1. Introduction
Endometriosis is a chronic, benign gynecological illness associated with infertility and pelvic pain. Despite having insufficient epidemiological data, it affects approximately 10% of
women in their reproductive age [1]. Endometriosis seems to be asymptomatic in one-third of affected females but markedly found to reduce the wellbeing of infected individuals [2].
Endometriosis is involved in several immune-mediated events associated with the atherogenic lipid profile, heightened oxidative stress, and systemic inflammation [2, 3]. Various mechanisms are involved in the upregulation of inflammatory gene activation and dysregulation of hormone receptors. The elevated levels of these circulating markers for each of these processes have been observed in the serum as well as the peritoneal fluid of females with endometriosis compared with healthy subjects [4, 5]. It has been suggested that the markers of reactive oxygen species and oxidative stress are involved in several diseases like autoimmune disorders, chronic systematic comorbidities, and rheumatoid arthritis [6]. On account of a comparable process, it has been proposed that endometriosis could be associated with harmful effects on other body functions [7]. Knowing the association between endometriosis and systemic inflammation [8–10], it has been proposed that endometriosis may prompt these patients to a variety of disorders including multiple cancers, atherosclerosis, and inflammatory and endocrine disorders later in life [11].
