The aim of this study was to provide a clinical reference for the acute postoperative changes to lipids and inflammation following premenopausal hysterectomy with bilateral oophorectomy and compare them to normal reference values.
Design
The study design was a planned secondary analysis of data from a randomized double-blind trial comparing the effectiveness of two different hormone therapies for preventing post-oophorectomy bone loss and controlling vasomotor symptoms. These data were obtained on hospital discharge before randomization to treatment.
Materials and Methods
Premenopausal women scheduled for a hysterectomy with bilateral oophorectomy for benign reasons were identified from preoperative lists and approached, prior to hospital discharge, to participate in this study. Postoperative data were compared with premenopausal reference intervals using Z scores.
Results
Thirty-three (33) women (mean age 45 ± 4.8 years) were studied an average of 7 days postsurgery. Hemoglobin, albumin, testosterone, and high-density lipoprotein values were decreased in comparison to the normal mean, having Z scores of −3.0, −2.5, −2.4, and −1.7, respectively. C-reactive protein levels were quite significantly elevated (Z score = 20.3).
Conclusions
The high levels of inflammation and abnormal lipids postsurgical menopause are important considerations for physicians when planning subsequent treatment and care. (J GYNECOL SURG 27:9)
premenopausal hysterectomy bilateral oophorectomy lipid changes, Prior JC surgical menopause inflammation markers, acute postoperative changes serum lipids after oophorectomy, C-reactive protein elevation after hysterectomy bilateral oophorectomy, surgical menopause HDL cholesterol testosterone changes, premenopausal oophorectomy hormonal values postoperative, hysterectomy benign reasons metabolic consequences premenopausal women, post-oophorectomy bone loss hormone therapy randomized trial, albumin hemoglobin decrease after gynecologic surgery, planned secondary analysis oophorectomy lipid inflammation
DOI 10.1089/gyn.2009.0098 10.1089/gyn.2009.0098 Kalyan et al. 2011, Kalyan 2011
Cite this article
Hitchcock, C. L., M, Pudek, M., & Prior, J. C. (2011). Acute effects of premenopausal hysterectomy with bilateral oophorectomy on serum lipids, hormonal values, inflammatory markers and metabolism. Journal of gynecologic surgery, 27(1), 9-15. https://doi.org/10.1089/gyn.2009.0098
Hitchcock CL, M, Pudek M, Prior JC. Acute effects of premenopausal hysterectomy with bilateral oophorectomy on serum lipids, hormonal values, inflammatory markers and metabolism. Journal of Gynecologic Surgery. 2011;27(1):9-15. doi:10.1089/gyn.2009.0098
Hitchcock, Christine L., et al. "Acute effects of premenopausal hysterectomy with bilateral oophorectomy on serum lipids, hormonal values, inflammatory markers and metabolism." Journal of gynecologic surgery, vol. 27, no. 1, 2011, pp. 9-15.
The present study investigated the role of melatonin (MT) in regulating mitochondrial function via sirtuin 3 (SIRT3) in granulosa cells (GCs) from patients with polycystic ovary syndrome (PCOS), with a focus on mitochondrial protection. Notably, GCs isolated from patients with PCOS exhibited mitochondrial dysfunction. Using an in vitro PCOS model established by treating KGN cells with dihydrotestosterone (DHT), decreased SIRT3 expression, dysregulated mitochondrial dynamics and hyperactivation of mitophagy were observed. Both SIRT3 overexpression and MT treatment restored the mitochondrial membrane potential, rebalanced mitochondrial dynamics and suppressed excessive autophagy in DHT-treated cells. Additionally, MT levels were shown to be reduced in the follicular fluid of patients with PCOS. Notably, the protective effects of MT on proteins associated with both mitochondrial dynamics and autophagy were abolished upon SIRT3 inhibition. In conclusion, mitochondrial dysfunction and aberrant mitophagy in GCs may serve a role in the pathogenesis of PCOS. MT appears to ameliorate these defects by modulating mitochondrial dynamics and function in a SIRT3-dependent manner. Moreover, the current study identified SIRT3 as a key molecular target of MT in PCOS.
Background Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine-metabolic disorder characterized by reproductive, hormonal, and metabolic disturbances. This study aimed to evaluate the association between clinical features, anthropometric indices, hormonal parameters, metabolic profile, ultrasonographic findings, and the second-to-fourth digit (2D:4D) ratio in women with PCOS compared to age-matched healthy controls. Methods A case-control study was conducted, including women diagnosed with PCOS and age-matched healthy controls. Clinical features, anthropometric measurements (BMI, waist-hip ratio (WHR), waist-height ratio (WHtR)), hormonal parameters (luteinizing hormone (LH), follicle-stimulating hormone (FSH), anti-Müllerian hormone (AMH)), metabolic variables (fasting glucose, lipid profile), ultrasonographic findings, and 2D:4D digit ratio were assessed. Statistical analysis was performed using appropriate tests, and a p-value < 0.05 was considered statistically significant. Results Women with PCOS exhibited a significantly higher prevalence of menstrual irregularity, polycystic ovarian morphology, hirsutism, and acne (p < 0.001). Hormonal analysis showed significantly elevated LH, FSH, and AMH levels in PCOS cases (p < 0.001). Anthropometric indices, including BMI, WHR, and WHtR, were significantly higher among PCOS cases (p < 0.01), indicating increased general and central adiposity. In contrast, fasting glucose and lipid profile levels did not differ significantly between groups. Additionally, the 2D:4D ratio was significantly lower in PCOS cases (p < 0.01) and showed significant negative correlations with BMI, WHR, WHtR, and cholesterol levels. Conclusion The study demonstrates that PCOS is associated with significant hormonal dysregulation, central obesity, and early metabolic alterations. The lower 2D:4D ratio observed in PCOS supports the role of prenatal androgen exposure in disease pathogenesis. These findings highlight the complex interplay between developmental, metabolic, and endocrine factors in PCOS and underscore the importance of early identification and comprehensive management strategies.
What is the association between endometriosis and the type and age of menopause? Women with endometriosis had a 7-fold increased risk of undergoing surgical menopause rather than natural menopause and were more likely to experience premature or early menopause, both surgically and naturally. Endometriosis is associated with reduced ovarian reserve, but evidence on its relationship with the type of menopause (surgical vs natural) and timing (especially premature and early menopause) is limited. Women with endometriosis are more likely to undergo hysterectomy and/or oophorectomy (either unilateral or bilateral), but the average age of these surgeries remains unclear. STUDY DESIGN, SIZE, The study analysed individual-level data from 279 948 women in five cohort studies conducted in the UK, Australia, Sweden, and Japan between 1996 and 2022. PARTICIPANTS/MATERIALS, SETTING, Women whose menopause type and age could not be determined due to premenopausal hysterectomy with ovarian preservation or use of menopausal hormone therapy were excluded. Endometriosis was identified through self-reports and administrative data. Surgical menopause was defined as premenopausal bilateral oophorectomy. Fine-Gray subdistribution hazard models estimated hazard ratios (HRs) for surgical and natural menopause. Age at menopause was determined by the ages at the final menstrual period or bilateral oophorectomy. Linear regression assessed mean differences in menopause age, while multinomial logistic regression estimated odds ratios (ORs) for categorical menopause age: <40 (premature), 40-44 (early), 45-49, 50-51 (reference), 52-54, and ≥55 years. Spontaneous premature ovarian insufficiency (POI) was defined as natural menopause before age 40 years. MAIN Endometriosis was identified in 3.7% of women. By the end of follow-up, 7.9% had surgical menopause and 58.2% experienced natural menopause. Using a competing risk model, women with endometriosis had a 7-fold increased risk of surgical menopause (HR: 7.54, 95% CI 6.84, 8.32) and were less likely to experience natural menopause (HR: 0.40, 95% CI 0.33, 0.49). On average, surgical menopause occurred 1.6 years (19 months) earlier (β: -1.59, 95% CI -1.77, -1.42) in women with endometriosis. Among women who experienced natural menopause, it was 0.4 years (5 months) earlier (β: -0.37, 95% CI -0.46, -0.28) for those with endometriosis. Women with endometriosis were twice as likely to experience premature surgical menopause (<40 years) (OR: 2.11, 95% CI 2.02, 2.20) or 1.4 times more likely to develop spontaneous POI (OR: 1.36, 95% CI 1.17, 1.59). They were also at increased odds of early surgical and natural menopause (40-44 years). LIMITATIONS, This study could not differentiate between subtypes and stages of endometriosis or assess treatments for ovarian endometrioma, which may impact ovarian reserve. Self-reported menopause type and age could introduce recall bias. Given the consistent findings across individual studies, our results are likely to be generalizable to different populations, highlighting the need for tailored management of endometriosis to prevent medically induced or premature menopause. Long-term monitoring of women with endometriosis is recommended, given their elevated risk of surgical menopause and premature or early menopause, which are associated with adverse health outcomes in later life. STUDY FUNDING/COMPETING INTEREST(S): The InterLACE Consortium is funded by the Australian National Health and Medical Research Council project grant (APP1027196) and Centres of Research Excellence (APP1153420). G.D.M. is funded by the Australian National Health and Medical Research Council Leadership Fellowship (APP2009577). This research is funded in part by the Japan Society for the Promotion of Science (JSPS 19KK0235, 23KK0167). The authors have no conflict of interest. Where authors are identified as personnel of the International Agency for Research on Cancer or WHO, the authors alone are responsible for the views expressed in this article, and they do not necessarily represent the decisions, policy, or views of the International Agency for Research on Cancer or WHO. N/A.
Senthilkumar H et al., 2025·Journal of translational medicine
Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects reproductive-aged women worldwide, causing hormonal imbalances and ovarian dysfunction. PCOS affects metabolic health and increases the risk of obesity, insulin resistance, and cardiovascular disease, in addition to infertility. This review delves deeper into the connections of gut microbiota with PCOS pathophysiology, particularly into its impact on hormone metabolism, obesity, inflammation, and insulin resistance by way of short-chain fatty acids, lipopolysaccharides, and gut-brain axis. Studies also show that changes in the metabolic processes and immune responses are seen in changes in the gut microbiota in PCOS subjects, such as changes in the Bacteroidetes and Firmicutes groups. Some bacteria, like Escherichia and Shigella, have been associated with dysbiosis in patients with PCOS, leading to systemic inflammation and changed hormone levels, which further worsen the clinical symptoms. Therapeutic interventions targeting the gut microbiota comprise probiotics, prebiotics, and fecal microbiota transplantation; these have potential to alleviate the symptoms of PCOS. Other precision microbiome-based therapies include postbiotics, and CRISPR-Cas9 genome editing, which are relatively new avenues toward precision treatment. This complex interlink of gut microbiota and PCOS pathophysiology will open the avenues for possible treatments for hormonal imbalances and metabolic problems that characterize these complex disorders. The review here focuses on the requirement of further studies to be able to elucidate the specific pathways relating gut microbiota dysregulation to PCOS and, thus, improve microbiome-based therapies for better clinical outcomes in affected individuals.