RESUMEN
Objectives: To determine the association between ovarian endometriomas and stage of endometriosis. Methods: A total of 222 women aged 18-55 years old, who underwent minimally invasive surgery between January 2016 and December 2021 for treatment of endometriosis were included in the study. Patients underwent laparoscopic and/or robotic treatment of endometriosis by a single surgeon (FRN) and were staged using the ASRM revised classification of endometriosis. Pre-operative imaging studies, and operative and pathology reports were reviewed for the presence of endometriomas and the final stage of endometriosis. Using univariate analyses for categorical variables and the two-sample t-test or Mann-Whitney test for continuous data, association between endometriomas, stage of endometriosis, type of endometrioma, and other patient parameters such as age, gravidity, parity, laterality of endometriomas, prior medical treatment, and indication for surgery was analyzed. Results: Of the 222 patients included in the study, 86 patients had endometrioma(s) and were found to have stage III-IV disease. All 36 patients with bilateral endometriomas and 70% of patients with unilateral endometriomas had stage IV disease. Conclusions: The presence of ovarian endometrioma(s) indicates a higher stage of disease, correlating most often with stage IV endometriosis. Understanding the association between endometriomas and anticipated stage of disease can aid in appropriate pre-operative planning and patient counseling.
RESUMEN
Human airway smooth muscle (HASM) cells are a rich source of inflammatory mediators that may propagate the airway inflammatory responses. Recent studies from our laboratory and others demonstrate that HASM cells express the proallergic cytokine thymic stromal lymphopoietin (TSLP) in vitro and in vivo. Compelling evidence from in vitro studies and animal models suggest that the TSLP is a critical factor sufficient and necessary to induce or maintain the allergic airway inflammation. Despite of an immense interest in pathophysiology of TSLP in allergic inflammation, the triggers and mechanisms of TSLP expression remain inadequately understood. In this study, we found that TNF-α upregulates the TSLP mRNA and induces high levels of TSLP protein release in primary human ASM cells. Interestingly, TNF-α induced the TSLP promoter activity (P < 0.05; n = 4) in HASM that was mediated by upstream NF-κB and activator protein-1 (AP-1) binding sites. Mutation in NF-κB and AP-1 binding sites completely abrogated the effect of TNF-α-mediated TSLP promoter activity and so did the expression of a dominant-negative mutant construct of IκB kinase. Furthermore, the peptide inhibitors of IκB kinase or NF-κB inhibited the TNF-α-induced TSLP protein release (P < 0.05; n = 3) in HASM. Collectively, our data suggest a novel important biological role for NF-κB pathway in TNF-α-induced TSLP expression in HASM and recommend this as a prime target for anti-inflammatory drugs.