemic immune system may help inform disease risk later in life.

Sections du résumé

BACKGROUND
Associations between benign gynecologic pathologies and circulating inflammatory markers are unknown. Our goal was to evaluate self-reported history of benign gynecologic pathology and subsequent alterations in systemic inflammation.
METHODS
Using nested case-control studies from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, study-specific associations between self-reported history of benign ovarian cysts, uterine fibroids, and endometriosis with inflammatory marker concentrations were evaluated using logistic regression and combined using meta-analysis. Inflammatory markers associated with individual benign pathologies were mutually adjusted for one another to evaluate independent associations.
RESULTS
Compared to women without a self-reported history of the pathology evaluated, benign ovarian cysts were associated with increased PAI-1 (OR [95% CI] 6.24 [2.53-15.39], P <.001) and TGF-β1 (3.79 [1.62-8.86], P =.002) and decreased BCA-1 (0.38 [0.19-0.73], P =.004). Uterine fibroids were associated with decreased CXCL11 (0.37 [0.22-0.63], P <.001) and VEGFR3 (0.40 [0.24-0.65], P <.001). Endometriosis was associated with increased SIL-4R (4.75 [1.84-12.26], P =.001).
CONCLUSIONS
Self-reported history of benign gynecologic pathologies were associated with alterations in inflammatory markers that have been previously linked to cancer risk. Understanding interactions between benign gynecologic pathologies and the systemic immune system may help inform disease risk later in life.

Identifiants

pubmed: 34906633
pii: S1047-2797(21)00344-6
doi: 10.1016/j.annepidem.2021.12.003
pmc: PMC8972075
mid: NIHMS1779310
pii:
doi:

Types de publication

Journal Article Meta-Analysis Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-8

Subventions

Organisme : Intramural NIH HHS
ID : ZIA CP010128
Pays : United States

Informations de copyright

Copyright © 2021. Published by Elsevier Inc.

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Auteurs

Lauren A King (LA)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD; University of Virginia School of Medicine, Department of Obstetrics and Gynecology, Charlottesville, VA. Electronic address: lak9um@virginia.edu.

Nicolas Wentzensen (N)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.

Mark P Purdue (MP)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.

Hormuzd A Katki (HA)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.

Ligia A Pinto (LA)

Frederick National Laboratory for Cancer Research, National Cancer Institute, Frederick, MD.

Britton Trabert (B)

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.

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Classifications MeSH