{"paper_id":"b512f48c-32f0-4da2-97a4-436904dc9b33","body_text":"Clin. Exp. Obstet. Gynecol. 2025; 52(12): 44674\nhttps://doi.org/10.31083/CEOG44674\nCopyright: © 2025 The Author(s). Published by IMR Press.\nThis is an open access article under the CC BY 4.0 license .\nPublisher’s Note: IMR Press stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.\nReview\nPost-Hysterectomy Ovarian Consequences: Mechanisms, Risks, and\nClinical Management Strategies—A Narrative Review\nYijun Chen1\n , Ling Min 2,*\n1Department of Gynecology and Obstetrics, Meishan Women and Children’s Hospital, Sichuan University, 620010 Meishan, Sichuan, China\n2Department of Gynecology and Obstetrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education,\nWest China Second Hospital, Sichuan University, 610041 Chengdu, Sichuan, China\n*Correspondence: dipper2001@163.com (Ling Min)\nAcademic Editor: Michael H. Dahan\nSubmitted: 9 July 2025 Revised: 29 August 2025 Accepted: 26 September 2025 Published: 25 December 2025\nAbstract\nObjective(s): To examine the mechanisms underlying changes in ovarian function after total hysterectomy, identify relevant risk factors,\nand summarize clinical management strategies for such changes. Mechanism: The pathogenesis of impaired ovarian function post-\ntotal hysterectomy involves three key pathways: (1) reduced ovarian blood supply due to uterine artery ligation; (2) neuroendocrine\nimbalance caused by abnormal gonadotropin levels; (3) oxidative stress and fibrosis induced by chronic inflammation. Findings in\nBrief: Total hysterectomy is associated with diminished ovarian reserve, including a 20–30% decrease in anti-Müllerian hormone (AMH),\nelevated serum follicle-stimulating hormone (FSH) levels, and an approximate 3–4-year acceleration of menopause. Risk factors include\nthe surgical approach (e.g., laparoscopic electrocoagulation decreases AMH by 40% vs. 20% with open surgery), unilateral ovarian\npreservation (increases the risk of menopause by 2.93-fold compared to bilateral preservation), and age <40 years (increases the risk of\npostoperative ovarian failure). Conclusions: Personalized clinical management, including preoperative assessment of AMH levels and\novarian blood flow, preference for ovarian and uterine artery-preserving techniques (e.g., STHMUV , uterine blood supply-preserving\nhysterectomy technique), and postoperative hormone/pelvic floor function monitoring may mitigate damage to ovarian function. To\noptimize long-term outcomes, future research should focus on vasoprotective strategies and precision interventions guided by biomarkers.\nKeywords: hysterectomy; ovarian function; ovarian reserve; anti-Müllerian hormone (AMH); premature menopause; surgical approach\n1. Introduction\n1.1 Background\nTotal hysterectomy is one of the most important surgi-\ncal procedures in many gynecologic conditions [ 1]. How-\never, changes in ovarian function after surgery (such as\nearly menopause and hormonal disorders) can have sig-\nnificant impacts on the reproductive and long-term health\nof women, including cardiovascular and cognitive issues\n[2,3]. There is currently a need for systematic integration\nof research on the mechanisms, risk stratification, and man-\nagement strategies for total hysterectomy.\n1.2 Objectives\nThe aims of this study were to elucidate the pathophys-\niological mechanisms underlying ovarian dysfunction fol-\nlowing total hysterectomy, systematically evaluate the clin-\nical evidence and epidemiological characteristics of postop-\nerative ovarian dysfunction, identify key risk factors affect-\ning postoperative ovarian function, and provide evidence-\nbased management strategies for preserving ovarian func-\ntion and improving long-term health outcomes after total\nhysterectomy.\n2. Methods\nArticles were identified via searches of Embase,\nPubMed, and Web of Science from each database’s in-\nception to June 2025, supplemented by manual screen-\ning of reference lists. The computerized search included\nonly English-language articles, using the keyword com-\nbination: “Hysterectomy” paired with “Ovarian function”\nor “Ovarian Reserve”, and supplemented by “premature\nmenopause”, “surgical approach”, “AMH/anti-Müllerian\nhormone”, etc.\nThis strategy initially yielded 383 records. After\nremoving duplicates, we focused on screening for meta-\nanalyses and clinical studies, while excluding abstracts (in-\ncomplete data) and review articles (non-original research);\nfinally, 39 eligible studies were selected, categorized as fol-\nlows: 7 on pathophysiologic mechanisms, 24 on clinical ev-\nidence and symptoms, and 8 on risk factors related to post-\nhysterectomy ovarian consequences.\n3. Pathophysiologic Mechanisms of Ovarian\nDysfunction After Total Hysterectomy\n3.1 Decreased Blood Supply and V ascular Damage\nThe uterine artery contributes approximately 50–70%\nof the blood supply to the ovary. Multiple studies using\nDoppler ultrasound have reported elevated resistance in-\n\ndex (RI) and pulsatility index (PI) post-hysterectomy, along\nwith reduced peak flow velocity (PSV) in the ovarian arter-\nies. These findings imply a diminished blood supply, pos-\nsibly due to direct vessel injury or induction of thrombo-\nsis by the surgical procedures. Halmesmäki et al . (2007)\n[4] reported the results of a randomized controlled trial (n\n= 107) in which post-operative pelvic ultrasound revealed\nsignificant alterations in ovarian blood flow. Specifically,\nthe PI showed a significant decrease ( p = 0.01), poten-\ntially due to vascular dilation as a consequence of sur-\ngical tissue trauma. Lee et al . (2010) [ 5] conducted a\nprospective cohort study (evidence level II) comprising 32\npatients who underwent hysterectomy and 21 control pa-\ntients. Three months after hysterectomy with bilateral ovar-\nian preservation, they found no significant changes in ovar-\nian artery blood flow indices (PI, RI) using transvaginal\nDoppler ultrasound, and no change in anti-Müllerian hor-\nmone (AMH) level using the Enzyme-Linked Immunosor-\nbent Assay (ELISA) method. Furthermore, no differences\nwere found between the laparoscopically-assisted vaginal\nhysterectomy (LA VH) and total abdominal hysterectomy\n(TAH) groups. An animal model showed a 32% absolute\nreduction in endothelium-dependent vasodilatory function\nafter ovariectomy, with impaired small-conductance Ca 2+-\nactivated K + (SK3) channels activity suggested to be the\nkey mechanism [6].\n3.2 Imbalance of Neuroendocrine Regulation\nThe uterus and ovaries are interconnected via the\nhypothalamic-pituitary-ovarian (HPO) axis and the auto-\nnomic nervous system (ANS). This regulatory balance be-\ntween the HPO and ANS can be disrupted following hys-\nterectomy. Postoperative changes include significant in-\ncreases in the levels of follicle-stimulating hormone (FSH)\nand luteinizing hormone (LH), along with a decrease in\nestradiol (E2), indicating ovarian hypoplasia. These hor-\nmonal shifts are most notable 3–6 months after surgery\nand may result from reduced negative feedback by ovarian\nsteroid hormones. Increased levels of sympathetic nerve\nactivity trigger the toll-like receptor 4 (TLR4)/Nucleotide-\nbinding oligomerization domain-like receptor protein 3\n(NLRP3) inflammasome pathway, resulting in the release\nof Interleukin-1 beta (IL-1 β),Interleukin-18 (IL-18), and\nother pro-inflammatory factors, thus accelerating follicular\natresia. Concurrently, diminished parasympathetic inhibi-\ntion intensifies the inflammatory cascade, while decreased\nexpression of estrogen receptors (ERα/β) reduces follicular\nsensitivity to gonadotropins, impairing follicular develop-\nment [7].\n3.3 Inflammatory Response and Oxidative Stress\nSurgical trauma can elicit sustained inflammatory re-\nsponses, fostering a pro-aging milieu. Inflammaging, de-\nnoted by chronic low-grade inflammation, is a pivotal fac-\ntor in ovarian senescence, influencing oxidative stress, fi-\nbrosis, and immune cell infiltration [ 8,9]. Elevated levels\nof ovarian oxidative stress driven by chronic inflammation\ncan impede follicular maturation and development, thereby\naccelerating the depletion of ovarian reserve and egg quality\n[8–10]. Furthermore, chronic inflammation is associated\nwith ovarian fibrosis, which disrupts the tissue architecture\nand compromises follicular growth. In addition, chronic in-\nflammation exacerbates apoptosis and DNA damage during\novarian aging through molecular mechanisms such as acti-\nvation of the NLRP3 inflammasome [ 7].\n4. Clinical Evidence and Epidemiological\nCharacteristics of Ovarian Dysfunction After\nTotal Hysterectomy\n4.1 Increased Risk of Early Menopause\nFollowing a total hysterectomy, patients may enter\nmenopause 3–4 years earlier. Siddle et al . (1987) [ 11]\nfound that hysterectomy was associated with an earlier on-\nset of ovarian failure compared to natural menopause (mean\nage: 45.4 ± 4.0 years vs. 49.5 ± 4.04 years, p < 0.001).\nAhn et al. (2002) [ 12] also reported that hysterectomy was\nassociated with a younger age at menopause (46.3 ± 3.0 vs.\n48.1 ± 3.2 years, p < 0.001). Farquhar et al. (2005) [ 13]\ncompared 257 women who underwent hysterectomy with\novarian preservation to 259 controls with intact uteri. These\nauthors found that hysterectomy advances ovarian failure\nby 3.7 years, and women who had a hysterectomy entered\nmenopause (FSH >40 IU/L) 3 years earlier than the con-\ntrols (95% confidence interval [CI]: 1.5–6.0). By 5 years\nafter surgery, 20.6% of hysterectomy patients had reached\nmenopause (95% CI: 6.8%) compared to only 7.3% of con-\ntrols ( p < 0.0001). Women who had unilateral oophorec-\ntomy (n = 28) were more likely to have reached menopause\n(35.7%) within 5 years, and they also reached menopause\n4.4 years earlier than women with bilateral ovarian preser-\nvation (95% CI: 0.6–7.9). In a prospective cohort study\nof 871 patients, Moorman et al. (2011) [ 14] demonstrated\nthat the 4-year cumulative incidence of ovarian failure was\n14.8% (60/406) in the hysterectomy group compared to\n8.0% (46/465) in the control group, with an adjusted hazard\nratio (HR) of 1.92 (95% CI: 1.29–2.86). These results sug-\ngest that hysterectomy is associated with an approximate\n2-fold increase in the likelihood of ovarian failure.\n4.2 Ovarian Reserve and Blood Supply Damage\nSince the uterine artery provides 50–70% of the blood\nsupply to the ovaries, surgical severance results in ischemic\ndamage to these organs. Postoperative Doppler ultrasound\nshowed elevated ovarian artery RI and PI, and decreased\nPSV , suggesting decreased blood supply [15]. Tapisiz et al.\n(2008) [16] examined histopathological changes in ovarian\ntissues after hysterectomy in a rat model. These authors\nobserved a 50% reduction in primordial follicle number ( p\n= 0.01), and a 300% increase in atretic follicle number ( p\n= 0.02). Hu et al. (2006) [ 17] found that hysterectomy af-\n2\n\n\nfected the ovarian vasculature and gland function in women\naged 32–45 years. A transient increase in Vmax was ob-\nserved 5 days after surgery (26.47 vs. 22.00 cm/s,p < 0.01),\nfollowed by a decline to 17.20–17.60 cm/s at 1–3 months (p\n< 0.001). A gradual increase in PI from 1.45 to 1.77 ( p <\n0.05) was also observed, suggesting a long-term decrease\nin blood flow.\n4.3 Changes in Serum Hormone Markers\n4.3.1 Serum Anti-Müllerian Hormone\nAMH is produced by small antral follicles and is the\nmost reliable circulating marker of ovarian reserve. Fol-\nlowing total hysterectomy, the concentration of AMH may\ndecline by 20–30%, and even more in patients with low\nreserve. Atabekoğlu et al . (2012) [ 18] reported that total\nhysterectomy resulted in a larger decrease in the ovarian re-\nserve, as measured by AMH level, at 4 months after surgery.\nSpecifically, the AMH level decreased by 30% more than\nin the controls. A prospective cohort study by Trabuco et\nal. (2016) [ 19] showed that hysterectomy resulted in a sig-\nnificant decrease of almost 20% in the AMH level at 1 year\ncompared with the control group. The hysterectomy group\nalso exhibited a significantly greater fall in AMH (–40.7%\nvs. 20.9%, p < 0.001), and a higher rate of undetectability\n(12.8% vs. 4.7%, p < 0.02). The postoperative decrease in\nAMH was 0.77 times greater than in the control group ( p <\n0.001). The low reserve group (AMH ≤1.2 ng/mL) showed\na greater decline in AMH in the hysterectomy group than\ncontrols (58.3% vs. 19.1%, p < 0.003), with 24.6% having\nundetectable postoperative AMH. In the high reserve group\n(AMH >1.2 ng/mL), the decline in AMH was not signifi-\ncantly different to controls (34.4% vs. –21.2%, p = 0.06),\nbut AMH was still lower (0.81-fold, p < 0.003). In a meta-\nanalysis of 14 studies with a total of 1457 women, Huang et\nal. (2023) [ 20] found significantly lower AMH levels in the\nhysterectomy group than the control group, with a weighted\nmean difference (WMD) of –0.56 (95% CI: –0.72 to –0.39,\np < 0.0001).\n4.3.2 Serum Follicle Stimulating Hormone\nSerum FSH levels are significantly elevated in pa-\ntients after hysterectomy. Huang et al . (2023) [ 20] re-\nported significantly elevated FSH levels in the hysterec-\ntomy group compared to the control group (WMD = 2.96,\n95% CI: 1.47–4.44, p < 0.001). Maiti et al . (2018) [ 21]\nfound that 1 year after hysterectomy, patients had signif-\nicantly increased serum FSH from baseline (7.5 IU/L to\n12.3 IU/L), as well as a significant ( p < 0.05) decrease in\novarian volume and PI, suggesting decreased blood flow\nwith atrophy. After 1 year, 20% had FSH >20 IU/L, indi-\ncating perimenopausal transition, while 5% had FSH >40\nIU/L, indicating menopausal transition. Cooper and Thorp\n(1999) [22] reported a strong association between hysterec-\ntomy and elevated serum FSH level ( >20 IU/L). Patients\nwith unilateral oophorectomy had 2.4-fold higher odds of\nelevated FSH ( >20 IU/L) compared to those with bilateral\novarian preservation (OR = 2.4, 95% CI: 1.3–4.6).\n4.3.3 Serum Inhibin B\nInhibin B is secreted by growing follicles and neg-\natively regulates pituitary FSH secretion, with its decline\nindicating a diminished follicular pool. Studies have con-\nsistently shown that inhibin B levels are significantly re-\nduced after hysterectomy. A meta-analysis conducted by\nHuang et al . (2023) [ 20] revealed the test group showed\na decrease of 14.34 pg/mL (95% CI: –24.69 to –3.99, p <\n0.001) in the level of inhibin B, aligning with changes in\nAMH and indicating a decline in follicular reserve. Tapisiz\net al . (2008) [ 16] also found that inhibin B was signifi-\ncantly lower in the hysterectomized group than in the con-\ntrol group ( p = 0.007), reflecting diminished ovarian feed-\nback inhibition, as demonstrated by experiments in rats. A\nrandomized controlled trial by Halmesmäki et al . (2007)\n[4] involving 107 participants found that serum inhibin B\nlevels were significantly decreased ( p < 0.05), with hys-\nterectomy emerging as an independent predictor ( p = 0.05)\nin multivariate regression analysis. Nahás et al. (2003) [23]\nconducted a prospective case-control study with 61 partici-\npants in the hysterectomy group and 30 in the control group.\nThey found a significant decline in serum inhibin B levels\npost-TAH, with median inhibin B levels decreasing notably\nat 6 and 12 months ( p < 0.05). Some patients experienced\nbiochemical failure, defined as FSH >40 mIU/mL and E2\n<20 pg/mL. Post-surgery, a percentage of patients exhib-\nited FSH >40 mIU/mL, E2 <20 pg/mL, and inhibin B <5\npg/mL at the 12-month mark.\n5. Clinical Symptoms and Long-Term Health\nRisks of Ovarian Dysfunction After Total\nHysterectomy\n5.1 V asomotor Symptoms\nWomen have a higher persistence of hot flashes and\nnight sweats following hysterectomy. A prospective obser-\nvational study by Maiti et al. (2018) [ 21] found that 34% of\npatients developed menopausal symptoms within one year\nfollowing hysterectomy. The observed symptoms were so-\nmatic (30% of cases), psychological (19%), and genitouri-\nnary (12%) in nature. A longitudinal study of 6106 women\nover 17 years found that those with a history of hysterec-\ntomy had higher incidences of persistent hot flashes (30%\nvs. 15%) and night sweats (19% vs. 9%) than women with-\nout hysterectomy. Moreover, women with a history of hys-\nterectomy had higher rates of persistent hot flashes (1.97%,\n95% CI: 1.64–2.35) and persistent night sweats (2.09%,\n95% CI: 1.70–2.55) compared to those without hysterec-\ntomy [24].\n5.2 Genitourinary Symptoms\nSeveral studies have found that about one-third of\npost-hysterectomy patients subsequently develop genitouri-\n3\n\nnary and vaginal prolapse problems. Following hysterec-\ntomy, many patients experience lower urinary tract dys-\nfunction (LUTD) caused by synergistic dysfunction of the\nbladder detrusor muscle with the urethral sphincter due\nto pelvic autonomic nerve injury. One study found that\nabout a third of post-hysterectomy patients develop geni-\ntourinary issues and vaginal prolapse [ 25]. Patients may\nexperience urinary frequency, dysuria (56–64%), urgency\nand/or stress urinary incontinence (37–60%), and incom-\nplete bladder emptying (36.7%) [ 26]. Compared to stan-\ndard hysterectomy, radical hysterectomy has a higher inci-\ndence of urinary complications (odds ratio [OR] = 15.63, p\n= 0.001), residual urine sensation (OR = 10.37, p < 0.001),\nand urinary tract infections (OR = 6.22, p < 0.001). Radi-\ncal hysterectomy is also associated with a higher incidence\nof urodynamic problems (max flow rate: 19.76 mL/s with\nstandard hysterectomy vs. 12.35 mL/s with radical hys-\nterectomy), increased residual urine volume (57.69 mL vs.\n221.28 mL), and abnormal urinary sensation (presence of\nsensation: 93.8% vs. 43.9%) [ 27]. In a prospective cohort\nstudy by Proshchenko and V entskivska (2022) [28] involv-\ning 160 women aged 40–49 years, the incidence of stress\nurinary incontinence increased from 13.75% before surgery\nto 41.02% at 5 years post-surgery ( p < 0.05). Abdomi-\nnal hysterectomy resulted in less favorable urodynamic out-\ncomes, including a larger reduction in bladder capacity (1.5-\nfold decrease), higher residual urine volume (+32%), and\nincreased rates of voiding dysfunction compared with vagi-\nnal or laparoscopic approaches [ 28].\n5.3 Cardiovascular Disease\nHysterectomy has been associated with a 27% reduc-\ntion in carotid artery compliance ( p = 0.004), independent\nof traditional cardiovascular risk factors [ 29]. A matched\ncase-control study (n = 246; 123 matched pairs) conducted\nby Punnonen et al . (1987) [ 8] found that premenopausal\nhysterectomy tripled the risk of cardiovascular disease rel-\native risk [RR] = 3.0, significant in McNemar test) com-\npared to myomectomy controls. Notably, hypertension was\nmore prevalent among hysterectomy cases (6/20) than con-\ntrols (1/6). A nationwide cohort study by Lai et al. (2018)\n[9] on 4986 women, including 1083 bilateral salpingo-\noophorectomy (BSO) cases, found that undergoing BSO\nduring hysterectomy did not significantly increase the over-\nall risk of stroke during a 13-year follow-up (HR = 0.84,\n95% CI: 0.63–1.13). However, BSO decreased the risk of\nstroke by 64% (HR = 0.36, 95% CI: 0.16–0.79) in women\naged 50 years or older who were using estrogen therapy.\nThis protective effect in older women receiving estrogen\ntherapy suggests that hormonal compensation may attenu-\nate the cardiovascular risks following BSO, offsetting the\neffects of surgical menopause. No increase in risk was ob-\nserved for either ischemic stroke (HR = 0.85, 95% CI: 0.61–\n1.18) or hemorrhagic stroke (HR = 0.82, 95% CI: 0.42–\n1.60). Analysis of the Nurses’ Health Study data by Parker\net al . (2009) [ 30] revealed a 17% increase in the risk of\ncoronary heart disease among women who had undergone\nhysterectomy (HR = 1.17, 95% CI: 1.02–1.35), irrespective\nof ovarian status. Gavin et al. (2012) [ 29] examined the re-\nlationship between hysterectomy (with or without bilateral\noophorectomy) and large artery stiffness. Both hysterec-\ntomy alone and hysterectomy with bilateral oophorectomy\nwere found to be associated with increased arterial stiffness,\nas indicated by reduced carotid compliance, and indepen-\ndently of traditional cardiovascular risk factors.\n5.4 Dementia\nPhung et al. (2010) [ 10] conducted a nationwide his-\ntorical cohort study (n = 2,313,388) to investigate the asso-\nciation between hysterectomy (with or without oophorec-\ntomy) and the risk of dementia. Their analysis revealed that\nhysterectomy was associated with an elevated risk of early-\nonset dementia (diagnosed before age 50), with the risk in-\ncreasing progressively according to the extent of surgery:\nhysterectomy alone (RR = 1.38, 95% CI: 1.07–1.78), hys-\nterectomy with unilateral oophorectomy (RR = 2.10, 95%\nCI: 1.28–3.45), and hysterectomy with bilateral oophorec-\ntomy (RR = 2.33, 95% CI: 1.44–3.77). Notably, the mag-\nnitude of risk exhibited a strong inverse relationship with\nage at surgery, with younger patients having a dispropor-\ntionately higher risk.\n6. Risk Factors for Ovarian Dysfunction\nAfter Total Hysterectomy\n6.1 Impact of the Surgical Procedure\n6.1.1 Opportunistic Bilateral Salpingectomy vs. Standard\nHysterectomy\nMost studies have shown that simultaneous removal\nof the fallopian tubes during hysterectomy (opportunis-\ntic salpingectomy (OS) or prophylactic bilateral salpingec-\ntomy (PBS)) does not cause significant acute damage to\novarian reserve markers (e.g., AMH, FSH, LH). Behnam-\nfar and Jabbari (2017) [ 31] compared combined BSO in\nhysterectomy with tubal preservation group, finding signif-\nicantly higher FSH and LH ( p < 0.001), but no difference\nbetween groups (FSH: p = 0.17; LH: p = 0.16). A retrospec-\ntive cohort study (n = 79) by Chen et al. (2022) [ 32] found\nthat hysterectomy with OS significantly reduced the time to\nmenopause (1.84 vs. 2.93 years, p = 0.031; p = 0.029 af-\nter adjusting for covariates). The OS group also had higher\nbody mass index (BMI) (25.27 vs. 22.97 kg/m 2, p = 0.01)\nand sleep disturbances (41% vs. 12%, p = 0.01). Tehranian\net al. (2017) [ 33] conducted a randomized controlled trial\non the effect of simultaneous salpingo-oophorectomy dur-\ning hysterectomy on ovarian reserve (n = 30). All patients\nshowed a significant postoperative decrease in AMH (1.32\n± 0.91 to 1.05 ± 0.88 ng/mL, p < 0.001), but no signifi-\ncant difference was found in the rate of decrease in AMH\nbetween the two groups (25% in salpingo-oophorectomy\ngroup vs. 26% in the control group, p = 0.23). A systematic\n4\n\n\nreview and meta-analysis of 9 studies by Gelderblom et al.\n(2022) [34] found that OS at the end of pregnancy did not\naffect ovarian reserve markers. In particular, there was no\nsignificant decrease in AMH at 3 months after salpingec-\ntomy (p = 0.21). V an Lieshout et al. (2018) [ 35] conducted\na Cochrane systematic review and found that combined OS\nduring hysterectomy did not significantly increase the sur-\ngical risk or impair ovarian function. A prospective cohort\nstudy (n = 60) by Naaman et al . (2017) [ 36] found that\nhysterectomy with bilateral salpingectomy or fimbriectomy\ndid not significantly affect ovarian reserve, as evidenced\nby changes in AMH (+0.53 vs. –0.02 ng/mL, p = 0.25),\nFSH (–2.53 vs. –7.20 IU/L, p = 0.30), and Doppler ultra-\nsound parameters (all p > 0.05). A recent multicenter ran-\ndomized controlled trial (n = 104) by V an Lieshout et al .\n(2019) [37] found that hysterectomy with opportunistic bi-\nlateral salpingectomy did not significantly impact ovarian\nreserve compared to standard hysterectomy. The study re-\nported a non-significant difference in AMH levels between\nthe two groups (change in AMH: –0.14 vs. 0.00 pmol/L,\np = 0.49). A prospective observational study (n = 71) con-\nducted by V enturella et al . (2017) [ 38] found that PBS in\ntotal laparoscopic hysterectomy (TLH) did not affect the\nlong-term ovarian reserve 3 years postoperatively (OvAge\nvs. chronological age: 49.22 ± 2.57 vs. 49.61 ± 2.15 years,\np = 0.900). The OvAge® model for AMH (0.12 ± 0.20\nng/mL), FSH (44.30 ± 219.92 mU/mL) and 3D-AFC (1.91\n± 1.28) showed equivalent slopes in the PBS and control\ngroups (r = 1.0008, p = 0.001).\n6.1.2 Total Laparoscopic Hysterectomy (TLH) vs\nLaparoscopic Supracervical Hysterectomy (LSH)\nThe prospective cohort study (n = 67 patients) by Y uan\net al . (2015) [ 39] revealed that TLH caused a greater de-\ncline in serum AMH levels than LSH at 4 months post-\nsurgery (p = 0.017).\n6.1.3 Bilateral Ovarian Preservation vs. Unilateral\nOvarian Preservation\nWomen with bilateral ovarian preservation show a sig-\nnificantly higher 5-year rate of normal ovarian function than\nthose with unilateral preservation (89% vs. 66%). Intra-\noperative preservation of both ovaries is therefore recom-\nmended as a priority. For women requiring unilateral ovar-\nian removal, postoperative monitoring of AMH should be\nperformed every 6 months for early detection of functional\ndecline. A prospective randomized study by Bukovsky et\nal. (1995) [ 40] found that abdominal hysterectomy with\nunilateral oophorectomy (USO) resulted in a higher dys-\nfunction rate (35% vs. 10%, p = 0.02) at the 6-month\nfollow-up assessment compared to ovarian conservation. A\nprospective cohort study by Farquhar et al . (2005) [ 13]\ninvolving 257 women in the hysterectomy group and 259\ncontrols found the 5-year menopausal rate was significantly\nhigher in women who retained one ovary (35.7%, 10/28)\ncompared to those retaining both ovaries (16.9%, p < 0.01).\nA prospective cohort study by Moorman et al. (2011) [ 14]\ninvolving 406 individuals in the hysterectomy group and\n465 controls found that USO was associated with a higher\nrisk (HR = 2.93) compared to women who retained bilateral\novaries (HR = 1.74).\n6.1.4 Laparoscopic vs. Non-Laparoscopic Surgery\nLaparoscopic hysterectomy has been associated with\nsubstantial short-term impacts on ovarian reserve function,\npossibly due to the thermal effects of electrocoagulation\nduring the procedure. In contrast, open surgical approaches\nor techniques that preserve the ovarian blood supply may\noffer superior protection of ovarian function. A prospec-\ntive cohort study by Chun and Ji (2020) [ 41] examined\nthe impact of hysterectomy with ovarian preservation on\novarian reserve in 86 premenopausal women aged 31–48\nyears. The results showed differential effects during the\nearly postoperative period depending on the surgical ap-\nproach. While the laparoscopic group experienced a greater\nreduction in AMH level (0.42 ng/mL) compared to the open\ngroup (0.01 ng/mL), this did not reach statistical signifi-\ncance ( p = 0.053). Cho et al . (2017) [ 42] prospectively\nmonitored the AMH level in 91 individuals and found no\nsignificant difference in the rate of decline between TLH\nand non-TLH groups at 6 months postoperatively (TLH\n42.1% vs. non-TLH 33.3%, p = 0.545). However, the TLH\ngroup exhibited a sustained decrease in the mean AMH\nvalue (3.5 to 1.6 ng/mL), whereas the AMH level remained\nrelatively stable in the non-TLH group (2.4 to 2.6 ng/mL).\nThe systematic review and meta-analysis of 9 studies by\nGelderblom et al . (2022) [ 34] found a significant decline\nof more than 40% in the AMH level at 2 months postoper-\natively in the TLH group ( p = 0.042), compared to a 20%\ndecline in the non-TLH group. This difference may be at-\ntributable to thermal damage from the electrocoagulation\nequipment used in laparoscopic procedures, which can ad-\nversely impact ovarian tissues or blood vessels through heat\ndiffusion. A randomized controlled trial (n = 100) con-\nducted by Cai et al. (2017) [ 43] compared traditional hys-\nterectomy with a novel hysterectomy technique that pre-\nserves the uterine blood supply (STHMUV , uterine blood\nsupply-preserving hysterectomy technique). Superior ovar-\nian protection was observed with the STHMUV technique,\nwhich maintained stable postoperative estradiol (E2) levels\n(346.12 pg/mL to 298.34 pg/mL) over 2 years ( p > 0.05).\nIn contrast, traditional hysterectomy exhibited a significant\ndecline in E2 (343.24 pg/mL to 203.17 pg/mL, p < 0.05),\nand significantly lower E2 levels compared to STHMUV .\nFurthermore, the STHMUV group showed a significantly\nsmaller increase in FSH (17.65 U/L to 20.17 U/L) compared\nto the traditional hysterectomy group (16.32 U/L to 89.01\nU/L, p < 0.05).\n5\n\n6.2 Patient Characteristics\n6.2.1 Age\nY ounger patients (<40 years) have a higher risk of\npostoperative ovarian failure and a stronger association\nwith surgery. Older patients ( ≥40 years) also have a sig-\nnificantly higher risk of ovarian failure (HR = 1.79) after\nhysterectomy. However, their risk is lower than for the\nyounger group, probably because their ovarian reserve is al-\nready in decline approaching the age of natural menopause,\nand hence the ‘extra blow’ of surgery is relatively limited.\nHuang et al . (2023) [ 20] conducted a systematic review\nand meta-analysis of 14 studies with 1457 premenopausal\nwomen. Their analysis revealed that women aged >40\nyears exhibited greater increases in FSH and LH levels,\nand more significant decreases in E2 concentrations, com-\npared to their younger counterparts. However, the reduc-\ntion in AMH did not show any significant age-related ef-\nfects, whereas some studies have suggested the decline in\nAMH levels following hysterectomy is more pronounced\nin younger patients. For instance, a study by Y uan et al .\n(2019) [44] involving 84 participants found a stronger neg-\native correlation between hysterectomy and AMH levels in\npatients aged <40 years (r = –0.48 at 6 weeks, p < 0.001).\nAdditionally, a prospective cohort study by Moorman et al.\n(2011) [ 14] involving 406 hysterectomy patients and 465\ncontrols reported a stronger association between hysterec-\ntomy and ovarian failure in women aged <40 years (HR =\n4.29, 95% CI: 0.83–22.3). While the risk of ovarian fail-\nure was also significantly elevated in the ≥40 years group,\nthe magnitude was lower (HR = 1.79, 95% CI: 1.18–2.71),\nlikely due to the wider confidence intervals resulting from\na limited sample size.\n6.2.2 Smoking\nCooper and Thorp (1999) [ 22] reported the impact\nof hysterectomy on FSH levels (OR = 1.5) was less pro-\nnounced than that of smoking (OR = 2.0), but significantly\ngreater than the natural aging process. This finding under-\nscores the importance of incorporating the effect of hys-\nterectomy on the FSH level into postoperative management\nstrategies.\n7. Clinical Management Strategies for\nOvarian Dysfunction After Total\nHysterectomy\nThe management of post-hysterectomy ovarian hy-\npoplasia and associated complications requires a full-cycle\napproach, incorporating detailed preoperative evaluation,\noptimized surgical techniques, and extended postoperative\nmonitoring. The following evidence-based strategy is rec-\nommended:\n7.1 Preoperative Assessment of Ovarian Function\nIn patients of childbearing age or those concerned\nabout endocrine function, preoperative testing of AMH,\nFSH, and E2 should be conducted to evaluate the risk of\npostoperative ovarian failure. The factors of age, BMI, and\nsmoking history should also be considered. Age >40 years\nand AMH levels below 1.2 ng/mL were identified as risk\nfactors for significant postoperative ovarian function de-\ncline [45]. When necessary, three-dimensional Doppler ul-\ntrasound should be used to assess ovarian blood flow (PI,\nRI), with increased risk of functional decline observed in\npatients with abnormal blood flow (PI >1.77, RI >0.8).\n7.2 Surgical Options\n7.2.1 Ovary Preservation\nIn the absence of clear ovarian pathology, bilateral\npreservation is favored (89% vs. 66% for unilateral preser-\nvation 5 years postoperatively) [ 13]. Patients undergoing\nunilateral oophorectomy should be informed of the 2–3-fold\nincreased risk of postoperative POI (HR = 2.93) [ 14].\n7.2.2 Salpingectomy Decision\nOpportunistic Salpingectomy (OS) does not cause sig-\nnificant acute damage to ovarian function, but may shorten\nthe time to menopause (1.84 years in the OS group vs. 2.93\nyears in the preserved group) [ 32,34], and should thus be\nconsidered in the context of the patient’s age and reproduc-\ntive needs. When tubal resection is required, fine dissection\nshould be used to avoid damage to the ovarian mesosalpinx\nvessels. AMH is monitored postoperatively until it stabi-\nlizes, usually after 3–6 months.\n7.2.3 Surgical Extent\nIn benign conditions, extrafascial subtotal resection is\nfavored over radical resection to minimize the decrease in\nAMH level ( p = 0.001) and to maintain the ovarian blood\nsupply provided by the uterine artery, which normally con-\ntributes 50–70% of the total supply [ 34].\n7.2.4 Laparoscopic Surgery\nCareful use of electrocoagulation equipment is re-\nquired, with preference given to cold knife separation or\nlow-power modes of energy instrumentation to minimize\novarian damage from heat spread [ 34,43].\n7.2.5 V ascular-Preserving Techniques\nSurgical techniques that preserve the uterine vascula-\nture, such as the STHMUV procedure, are recommended to\nmaintain postoperative estrogen homeostasis. These mod-\nified approaches result in a less pronounced decrease in\nestradiol levels (<15%) compared to conventional methods\n(>40%), which is a desirable outcome [ 43].\n6\n\n\n7.3 Postoperative Monitoring and Management\nIn line with the 2022 European Society of Human Re-\nproduction and Embryology (ESHRE) Guidelines on the\nmanagement of premature ovarian insufficiency [ 46], as\nwell as the expert consensus [ 20], the levels of AMH,\nFSH and E2 should be monitored postoperatively. Inter-\nvals should be shortened for patients who undergo laparo-\nscopic hysterectomy, or who retained only one ovary. An-\nnual evaluation should focus on FSH levels that exceed 40\nIU/L (indicative of menopausal status), as well as the pres-\nence of perimenopausal symptoms such as hot flashes and\nvaginal dryness. Particular consideration should be given\nto interventions for individuals who experience early-onset\nmenopause (<40 years of age).\nPostoperative screening of pelvic floor function, in-\ncluding urodynamics, is recommended from 6 months on-\nward in patients undergoing transvaginal surgery or radical\nresection. These should have careful monitoring for vaginal\nprolapse (37.8% incidence) and urethral dysfunction such\nas stress urinary incontinence (41% incidence at five years\npostoperatively).\n8. Conclusions\nPost-hysterectomy ovarian function undergoes signif-\nicant changes, including diminished ovarian reserve, men-\nstrual alterations, and early menopausal symptoms. The im-\npact of surgical techniques and adjunct procedures on ovar-\nian function is varied, and can influence the patients’ quality\nof life and psychological well-being. Clinicians should con-\nsider factors such as age, fertility desires, and disease sta-\ntus when selecting surgical methods and devising treatment\nplans. Surgical benefits and drawbacks must be balanced\nwith ovarian function to tailor patient-specific strategies.\nCareful monitoring and management of postoperative ovar-\nian function are crucial to promptly address issues, thereby\nimproving the quality of life and health of patients. Future\nresearch should focus on personalized surgical designs such\nas vascular refinement protection, novel biomarkers includ-\ning inflammatory factor profiles, and targeted interventions\nsuch as antifibrotic drugs. Advances in these areas should\nhelp to refine clinical management and improve long-term\npatient outcomes.\nAbbreviations\nAMH, anti-Müllerian hormone; FSH, follicle-\nstimulating hormone; STHMUV , uterine blood supply-\npreserving hysterectomy technique; HPO, hypothalamic-\npituitary-ovarian; ANS, autonomic nervous system; PI,\npulsatility index; RI, resistance index; PSV , peak flow\nvelocity; LA VH, laparoscopically-assisted vaginal hys-\nterectomy; TAH, total abdominal hysterectomy; LUTD,\nlower urinary tract dysfunction; OS, opportunistic salp-\ningectomy; PBS, prophylactic bilateral salpingectomy;\nBSO, bilateral salpingo-oophorectomy; LH, luteinizing\nhormone; E2, estradiol; USO, unilateral oophorectomy;\nTLH, total laparoscopic hysterectomy; LSH, laparoscopic\nsupracervical hysterectomy.\nAuthor Contributions\nYC conceptualized and designed the review, con-\nducted comprehensive literature search and selection, and\ncompiled and synthesized the relevant data. LM not only\nprovided critical advice on data collation and interpretation\nof the review findings, but also took the lead in formulat-\ning literature inclusion and exclusion criteria, participated\nin the quality assessment of included literature, and con-\nstructed the core argumentation. Both authors contributed\nto editorial changes in the manuscript. Both authors read\nand approved the final manuscript. Both authors have par-\nticipated sufficiently in the work and agreed to be account-\nable for all aspects of the work.\nEthics Approval and Consent to Participate\nNot applicable.\nAcknowledgment\nWe would like to express our gratitude to all those who\nprovided assistance during the writing of this manuscript.\nWe also thank all peer reviewers for their valuable opinions\nand suggestions.\nFunding\nThis research received no external funding.\nConflict of Interest\nThe authors declare no conflict of interest.\nReferences\n[1] Papadopoulos MS, Tolikas AC, Miliaras DE. 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