Post-Hysterectomy Ovarian Consequences: Mechanisms, Risks, and Clinical Management Strategies—A Narrative Review

Objective(s): To examine the mechanisms underlying changes in ovarian function after total hysterectomy, identify relevant risk factors, and summarize clinical management strategies for such changes. Mechanism: The pathogenesis of impaired ovarian function post- total hysterectomy involves three key pathways: (1) reduced ovarian blood supply due to uterine artery ligation; (2) neuroendocrine imbalance caused by abnormal gonadotropin levels; (3) oxidative stress and fibrosis induced by chronic inflammation. Findings in Brief: Total hysterectomy is associated with diminished ovarian reserve, including a 20–30% decrease in anti-Müllerian hormone (AMH), elevated serum follicle-stimulating hormone (FSH) levels, and an approximate 3–4-year acceleration of menopause. Risk factors include the surgical approach (e.g., laparoscopic electrocoagulation decreases AMH by 40% vs. 20% with open surgery), unilateral ovarian preservation (increases the risk of menopause by 2.93-fold compared to bilateral preservation), and age <40 years (increases the risk of postoperative ovarian failure). Conclusions: Personalized clinical management, including preoperative assessment of AMH levels and ovarian blood flow, preference for ovarian and uterine artery-preserving techniques (e.g., STHMUV , uterine blood supply-preserving hysterectomy technique), and postoperative hormone/pelvic floor function monitoring may mitigate damage to ovarian function. To optimize long-term outcomes, future research should focus on vasoprotective strategies and precision interventions guided by biomarkers.

hysterectomy; ovarian function; ovarian reserve; anti-Müllerian hormone (AMH); premature menopause; surgical approach 1. Introduction 1.1 Background Total hysterectomy is one of the most important surgi- cal procedures in many gynecologic conditions [ 1]. How- ever, changes in ovarian function after surgery (such as early menopause and hormonal disorders) can have sig- nificant impacts on the reproductive and long-term health of women, including cardiovascular and cognitive issues [2,3]. There is currently a need for systematic integration of research on the mechanisms, risk stratification, and man- agement strategies for total hysterectomy. 1.2 Objectives The aims of this study were to elucidate the pathophys- iological mechanisms underlying ovarian dysfunction fol- lowing total hysterectomy, systematically evaluate the clin- ical evidence and epidemiological characteristics of postop- erative ovarian dysfunction, identify key risk factors affect- ing postoperative ovarian function, and provide evidence- based management strategies for preserving ovarian func- tion and improving long-term health outcomes after total hysterectomy. 2. Methods Articles were identified via searches of Embase, PubMed, and Web of Science from each database’s in- ception to June 2025, supplemented by manual screen- ing of reference lists. The computerized search included only English-language articles, using the keyword com- bination: “Hysterectomy” paired with “Ovarian function” or “Ovarian Reserve”, and supplemented by “premature menopause”, “surgical approach”, “AMH/anti-Müllerian hormone”, etc. This strategy initially yielded 383 records. After removing duplicates, we focused on screening for meta- analyses and clinical studies, while excluding abstracts (in- complete data) and review articles (non-original research); finally, 39 eligible studies were selected, categorized as fol- lows: 7 on pathophysiologic mechanisms, 24 on clinical ev- idence and symptoms, and 8 on risk factors related to post- hysterectomy ovarian consequences. 3. Pathophysiologic Mechanisms of Ovarian Dysfunction After Total Hysterectomy 3.1 Decreased Blood Supply and V ascular Damage The uterine artery contributes approximately 50–70% of the blood supply to the ovary. Multiple studies using Doppler ultrasound have reported elevated resistance in- dex (RI) and pulsatility index (PI) post-hysterectomy, along with reduced peak flow velocity (PSV) in the ovarian arter- ies. These findings imply a diminished blood supply, pos- sibly due to direct vessel injury or induction of thrombo- sis by the surgical procedures. Halmesmäki et al . (2007) [4] reported the results of a randomized controlled trial (n = 107) in which post-operative pelvic ultrasound revealed significant alterations in ovarian blood flow. Specifically, the PI showed a significant decrease ( p = 0.01), poten- tially due to vascular dilation as a consequence of sur- gical tissue trauma. Lee et al . (2010) [ 5] conducted a prospective cohort study (evidence level II) comprising 32 patients who underwent hysterectomy and 21 control pa- tients. Three months after hysterectomy with bilateral ovar- ian preservation, they found no significant changes in ovar- ian artery blood flow indices (PI, RI) using transvaginal Doppler ultrasound, and no change in anti-Müllerian hor- mone (AMH) level using the Enzyme-Linked Immunosor- bent Assay (ELISA) method. Furthermore, no differences were found between the laparoscopically-assisted vaginal hysterectomy (LA VH) and total abdominal hysterectomy (TAH) groups. An animal model showed a 32% absolute reduction in endothelium-dependent vasodilatory function after ovariectomy, with impaired small-conductance Ca 2+- activated K + (SK3) channels activity suggested to be the key mechanism [6]. 3.2 Imbalance of Neuroendocrine Regulation The uterus and ovaries are interconnected via the hypothalamic-pituitary-ovarian (HPO) axis and the auto- nomic nervous system (ANS). This regulatory balance be- tween the HPO and ANS can be disrupted following hys- terectomy. Postoperative changes include significant in- creases in the levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH), along with a decrease in estradiol (E2), indicating ovarian hypoplasia. These hor- monal shifts are most notable 3–6 months after surgery and may result from reduced negative feedback by ovarian steroid hormones. Increased levels of sympathetic nerve activity trigger the toll-like receptor 4 (TLR4)/Nucleotide- binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome pathway, resulting in the release of Interleukin-1 beta (IL-1 β),Interleukin-18 (IL-18), and other pro-inflammatory factors, thus accelerating follicular atresia. Concurrently, diminished parasympathetic inhibi- tion intensifies the inflammatory cascade, while decreased expression of estrogen receptors (ERα/β) reduces follicular sensitivity to gonadotropins, impairing follicular develop- ment [7]. 3.3 Inflammatory Response and Oxidative Stress Surgical trauma can elicit sustained inflammatory re- sponses, fostering a pro-aging milieu. Inflammaging, de- noted by chronic low-grade inflammation, is a pivotal fac- tor in ovarian senescence, influencing oxidative stress, fi- brosis, and immune cell infiltration [ 8,9]. Elevated levels of ovarian oxidative stress driven by chronic inflammation can impede follicular maturation and development, thereby accelerating the depletion of ovarian reserve and egg quality [8–10]. Furthermore, chronic inflammation is associated with ovarian fibrosis, which disrupts the tissue architecture and compromises follicular growth. In addition, chronic in- flammation exacerbates apoptosis and DNA damage during ovarian aging through molecular mechanisms such as acti- vation of the NLRP3 inflammasome [ 7]. 4. Clinical Evidence and Epidemiological Characteristics of Ovarian Dysfunction After Total Hysterectomy 4.1 Increased Risk of Early Menopause Following a total hysterectomy, patients may enter menopause 3–4 years earlier. Siddle et al . (1987) [ 11] found that hysterectomy was associated with an earlier on- set of ovarian failure compared to natural menopause (mean age: 45.4 ± 4.0 years vs. 49.5 ± 4.04 years, p < 0.001). Ahn et al. (2002) [ 12] also reported that hysterectomy was associated with a younger age at menopause (46.3 ± 3.0 vs. 48.1 ± 3.2 years, p < 0.001). Farquhar et al. (2005) [ 13] compared 257 women who underwent hysterectomy with ovarian preservation to 259 controls with intact uteri. These authors found that hysterectomy advances ovarian failure by 3.7 years, and women who had a hysterectomy entered menopause (FSH >40 IU/L) 3 years earlier than the con- trols (95% confidence interval [CI]: 1.5–6.0). By 5 years after surgery, 20.6% of hysterectomy patients had reached menopause (95% CI: 6.8%) compared to only 7.3% of con- trols ( p < 0.0001). Women who had unilateral oophorec- tomy (n = 28) were more likely to have reached menopause (35.7%) within 5 years, and they also reached menopause 4.4 years earlier than women with bilateral ovarian preser- vation (95% CI: 0.6–7.9). In a prospective cohort study of 871 patients, Moorman et al. (2011) [ 14] demonstrated that the 4-year cumulative incidence of ovarian failure was 14.8% (60/406) in the hysterectomy group compared to 8.0% (46/465) in the control group, with an adjusted hazard ratio (HR) of 1.92 (95% CI: 1.29–2.86). These results sug- gest that hysterectomy is associated with an approximate 2-fold increase in the likelihood of ovarian failure. 4.2 Ovarian Reserve and Blood Supply Damage Since the uterine artery provides 50–70% of the blood supply to the ovaries, surgical severance results in ischemic damage to these organs. Postoperative Doppler ultrasound showed elevated ovarian artery RI and PI, and decreased PSV , suggesting decreased blood supply [15]. Tapisiz et al. (2008) [16] examined histopathological changes in ovarian tissues after hysterectomy in a rat model. These authors observed a 50% reduction in primordial follicle number ( p = 0.01), and a 300% increase in atretic follicle number ( p = 0.02). Hu et al. (2006) [ 17] found that hysterectomy af- 2 fected the ovarian vasculature and gland function in women aged 32–45 years. A transient increase in Vmax was ob- served 5 days after surgery (26.47 vs. 22.00 cm/s,p < 0.01), followed by a decline to 17.20–17.60 cm/s at 1–3 months (p < 0.001). A gradual increase in PI from 1.45 to 1.77 ( p < 0.05) was also observed, suggesting a long-term decrease in blood flow. 4.3 Changes in Serum Hormone Markers 4.3.1 Serum Anti-Müllerian Hormone AMH is produced by small antral follicles and is the most reliable circulating marker of ovarian reserve. Fol- lowing total hysterectomy, the concentration of AMH may decline by 20–30%, and even more in patients with low reserve. Atabekoğlu et al . (2012) [ 18] reported that total hysterectomy resulted in a larger decrease in the ovarian re- serve, as measured by AMH level, at 4 months after surgery. Specifically, the AMH level decreased by 30% more than in the controls. A prospective cohort study by Trabuco et al. (2016) [ 19] showed that hysterectomy resulted in a sig- nificant decrease of almost 20% in the AMH level at 1 year compared with the control group. The hysterectomy group also exhibited a significantly greater fall in AMH (–40.7% vs. 20.9%, p < 0.001), and a higher rate of undetectability (12.8% vs. 4.7%, p < 0.02). The postoperative decrease in AMH was 0.77 times greater than in the control group ( p < 0.001). The low reserve group (AMH ≤1.2 ng/mL) showed a greater decline in AMH in the hysterectomy group than controls (58.3% vs. 19.1%, p 1.2 ng/mL), the decline in AMH was not signifi- cantly different to controls (34.4% vs. –21.2%, p = 0.06), but AMH was still lower (0.81-fold, p < 0.003). In a meta- analysis of 14 studies with a total of 1457 women, Huang et al. (2023) [ 20] found significantly lower AMH levels in the hysterectomy group than the control group, with a weighted mean difference (WMD) of –0.56 (95% CI: –0.72 to –0.39, p < 0.0001). 4.3.2 Serum Follicle Stimulating Hormone Serum FSH levels are significantly elevated in pa- tients after hysterectomy. Huang et al . (2023) [ 20] re- ported significantly elevated FSH levels in the hysterec- tomy group compared to the control group (WMD = 2.96, 95% CI: 1.47–4.44, p < 0.001). Maiti et al . (2018) [ 21] found that 1 year after hysterectomy, patients had signif- icantly increased serum FSH from baseline (7.5 IU/L to 12.3 IU/L), as well as a significant ( p 20 IU/L, indi- cating perimenopausal transition, while 5% had FSH >40 IU/L, indicating menopausal transition. Cooper and Thorp (1999) [22] reported a strong association between hysterec- tomy and elevated serum FSH level ( >20 IU/L). Patients with unilateral oophorectomy had 2.4-fold higher odds of elevated FSH ( >20 IU/L) compared to those with bilateral ovarian preservation (OR = 2.4, 95% CI: 1.3–4.6). 4.3.3 Serum Inhibin B Inhibin B is secreted by growing follicles and neg- atively regulates pituitary FSH secretion, with its decline indicating a diminished follicular pool. Studies have con- sistently shown that inhibin B levels are significantly re- duced after hysterectomy. A meta-analysis conducted by Huang et al . (2023) [ 20] revealed the test group showed a decrease of 14.34 pg/mL (95% CI: –24.69 to –3.99, p < 0.001) in the level of inhibin B, aligning with changes in AMH and indicating a decline in follicular reserve. Tapisiz et al . (2008) [ 16] also found that inhibin B was signifi- cantly lower in the hysterectomized group than in the con- trol group ( p = 0.007), reflecting diminished ovarian feed- back inhibition, as demonstrated by experiments in rats. A randomized controlled trial by Halmesmäki et al . (2007) [4] involving 107 participants found that serum inhibin B levels were significantly decreased ( p < 0.05), with hys- terectomy emerging as an independent predictor ( p = 0.05) in multivariate regression analysis. Nahás et al. (2003) [23] conducted a prospective case-control study with 61 partici- pants in the hysterectomy group and 30 in the control group. They found a significant decline in serum inhibin B levels post-TAH, with median inhibin B levels decreasing notably at 6 and 12 months ( p 40 mIU/mL and E2 40 mIU/mL, E2 <20 pg/mL, and inhibin B <5 pg/mL at the 12-month mark. 5. Clinical Symptoms and Long-Term Health Risks of Ovarian Dysfunction After Total Hysterectomy 5.1 V asomotor Symptoms Women have a higher persistence of hot flashes and night sweats following hysterectomy. A prospective obser- vational study by Maiti et al. (2018) [ 21] found that 34% of patients developed menopausal symptoms within one year following hysterectomy. The observed symptoms were so- matic (30% of cases), psychological (19%), and genitouri- nary (12%) in nature. A longitudinal study of 6106 women over 17 years found that those with a history of hysterec- tomy had higher incidences of persistent hot flashes (30% vs. 15%) and night sweats (19% vs. 9%) than women with- out hysterectomy. Moreover, women with a history of hys- terectomy had higher rates of persistent hot flashes (1.97%, 95% CI: 1.64–2.35) and persistent night sweats (2.09%, 95% CI: 1.70–2.55) compared to those without hysterec- tomy [24]. 5.2 Genitourinary Symptoms Several studies have found that about one-third of post-hysterectomy patients subsequently develop genitouri- 3 nary and vaginal prolapse problems. Following hysterec- tomy, many patients experience lower urinary tract dys- function (LUTD) caused by synergistic dysfunction of the bladder detrusor muscle with the urethral sphincter due to pelvic autonomic nerve injury. One study found that about a third of post-hysterectomy patients develop geni- tourinary issues and vaginal prolapse [ 25]. Patients may experience urinary frequency, dysuria (56–64%), urgency and/or stress urinary incontinence (37–60%), and incom- plete bladder emptying (36.7%) [ 26]. Compared to stan- dard hysterectomy, radical hysterectomy has a higher inci- dence of urinary complications (odds ratio [OR] = 15.63, p = 0.001), residual urine sensation (OR = 10.37, p < 0.001), and urinary tract infections (OR = 6.22, p < 0.001). Radi- cal hysterectomy is also associated with a higher incidence of urodynamic problems (max flow rate: 19.76 mL/s with standard hysterectomy vs. 12.35 mL/s with radical hys- terectomy), increased residual urine volume (57.69 mL vs. 221.28 mL), and abnormal urinary sensation (presence of sensation: 93.8% vs. 43.9%) [ 27]. In a prospective cohort study by Proshchenko and V entskivska (2022) [28] involv- ing 160 women aged 40–49 years, the incidence of stress urinary incontinence increased from 13.75% before surgery to 41.02% at 5 years post-surgery ( p < 0.05). Abdomi- nal hysterectomy resulted in less favorable urodynamic out- comes, including a larger reduction in bladder capacity (1.5- fold decrease), higher residual urine volume (+32%), and increased rates of voiding dysfunction compared with vagi- nal or laparoscopic approaches [ 28]. 5.3 Cardiovascular Disease Hysterectomy has been associated with a 27% reduc- tion in carotid artery compliance ( p = 0.004), independent of traditional cardiovascular risk factors [ 29]. A matched case-control study (n = 246; 123 matched pairs) conducted by Punnonen et al . (1987) [ 8] found that premenopausal hysterectomy tripled the risk of cardiovascular disease rel- ative risk [RR] = 3.0, significant in McNemar test) com- pared to myomectomy controls. Notably, hypertension was more prevalent among hysterectomy cases (6/20) than con- trols (1/6). A nationwide cohort study by Lai et al. (2018) [9] on 4986 women, including 1083 bilateral salpingo- oophorectomy (BSO) cases, found that undergoing BSO during hysterectomy did not significantly increase the over- all risk of stroke during a 13-year follow-up (HR = 0.84, 95% CI: 0.63–1.13). However, BSO decreased the risk of stroke by 64% (HR = 0.36, 95% CI: 0.16–0.79) in women aged 50 years or older who were using estrogen therapy. This protective effect in older women receiving estrogen therapy suggests that hormonal compensation may attenu- ate the cardiovascular risks following BSO, offsetting the effects of surgical menopause. No increase in risk was ob- served for either ischemic stroke (HR = 0.85, 95% CI: 0.61– 1.18) or hemorrhagic stroke (HR = 0.82, 95% CI: 0.42– 1.60). Analysis of the Nurses’ Health Study data by Parker et al . (2009) [ 30] revealed a 17% increase in the risk of coronary heart disease among women who had undergone hysterectomy (HR = 1.17, 95% CI: 1.02–1.35), irrespective of ovarian status. Gavin et al. (2012) [ 29] examined the re- lationship between hysterectomy (with or without bilateral oophorectomy) and large artery stiffness. Both hysterec- tomy alone and hysterectomy with bilateral oophorectomy were found to be associated with increased arterial stiffness, as indicated by reduced carotid compliance, and indepen- dently of traditional cardiovascular risk factors. 5.4 Dementia Phung et al. (2010) [ 10] conducted a nationwide his- torical cohort study (n = 2,313,388) to investigate the asso- ciation between hysterectomy (with or without oophorec- tomy) and the risk of dementia. Their analysis revealed that hysterectomy was associated with an elevated risk of early- onset dementia (diagnosed before age 50), with the risk in- creasing progressively according to the extent of surgery: hysterectomy alone (RR = 1.38, 95% CI: 1.07–1.78), hys- terectomy with unilateral oophorectomy (RR = 2.10, 95% CI: 1.28–3.45), and hysterectomy with bilateral oophorec- tomy (RR = 2.33, 95% CI: 1.44–3.77). Notably, the mag- nitude of risk exhibited a strong inverse relationship with age at surgery, with younger patients having a dispropor- tionately higher risk. 6. Risk Factors for Ovarian Dysfunction After Total Hysterectomy 6.1 Impact of the Surgical Procedure 6.1.1 Opportunistic Bilateral Salpingectomy vs. Standard Hysterectomy Most studies have shown that simultaneous removal of the fallopian tubes during hysterectomy (opportunis- tic salpingectomy (OS) or prophylactic bilateral salpingec- tomy (PBS)) does not cause significant acute damage to ovarian reserve markers (e.g., AMH, FSH, LH). Behnam- far and Jabbari (2017) [ 31] compared combined BSO in hysterectomy with tubal preservation group, finding signif- icantly higher FSH and LH ( p < 0.001), but no difference between groups (FSH: p = 0.17; LH: p = 0.16). A retrospec- tive cohort study (n = 79) by Chen et al. (2022) [ 32] found that hysterectomy with OS significantly reduced the time to menopause (1.84 vs. 2.93 years, p = 0.031; p = 0.029 af- ter adjusting for covariates). The OS group also had higher body mass index (BMI) (25.27 vs. 22.97 kg/m 2, p = 0.01) and sleep disturbances (41% vs. 12%, p = 0.01). Tehranian et al. (2017) [ 33] conducted a randomized controlled trial on the effect of simultaneous salpingo-oophorectomy dur- ing hysterectomy on ovarian reserve (n = 30). All patients showed a significant postoperative decrease in AMH (1.32 ± 0.91 to 1.05 ± 0.88 ng/mL, p < 0.001), but no signifi- cant difference was found in the rate of decrease in AMH between the two groups (25% in salpingo-oophorectomy group vs. 26% in the control group, p = 0.23). A systematic 4 review and meta-analysis of 9 studies by Gelderblom et al. (2022) [34] found that OS at the end of pregnancy did not affect ovarian reserve markers. In particular, there was no significant decrease in AMH at 3 months after salpingec- tomy (p = 0.21). V an Lieshout et al. (2018) [ 35] conducted a Cochrane systematic review and found that combined OS during hysterectomy did not significantly increase the sur- gical risk or impair ovarian function. A prospective cohort study (n = 60) by Naaman et al . (2017) [ 36] found that hysterectomy with bilateral salpingectomy or fimbriectomy did not significantly affect ovarian reserve, as evidenced by changes in AMH (+0.53 vs. –0.02 ng/mL, p = 0.25), FSH (–2.53 vs. –7.20 IU/L, p = 0.30), and Doppler ultra- sound parameters (all p > 0.05). A recent multicenter ran- domized controlled trial (n = 104) by V an Lieshout et al . (2019) [37] found that hysterectomy with opportunistic bi- lateral salpingectomy did not significantly impact ovarian reserve compared to standard hysterectomy. The study re- ported a non-significant difference in AMH levels between the two groups (change in AMH: –0.14 vs. 0.00 pmol/L, p = 0.49). A prospective observational study (n = 71) con- ducted by V enturella et al . (2017) [ 38] found that PBS in total laparoscopic hysterectomy (TLH) did not affect the long-term ovarian reserve 3 years postoperatively (OvAge vs. chronological age: 49.22 ± 2.57 vs. 49.61 ± 2.15 years, p = 0.900). The OvAge® model for AMH (0.12 ± 0.20 ng/mL), FSH (44.30 ± 219.92 mU/mL) and 3D-AFC (1.91 ± 1.28) showed equivalent slopes in the PBS and control groups (r = 1.0008, p = 0.001). 6.1.2 Total Laparoscopic Hysterectomy (TLH) vs Laparoscopic Supracervical Hysterectomy (LSH) The prospective cohort study (n = 67 patients) by Y uan et al . (2015) [ 39] revealed that TLH caused a greater de- cline in serum AMH levels than LSH at 4 months post- surgery (p = 0.017). 6.1.3 Bilateral Ovarian Preservation vs. Unilateral Ovarian Preservation Women with bilateral ovarian preservation show a sig- nificantly higher 5-year rate of normal ovarian function than those with unilateral preservation (89% vs. 66%). Intra- operative preservation of both ovaries is therefore recom- mended as a priority. For women requiring unilateral ovar- ian removal, postoperative monitoring of AMH should be performed every 6 months for early detection of functional decline. A prospective randomized study by Bukovsky et al. (1995) [ 40] found that abdominal hysterectomy with unilateral oophorectomy (USO) resulted in a higher dys- function rate (35% vs. 10%, p = 0.02) at the 6-month follow-up assessment compared to ovarian conservation. A prospective cohort study by Farquhar et al . (2005) [ 13] involving 257 women in the hysterectomy group and 259 controls found the 5-year menopausal rate was significantly higher in women who retained one ovary (35.7%, 10/28) compared to those retaining both ovaries (16.9%, p < 0.01). A prospective cohort study by Moorman et al. (2011) [ 14] involving 406 individuals in the hysterectomy group and 465 controls found that USO was associated with a higher risk (HR = 2.93) compared to women who retained bilateral ovaries (HR = 1.74). 6.1.4 Laparoscopic vs. Non-Laparoscopic Surgery Laparoscopic hysterectomy has been associated with substantial short-term impacts on ovarian reserve function, possibly due to the thermal effects of electrocoagulation during the procedure. In contrast, open surgical approaches or techniques that preserve the ovarian blood supply may offer superior protection of ovarian function. A prospec- tive cohort study by Chun and Ji (2020) [ 41] examined the impact of hysterectomy with ovarian preservation on ovarian reserve in 86 premenopausal women aged 31–48 years. The results showed differential effects during the early postoperative period depending on the surgical ap- proach. While the laparoscopic group experienced a greater reduction in AMH level (0.42 ng/mL) compared to the open group (0.01 ng/mL), this did not reach statistical signifi- cance ( p = 0.053). Cho et al . (2017) [ 42] prospectively monitored the AMH level in 91 individuals and found no significant difference in the rate of decline between TLH and non-TLH groups at 6 months postoperatively (TLH 42.1% vs. non-TLH 33.3%, p = 0.545). However, the TLH group exhibited a sustained decrease in the mean AMH value (3.5 to 1.6 ng/mL), whereas the AMH level remained relatively stable in the non-TLH group (2.4 to 2.6 ng/mL). The systematic review and meta-analysis of 9 studies by Gelderblom et al . (2022) [ 34] found a significant decline of more than 40% in the AMH level at 2 months postoper- atively in the TLH group ( p = 0.042), compared to a 20% decline in the non-TLH group. This difference may be at- tributable to thermal damage from the electrocoagulation equipment used in laparoscopic procedures, which can ad- versely impact ovarian tissues or blood vessels through heat diffusion. A randomized controlled trial (n = 100) con- ducted by Cai et al. (2017) [ 43] compared traditional hys- terectomy with a novel hysterectomy technique that pre- serves the uterine blood supply (STHMUV , uterine blood supply-preserving hysterectomy technique). Superior ovar- ian protection was observed with the STHMUV technique, which maintained stable postoperative estradiol (E2) levels (346.12 pg/mL to 298.34 pg/mL) over 2 years ( p > 0.05). In contrast, traditional hysterectomy exhibited a significant decline in E2 (343.24 pg/mL to 203.17 pg/mL, p < 0.05), and significantly lower E2 levels compared to STHMUV . Furthermore, the STHMUV group showed a significantly smaller increase in FSH (17.65 U/L to 20.17 U/L) compared to the traditional hysterectomy group (16.32 U/L to 89.01 U/L, p < 0.05). 5 6.2 Patient Characteristics 6.2.1 Age Y ounger patients (<40 years) have a higher risk of postoperative ovarian failure and a stronger association with surgery. Older patients ( ≥40 years) also have a sig- nificantly higher risk of ovarian failure (HR = 1.79) after hysterectomy. However, their risk is lower than for the younger group, probably because their ovarian reserve is al- ready in decline approaching the age of natural menopause, and hence the ‘extra blow’ of surgery is relatively limited. Huang et al . (2023) [ 20] conducted a systematic review and meta-analysis of 14 studies with 1457 premenopausal women. Their analysis revealed that women aged >40 years exhibited greater increases in FSH and LH levels, and more significant decreases in E2 concentrations, com- pared to their younger counterparts. However, the reduc- tion in AMH did not show any significant age-related ef- fects, whereas some studies have suggested the decline in AMH levels following hysterectomy is more pronounced in younger patients. For instance, a study by Y uan et al . (2019) [44] involving 84 participants found a stronger neg- ative correlation between hysterectomy and AMH levels in patients aged <40 years (r = –0.48 at 6 weeks, p < 0.001). Additionally, a prospective cohort study by Moorman et al. (2011) [ 14] involving 406 hysterectomy patients and 465 controls reported a stronger association between hysterec- tomy and ovarian failure in women aged <40 years (HR = 4.29, 95% CI: 0.83–22.3). While the risk of ovarian fail- ure was also significantly elevated in the ≥40 years group, the magnitude was lower (HR = 1.79, 95% CI: 1.18–2.71), likely due to the wider confidence intervals resulting from a limited sample size. 6.2.2 Smoking Cooper and Thorp (1999) [ 22] reported the impact of hysterectomy on FSH levels (OR = 1.5) was less pro- nounced than that of smoking (OR = 2.0), but significantly greater than the natural aging process. This finding under- scores the importance of incorporating the effect of hys- terectomy on the FSH level into postoperative management strategies. 7. Clinical Management Strategies for Ovarian Dysfunction After Total Hysterectomy The management of post-hysterectomy ovarian hy- poplasia and associated complications requires a full-cycle approach, incorporating detailed preoperative evaluation, optimized surgical techniques, and extended postoperative monitoring. The following evidence-based strategy is rec- ommended: 7.1 Preoperative Assessment of Ovarian Function In patients of childbearing age or those concerned about endocrine function, preoperative testing of AMH, FSH, and E2 should be conducted to evaluate the risk of postoperative ovarian failure. The factors of age, BMI, and smoking history should also be considered. Age >40 years and AMH levels below 1.2 ng/mL were identified as risk factors for significant postoperative ovarian function de- cline [45]. When necessary, three-dimensional Doppler ul- trasound should be used to assess ovarian blood flow (PI, RI), with increased risk of functional decline observed in patients with abnormal blood flow (PI >1.77, RI >0.8). 7.2 Surgical Options 7.2.1 Ovary Preservation In the absence of clear ovarian pathology, bilateral preservation is favored (89% vs. 66% for unilateral preser- vation 5 years postoperatively) [ 13]. Patients undergoing unilateral oophorectomy should be informed of the 2–3-fold increased risk of postoperative POI (HR = 2.93) [ 14]. 7.2.2 Salpingectomy Decision Opportunistic Salpingectomy (OS) does not cause sig- nificant acute damage to ovarian function, but may shorten the time to menopause (1.84 years in the OS group vs. 2.93 years in the preserved group) [ 32,34], and should thus be considered in the context of the patient’s age and reproduc- tive needs. When tubal resection is required, fine dissection should be used to avoid damage to the ovarian mesosalpinx vessels. AMH is monitored postoperatively until it stabi- lizes, usually after 3–6 months. 7.2.3 Surgical Extent In benign conditions, extrafascial subtotal resection is favored over radical resection to minimize the decrease in AMH level ( p = 0.001) and to maintain the ovarian blood supply provided by the uterine artery, which normally con- tributes 50–70% of the total supply [ 34]. 7.2.4 Laparoscopic Surgery Careful use of electrocoagulation equipment is re- quired, with preference given to cold knife separation or low-power modes of energy instrumentation to minimize ovarian damage from heat spread [ 34,43]. 7.2.5 V ascular-Preserving Techniques Surgical techniques that preserve the uterine vascula- ture, such as the STHMUV procedure, are recommended to maintain postoperative estrogen homeostasis. These mod- ified approaches result in a less pronounced decrease in estradiol levels (40%), which is a desirable outcome [ 43]. 6 7.3 Postoperative Monitoring and Management In line with the 2022 European Society of Human Re- production and Embryology (ESHRE) Guidelines on the management of premature ovarian insufficiency [ 46], as well as the expert consensus [ 20], the levels of AMH, FSH and E2 should be monitored postoperatively. Inter- vals should be shortened for patients who undergo laparo- scopic hysterectomy, or who retained only one ovary. An- nual evaluation should focus on FSH levels that exceed 40 IU/L (indicative of menopausal status), as well as the pres- ence of perimenopausal symptoms such as hot flashes and vaginal dryness. Particular consideration should be given to interventions for individuals who experience early-onset menopause (<40 years of age). Postoperative screening of pelvic floor function, in- cluding urodynamics, is recommended from 6 months on- ward in patients undergoing transvaginal surgery or radical resection. These should have careful monitoring for vaginal prolapse (37.8% incidence) and urethral dysfunction such as stress urinary incontinence (41% incidence at five years postoperatively). 8. Conclusions Post-hysterectomy ovarian function undergoes signif- icant changes, including diminished ovarian reserve, men- strual alterations, and early menopausal symptoms. The im- pact of surgical techniques and adjunct procedures on ovar- ian function is varied, and can influence the patients’ quality of life and psychological well-being. Clinicians should con- sider factors such as age, fertility desires, and disease sta- tus when selecting surgical methods and devising treatment plans. Surgical benefits and drawbacks must be balanced with ovarian function to tailor patient-specific strategies. Careful monitoring and management of postoperative ovar- ian function are crucial to promptly address issues, thereby improving the quality of life and health of patients. Future research should focus on personalized surgical designs such as vascular refinement protection, novel biomarkers includ- ing inflammatory factor profiles, and targeted interventions such as antifibrotic drugs. Advances in these areas should help to refine clinical management and improve long-term patient outcomes. Abbreviations AMH, anti-Müllerian hormone; FSH, follicle- stimulating hormone; STHMUV , uterine blood supply- preserving hysterectomy technique; HPO, hypothalamic- pituitary-ovarian; ANS, autonomic nervous system; PI, pulsatility index; RI, resistance index; PSV , peak flow velocity; LA VH, laparoscopically-assisted vaginal hys- terectomy; TAH, total abdominal hysterectomy; LUTD, lower urinary tract dysfunction; OS, opportunistic salp- ingectomy; PBS, prophylactic bilateral salpingectomy; BSO, bilateral salpingo-oophorectomy; LH, luteinizing hormone; E2, estradiol; USO, unilateral oophorectomy; TLH, total laparoscopic hysterectomy; LSH, laparoscopic supracervical hysterectomy. Author Contributions YC conceptualized and designed the review, con- ducted comprehensive literature search and selection, and compiled and synthesized the relevant data. LM not only provided critical advice on data collation and interpretation of the review findings, but also took the lead in formulat- ing literature inclusion and exclusion criteria, participated in the quality assessment of included literature, and con- structed the core argumentation. Both authors contributed to editorial changes in the manuscript. Both authors read and approved the final manuscript. Both authors have par- ticipated sufficiently in the work and agreed to be account- able for all aspects of the work. Ethics Approval and Consent to Participate Not applicable. Acknowledgment We would like to express our gratitude to all those who provided assistance during the writing of this manuscript. We also thank all peer reviewers for their valuable opinions and suggestions. Funding This research received no external funding. Conflict of Interest The authors declare no conflict of interest.

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