Abstract
BackgroundInflammation is emerging as a potential mechanism of cervical carcinogenesis. However, few studies have investigated the association between host inflammatory status and the natural course of cervical precursor lesion. The aim of this study was to assess the probability of LSIL regression, associated with an inflammatory biomarker, high-sensitivity C-reactive protein (hs-CRP).MethodsIn a longitudinal cohort study, female participants were examined annually or biannually using cervical cytology between 2006 and 2015. Incident LSIL cases were included in the analysis, with regression defined as at least one consecutive normal cytologic result. A total of 520 women aged 22–64 years were followed up for LSIL regression. The multivariable-adjusted hazard ratios (HRs) for LSIL regression were estimated using a parametric proportional hazards model.ResultsDuring 827.5 person-years of follow-up, 486 out of 520 subjects (93.5%) showed LSIL regression. After adjusting several important potential confounders, a higher quartile of hs-CRP levels was significantly associated with a lower rate of regression (for quartile 4 vs quartile 1, inverse HR 1.33; 95% CI, 1.04–1.69; P for trend = 0.028).ConclusionsThe low rate of spontaneous regression recorded in women with higher hs-CRP lends support to the role of the perturbated host inflammatory status in cervical carcinogenesis, and suggests that hs-CRP level could help monitor LSIL.
Highlights
Cervical infection with high-risk types of human papillomavirus (HPV) is the cause of most cervical cancers and their precursors.[1]
Glucose, and homeostatic model assessment of insulin resistance (HOMA-IR) were positively associated with the high-sensitivity C-reactive protein (hs-CRP) level
After adjusting for age, the year of a screening exam, smoking status, alcohol intake, marital status, education level, HPV infection, and history of diabetes, inverse hazard ratios (HRs) for Low-grade squamous intraepithelial lesion (LSIL) regression comparing quartiles 2–4 vs quartile 1 of hs-CRP, were 1.00, 1.05, and 1.33, respectively (P for trend = 0.03)
Summary
Cervical infection with high-risk types of human papillomavirus (HPV) is the cause of most cervical cancers and their precursors.[1]. Inflammation has emerged as a potential mechanism of cancer development,[18,19,20] including cervical cancer.[21,22] Recently, a gene signature for low-grade inflammatory status, which is an intermediate state between tissue homeostasis and classic inflammation,[23] was found in several cancers, suggesting that inflammatory status plays a role in carcinogenesis.[24] In cervical cancer, only a few studies have explored the associations between systemic[25,26,27,28,29,30] or cervical (local) inflammation[31,32,33,34] and the risk of persistent HPV infection and=or cervical precursor progression, exhibiting a positive correlation.[25,26,27,28,29,30,31,32,33,34] the evaluation of Address for correspondence. The aim of this study was to assess the probability of LSIL regression, associated with an inflammatory biomarker, high-sensitivity C-reactive protein (hs-CRP)
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