cervical squamous intraepithelial lesions

The role of human papillomavirus infection as etiological factor for cervical squamous intraepithelial lesions and cervical cancer is well established. However, the presence of this virus is not sufficient condition for developing of cervical cancer. Currently, the contribution of other viral, environmental and host cofactors in triggering of this neoplasm is being investigated. Some metabolic risk factors have been associated with the development of several gynecological cancers such as endometrium, ovary and cervix. However, the mechanisms through which these factors contribute to carcinogenesis are complex and not fully elucidated. Few interventions regarding host metabolic factors have been performed on women at risk of developing cervical cancer. Some specific treatments and or changes in lifestyles could be carried out to avoid or delay progression to this kind of cancer. This paper aims to enlarge and update this topic based on the article ¨Association between components of the metabolic syndrome and degree of cervical squamous intraepithelial lesions in Cuban women¨, with emphasis on possible mechanisms that explain the link between central adiposity, insulin resistance and dyslipidemia with risk of premalignant lesions and cervical cancer. 

Introduction: Few studies have explored the vulnerability of women with polycystic ovary syndrome (PCOS) to developing cervical cancer and its precursor lesions. Objective: To describe the clinical, metabolic, and endocrine characteristics of a series of women with cervical squamous intraepithelial lesions and polycystic ovary syndrome, aiming to generate hypotheses regarding the potential pathophysiological mechanisms linking both conditions.Methods: A descriptive and hypothesis-generating study was conducted. The series consisted of nine women with a cytological diagnosis of cervical squamous intraepithelial lesions (SIL) who also met the Rotterdam criteria for PCOS. Characterization included age, sexual behavior, toxic habits, history of hypertension and diabetes mellitus, body mass index (BMI) and waist-to-hip ratio (WHR), metabolic parameters (insulin resistance, dyslipidemia), serum hormone levels (testosterone, prolactin, estradiol), human papillomavirus (HPV) 16/18 infection, grade of the lesion, and PCOS phenotypes. Results: The mean age was 37,11 ± 12,8 years. Abdominal obesity was detected in 55,5% and insulin resistance in 44,4% of cases. Hyperprolactinemia was present in 33,3%. HPV 16/18 infection was identified in 77,7% of cases. Most patients presented high-grade squamous intraepithelial lesions (HSIL) and PCOS phenotype D. Conclusion: The presence of HSIL in more than a third of the women in this case series is compatible with the hypothesis that PCOS, particularly those with insulin resistance, abdominal obesity, or hyperprolactinemia, may act as a multifactorial risk factor for cervical lesions, either independently or synergistically through metabolic and hormonal pathways that interact with HPV. These findings should be interpreted as preliminary observations that warrant confirmation in larger, controlled studies.