This chapter should be cited as follows:
Andersson KL, Glob Libr Women's Med
ISSN: 1756-2228; DOI 10.3843/GLOWM.418583
The Continuous Textbook of Women’s Medicine Series – Gynecology Module
Volume 4
Benign gynecology
Volume Editor: Professor Shilpa Nambiar, Prince Court Medical Centre, Kuala Lumpur, Malaysia
Chapter
Uterine Fibroids: from Molecular Pathogenesis to Contemporary Management
First published: February 2026
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PATHOGENESIS
The pathogenesis of uterine fibroids is complex and remains uncertain but is thought to involve the transformation of smooth muscle cell stem-cell precursors into fibroids after cumulative 'hits' related to traditional risk factors (age, ethnicity, obesity), coupled with hormonal, genetic, environmental and molecular influences.
Uterine fibroids have been described as monoclonal tumors of the myometrial smooth muscle cells that are benign, a description that has been reinforced by histological findings as well as biochemical evidence, including glucose-6-phosphate dehydrogenase isoform expression,1 X-chromosome-linked phosphoglycerokinase (PGK) gene expression via differential inactivation,2 and non-random X-chromosome inactivation as assessed using the human androgen receptor (HUMARA) assay.3,4 Cumulatively, these findings prove that each leiomyoma is unicellular in origin, even if multiple fibroids arise independently within the uterus.1,2,4 More recently, single-cell analysis has demonstrated cellular heterogeneity within fibroids, reporting multiple subpopulations of smooth muscle cells and fibroblasts. These findings contradict the longstanding monoclonal theory and have important implications for disease mechanisms and personalized treatment in the future.5
Besides their monoclonal origin, leiomyomas are heterogeneous tumors characterized by aberrant extracellular matrix (ECM) deposition that plays a fundamental role in their biology. Fibroblasts in leiomyomas – occasionally referred to as 'myofibroblasts – express increased levels of type-I and -III collagen mRNA and proteins during the proliferative phase of the menstrual cycle compared to normal myometrium.6 This remodeled ECM provides a reservoir of growth factors, cytokines, chemokines and proteases essential for tumor growth.4,7,8,9 Uterine leiomyoma cells cultured with leiomyoma-derived fibroblasts in co-culture experiments have been shown to exhibit enhanced proliferation, increased ECM collagen type I, and greater secretion of growth factors VEGF, EGF, FGF-2, PDGF and TGF-β, as well as activation of receptor tyrosine kinases. These effects were not observed in co-cultures with normal myometrial fibroblasts,9 emphasizing the importance of cross-talk among leiomyoma smooth muscle cells, fibroblasts and the stromal compartment for sustaining tumor growth.
ECM turnover abnormalities also lead to fibrosis and tumor stiffness, with collagen gene dysregulation and altered fibril structure in leiomyomas.10 Transforming growth factor-β (particularly TGF-β3) has been identified as a major mediator in this process, promoting overexpression of ECM-related genes (collagen 1A1, fibronectin 1 and connective tissue growth factor) and repression of ECM-degrading enzymes such as matrix metalloproteinase 2.11 Exogenous TGF-β3 can even induce a leiomyoma-like phenotype in normal myometrial cells, and therapies such as GnRHa downregulate the expression of TGF-β.12,13 Other mediators, e.g. GM-CSF, also regulate TGF-β activity, inducing fibrosis.13
Genetic alterations also play a central role, with mutations in MED12, HMGA2, CYP1A1, CYP1B1 and proto-oncogenes such as p27 and p53, as well as dysregulation of signaling pathways (e.g. PI3K–AKT–mTOR) and epigenetics.14 MED12 is the most frequently altered gene (50–85%), with a driver role for TGF-β overexpression and abnormal ECM deposition.15,16,17 A smaller percentage of fibroids are associated with HMGA2 overexpression or COL4A5–COL4A6 locus disruption.18,19 More recent multi-omic studies deduce that these alterations (MED12, AHR, COL4A6) can additionally disrupt RNA splicing in the adjacent endometrium, providing a mechanistic link between fibroids and abnormal uterine bleeding.20 Also, dysregulated expression of small non-coding RNAs, including miRNAs (miR-21, miR-29, miR-200, miR-93) and lncRNAs (H19, MIAT, XIST), influences proliferation, apoptosis, ECM remodeling, angiogenesis and inflammation, pointing to their potential as biomarkers and therapeutic targets.21,22,23
Family linkage analyses of syndromes associated with leiomyomas support a genetic susceptibility to their development, such as in the autosomal dominant syndrome hereditary leiomyomatosis and renal cell cancer.24 The syndrome is due to mutations in the fumarate hydratase gene that interfere with tumor suppressor function and may also be involved in the pathogenesis of non-syndromic leiomyomas, particularly in white women.25
In addition to genetic, molecular and microenvironmental processes, vascular dysregulation is also key to the symptoms of leiomyoma. Disordered angiogenesis and vessel growth have been implicated in abnormal uterine bleeding in women with fibroids since Sampson's early descriptions in 1912.26 Abnormal bleeding in this context is associated with structural and functional alterations of the endometrium and its vessels. Exuberant ECM deposition and TGF-β signaling account for uterine stiffness, contractile dysfunction and reduced receptivity, as well as disrupting vascular remodeling by dysregulating angiogenic factors (TGF-β, VEGF, PDGF, EGF, TNF-α, PGF2α, ET-1), immune imbalance, and aberrant microRNA networks, thereby promoting aberrant bleeding and infertility.27 Moreover, fibroids display a distinctive vascular architecture, with a hypovascular core encircled by a vascularized capsule, reflecting an aberrant angiogenic response. Despite their hypoxic environment, they possess a defective HIF-1α pathway, which may be the reason for their abnormal growth pattern. All of these features render fibroids extremely vulnerable to anti-angiogenic mechanisms, a process that is already being exploited by GnRH agonists and uterine artery embolization.28
Ovarian steroid hormones are essential for fibroid growth, and most tumors regress after menopause. Estrogen and progesterone act synergistically, with estradiol inducing progesterone receptor expression, and progesterone promoting fibroid growth through stimulation of the Ras–Raf–MEK–MAPK and PI3K–Akt–mTOR signaling pathways..29,30,31,32,33,34 The progesterone receptor isoforms, in particular PR-A, dominate in leiomyomas, and aromatase overexpression leads to increased local estrogen production.35,36 The high level of PR-B in leiomyomas is associated with more tumor burden but with decreased bleeding and pain, implicating that PR-B promotes growth but inhibits symptoms.37 Other pathways involved include paracrine WNT/β-catenin signaling in stem-like leiomyoma cells (LMSPs), which appear to be necessary for tumor growth in vivo and hormone-dependent growth of the lesions.38,39 Leiomyomas exhibit moderate in-situ upregulation of 17β-hydroxysteroid dehydrogenase type 1 (17β-HSD1) relative to myometrium, resulting in increased local conversion of estrone to estradiol..40
The gut microbiota may also play a role in fibroid pathogenesis by modulating systemic estrogen levels through the so-called estrobolome. Certain individual species, such as Clostridium and Pneumococcus, play important roles in estrogen metabolism.41,42 This raises the intriguing possibility that the makeup of the gut microbiota might influence fibroid risk, for which direct evidence is still awaited. Similarly, while the uterine cavity does indeed harbor a distinct microbiome, its role in leiomyoma pathogenesis remains unproven and is awaiting investigation.43
Non-hormonal pathways have also been involved. Deficiency in vitamin D worsens TGF-β-mediated fibrotic reactions, with supplementation blocking the effects.44,45 Accordingly, 1,25(OH)2D3 downregulates ER-α, PR-A and PR-B, and induces VDR and VDR–RXRα complexes in leiomyoma cells, acting as an antagonist of sex steroid receptors.46 Other systemic disorders, including hypertension, diabetes, pelvic infection and perineal talc exposure, can also stimulate the growth of fibroids through the induction of hypoxic reactions in myometrial cells.47
Finally, endocrine-disrupting chemicals (EDs), including plasticizers, dioxins, polychlorinated biphenyls, organochlorines, phthalates and diethylstilbestrol, may play a role in fibroid pathogenesis by binding nuclear receptors, mimicking endogenous hormones, and inducing epigenetic reprogramming of myometrial stem cells (MMSCs).48,49 Developmental exposure to EDs can lead to a permanent hormonal imprint on key signaling pathways, with predisposition to hormone-dependent fibroids. According to the 'two-hit' hypothesis,49 MMSC epigenetic reprogramming during early life may be the first hit, and later-life adverse exposures may be the second hit that transforms reprogrammed cells into tumor-initiating stem cells.
Overall, uterine leiomyomas can be considered the product of cumulative genetic alterations in myometrial stem cells, sustained by hormonal stimulation, ECM remodeling and complex interactions with the tumor microenvironment and systemic hormones. Such multifactorial interaction explains their heterogeneity and wide spectrum of clinical presentations in affected women.
MANAGEMENT
The management of uterine fibroids is multifaceted, with treatment options ranging from expectant management, medical therapy and minimally invasive procedures, to surgical intervention. Medical therapy is considered first-line, particularly in women desiring fertility preservation or aiming to delay surgical procedures. Importantly, medical management can address symptoms such as menorrhagia, anemia, pelvic pain, and pressure effects, without the immediate need for invasive interventions.
MEDICAL THERAPY
Non-hormonal therapy (tranexamic acid)
Tranexamic acid (TXA) is a synthetic analog of lysine that inhibits fibrinolysis. It reduces menstrual blood loss effectively; studies indicate an average reduction of approximately 89 mL per cycle, making it a valuable agent for heavy menstrual bleeding (HMB) in fibroid-affected women.50 Its mode of action involves stabilizing clots, thus managing bleeding without affecting fibroid size.
The safety profile of TXA is favorable, with gastrointestinal discomfort, headaches, dizziness and mood swings being the most common adverse events. Importantly, no thromboembolic complications have been reported with TXA.50 However, contraindications include a history of thromboembolism or active thrombotic disease, limiting its use in some patient populations.
Hormonal therapy
Progesterone receptor modulators (ulipristal acetate and others)
Ulipristal acetate (UPA), a selective progesterone receptor modulator (SPRM), was widely used until safety concerns prompted restrictions. Prior to these, UPA demonstrated significant efficacy in reducing fibroid volume and controlling bleeding. The PEARL studies illustrated this benefit, providing a substantial reduction in fibroid size and bleeding severity.51 However, reports of serious liver injury led to its restricted use in Europe and withdrawal in some markets, including the USA.52
Other SPRMs under investigation continue to show promise, with ongoing trials assessing their safety and efficacy. These agents modulate progesterone activity, which is critical in fibroid pathogenesis, leading to decreased cell proliferation and fibroid shrinkage.
Oral progestins and levonorgestrel-releasing intrauterine system (LNG-IUD)
Oral progestins, such as medroxyprogesterone acetate, are primarily employed for symptomatic control of menorrhagia, with benefits including affordability and widespread availability. However, evidence suggests they do not significantly reduce fibroid size.50 The LNG-IUD, releasing levonorgestrel locally within the uterus, effectively reduces menstrual bleeding and has been associated with decreases in uterine volume, though its impact on fibroid size remains modest (<10%).50
The LNG-IUD has the additional advantage of contraception and can be particularly useful in women with heavy bleeding caused by fibroids, especially when fibroids are small or medium-sized (< 3 cm).
Combined hormonal contraceptives (CHCs)
The use of CHCs moderates menstrual bleeding and provides contraception, with studies indicating a modest reduction in menstrual blood loss (~13%) and no evidence of fibroid growth promotion.50 Their role is primarily symptom control rather than fibroid size reduction. Older women or those with thrombotic risk factors should avoid estrogen-containing formulations due to increased thromboembolic risks.
Gonadotropin-releasing hormone (GnRH) agonists
GnRH agonists like leuprolide induce an initial flare response followed by downregulation of gonadotropins, resulting in hypoestrogenism. They effectively reduce fibroid volume by approximately 50%, improve anemia and decrease bleeding.50 Their role is mainly preoperative or short-term, as their adverse effects – hot flushes, bone mineral density loss, vaginal dryness – preclude prolonged use.
Gonadotropin-releasing hormone (GnRH) antagonists
GnRH antagonists have emerged as a medical treatment option for symptomatic uterine fibroids offering an effective balance of efficacy, rapid symptom control and an improved safety profile compared with traditional medical treatments.
- Mechanism of Action and Pharmacology
Relugolix and linzagolix are reversible GnRH antagonists that suppress gonadotropin release by competitively binding to GnRH receptors in the pituitary gland, thereby promptly suppressing the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Unlike GnRH agonists, antagonists do not cause the initial hormone 'flare' effect, which can worsen symptoms temporarily. Through rapid receptor blockade, these agents induce a reversible hypoestrogenic state that reduces fibroid volume and controls menstrual bleeding effectively within days to weeks of therapy initiation.53
- Clinical efficacy
Data from multiple randomized clinical trials involving over 4000 premenopausal women demonstrate that GnRH antagonists – such as relugolix, elagolix, and linzagolix – significantly reduce menstrual blood loss and fibroid size compared to placebo. Symptom relief is rapid and sustained, improving quality of life and anemia. For example, meta-analyses show a pooled relative risk of approximately 5 for controlling uterine bleeding and mean fibroid volume reduction around 27% during treatment courses.54
Targeted medical treatment for uterine fibroids may delay or obviate the need for surgery, especially in the patient groups with a desire for uterus preservation. Access and affordability of medical treatments affect global management, highlighting the need for equitable care delivery, especially in populations with a higher fibroid burden.55
SURGICAL TREATMENT
Surgical treatment of fibroids involves several approaches focused on removing or reducing fibroids to relieve symptoms while considering factors such as fibroid size, number, location and the patient’s desire to preserve the fertility as well as previous obstetric history.
Laparoscopic and robotic myomectomy
Laparoscopic and robotic myomectomy are minimally invasive surgical techniques that offer uterus-preserving treatment options for women with symptomatic uterine fibroids. Both approaches have evolved significantly over recent years, providing alternatives to traditional open surgery with benefits including lower blood loss, shorter hospital stays and expedited recovery.
Indications and patient selection
Both laparoscopic myomectomy (LM) and robotic myomectomy (RM) are indicated in women with symptomatic fibroids causing menorrhagia, pelvic pain, pressure symptoms, bulk-related complaints, or infertility, who wish to preserve their uterus. Careful preoperative assessment including imaging with ultrasound or MRI is essential to evaluate fibroid size, number and location, guiding surgical approach selection. LM is generally preferred for fibroids up to 10 cm and limited number, while RM can facilitate removal of larger or more complexly located fibroids due to enhanced dexterity and visualization.56,57
Surgical techniques
In laparoscopic myomectomy, small incisions are made for trocar placement. After vasopressin injection for hemostasis, the myometrium is incised and fibroids are enucleated using laparoscopic instruments. Multilayered suturing of the myometrial defect is critical to restore uterine integrity, typically achieved using intracorporeal knot tying or barbed sutures. Patients undergoing barbed suture laparoscopic myomectomy experienced significantly lower suturing time and blood loss. Regarding obstetric outcomes, barbed sutures in myomectomy are as safe as conventional sutures and do not adversely affect pregnancy outcomes.58,59,60
Robotic myomectomy utilizes a robotic platform providing 3D visualization and wristed instruments improving suturing precision and access, especially for fibroids in challenging locations such as posterior or fundal fibroids. Docking and setup increase operative time, but the ergonomics and enhanced dexterity facilitate performance of complex cases.56,61
In both approaches, fibroid extraction is commonly performed via morcellation. Due to concerns about spreading occult malignancy, contained morcellation within specimen bags is increasingly recommended.56
Comparative outcomes
Several studies comparing LM and RM reveal both techniques significantly reduce blood loss and postoperative pain compared with abdominal myomectomy (AM). RM tends to have longer operative times, primarily due to robotic setup, but has been associated with reduced estimated blood loss and shorter hospital stays relative to LM.57,62
RM has been demonstrated to allow removal of larger and less accessible myomas, with potentially lower conversion rates to open surgery. However, LM outcomes improve with surgical experience, making operative durations and complication rates comparable in high-volume centers.56,61
Cost considerations remain relevant, as RM entails significantly higher direct surgical expenses compared to LM, potentially limiting accessibility.57
Fertility outcomes and postoperative pregnancy guidance
Both LM and RM preserve fertility, with postoperative pregnancy rates reported between 60% and 85%. The minimally invasive nature of these procedures contributes to favorable uterine healing and reduced adhesion formation compared to open surgery.63
Pregnancy is generally recommended to be deferred for 3 to 6 months postoperatively to allow adequate myometrial healing.64 Cesarean delivery may be advised depending on surgical complexity and extent of uterine repair, although vaginal delivery is feasible in selected patients.65,66
Limitations
Both techniques require advanced surgical skills. LM necessitates proficiency in laparoscopic suturing, while RM’s longer operative time and higher cost may limit routine use. Potential risks include intraoperative hemorrhage and fertility-impacting uterine rupture, mandating careful patient selection and counseling.56,61
Summary
Laparoscopic and robotic myomectomy represent safe, effective minimally invasive approaches for fibroid management in women desiring uterine preservation. Each modality has distinct advantages: LM benefits from shorter operative times and lower costs, while RM offers ergonomic ease, potentially improved access to complex myomas, and reduced conversion rates. Both result in favorable clinical and reproductive outcomes with reduced morbidity compared to open surgery. Selection should consider surgeon expertise, patient anatomy, surgical complexity and resource availability.
Hysteroscopic myomectomy
Indications
HM is primarily indicated for submucosal fibroids classified as FIGO Types-0, -1 and selected Type-2 lesions that significantly distort the uterine cavity and cause symptoms such as menorrhagia, prolonged menstrual bleeding and infertility due to mechanical disruption of the endometrial cavity. It is especially favored in women seeking fertility preservation since it avoids uterine incision and extensive myometrial trauma seen in abdominal surgery. Fibroids larger than 3–4 cm, multiple fibroids or those with deep intramural components (Type 2, large size) frequently require staged procedures or alternative approaches due to increased procedural complexity.67,68
Surgical technique
The procedure is carried out under either general or regional anesthesia, and bipolar resectoscopes are usually favored because they offer greater safety and efficient coagulation. Vasoconstrictive agents may be administered to reduce intraoperative bleeding and improve visualization. Submucosal fibroids are resected using a loop electrode or mechanical shaver, preferably with complete removal in the first session to minimize the need for repeat surgery.
For large or Type-2 fibroids, which are partly intramural, multiple staged resections may be necessary to avoid uterine perforation or fluid overload. Fluid management protocols and careful monitoring of fluid balance are critical to minimize risks of hyponatremia.69,70
Clinical outcomes
Hysteroscopic myomectomy effectively improves symptoms of heavy menstrual bleeding, with success rates ranging from 70% to 99% depending on fibroid characteristics, extent of removal and follow-up duration. Symptom recurrence primarily occurs within the first year, often attributed to incomplete resection or the development of other endometrial dysfunctions. Patients frequently report high satisfaction postoperatively due to rapid alleviation of bleeding and improved uterine function.67,69
Reproductive outcomes also improve considerably; cumulative live birth rates increase following HM, with studies reporting live birth rates reaching approximately 43% in women with prior infertility. However, post-surgical intrauterine adhesions (Asherman syndrome) occur in some cases, sometimes necessitating additional treatment to restore uterine cavity patency.70
Advantages and complications
Advantages of HM include minimal invasiveness, preservation of uterine anatomy, avoidance of abdominal incisions and short hospital stays or outpatient performance. Bipolar instruments reduce the risk of fluid overload and electrolyte disturbances traditionally associated with monopolar resection.68
Complications include uterine perforation, fluid overload, bleeding, infection and formation of intrauterine adhesions. Careful patient selection, surgical expertise and adherence to safety protocols reduce these risks substantially. Avoidance of multiple procedures through complete removal during the initial surgery lowers morbidity and improves outcomes.69
Fertility implications
HM represents the treatment of choice for women with submucosal fibroids and fertility issues, improving pregnancy rates by restoring normal uterine cavity architecture. Fertility outcomes are generally favorable, although risk of adhesion formation warrants the use of postoperative adhesion prevention strategies and possibly hysteroscopic assessment before conception attempts. Time to conception is typically recommended to be at least 1–2 menstrual cycles post-resection.70
MINIMALLY INVASIVE APPROACHES
Minimally invasive uterus-preserving treatments for symptomatic uterine fibroids, which offer alternatives to hysterectomy or myomectomy and are associated with reduced morbidity, include ablative techniques (transvaginal radiofrequency ablation (TVRFA) and microwave ablation (MWA)), uterine artery embolization (UAE) and high-intensity focused ultrasound (HIFU).
Transvaginal radiofrequency ablation
TVRFA is an emerging minimally invasive technique for the treatment of symptomatic uterine fibroids, offering a uterus-preserving alternative to traditional surgical methods. Guided by transvaginal ultrasound, this approach uses targeted radiofrequency energy to induce thermal coagulative necrosis within fibroid tissue, leading to fibroid shrinkage and symptom relief without significant injury to surrounding myometrium.71,72
Procedure and technique
TVRFA is performed under sedation or local anesthesia in an outpatient setting. Using real-time transvaginal ultrasound guidance, a dedicated cooled radiofrequency needle is inserted transvaginally directly into the fibroid. Advanced virtual needle tracking technology enhances accurate probe placement, minimizing the number of punctures and procedural risks. Ablation employs either a fixed needle or a moving shot technique to ensure comprehensive treatment of the fibroid volume. Continuous ultrasound monitoring enables visualization of echogenic changes confirming effective thermal injury of the targeted tissue.71,72
Clinical outcomes and safety
Clinical studies demonstrate that TVRFA achieves significant fibroid volume reduction accompanied by marked improvements in quality of life and symptom severity scores. The procedure shows high technical success with negligible major complications.72,73,74 Minor adverse events such as transient pelvic pain and mild vaginal bleeding are uncommon and self-limited. Notably, the minimally invasive, incision-free nature of TVRFA facilitates a rapid return to daily activities.
Advantages and considerations
Radiofrequency ablation, also feasible via laparoscopic and abdominal access,75 has in recent years been largely replaced by the transvaginal approach, which is more cost‑effective and straightforward for gynecologists in daily practice. The technique avoids abdominal incisions and general anesthesia, improving patient comfort and reducing healthcare costs. Transvaginal access allows direct fibroid targeting with minimal tissue disruption. The technique circumvents concerns related to morcellation and uterine repair required in surgical myomectomy.
Patient selection is critical; TVRFA is currently best suited for solitary or limited numbers of fibroids up to approximately 5 cm in diameter and with suitable transvaginal accessibility. Fibroids with large intramural components or very large volumes may require alternative treatments. Long-term data on fertility outcomes are still limited, so counseling regarding reproductive planning remains essential.73
TRFA ablation represents a feasible, safe and effective minimally invasive treatment for uterine fibroids, providing substantial symptom improvement and fibroid shrinkage with minimal morbidity. Its outpatient applicability, rapid recovery time and uterus-sparing profile make it an attractive option for selected patients. Ongoing research is needed to better define long-term reproductive outcomes and refine patient selection criteria.76,77
More detailed information on TVRFA can be obtained from Current Role of Radiofrequency Ablation in the Management of Uterine Fibroids in GLOWM's Continuous Textbook of Women's Medicine.
Microwave ablation
Microwave ablation (MWA) represents a minimally invasive, uterus-preserving treatment for symptomatic uterine fibroids, utilizing ultrasound-guided percutaneous or vaginal insertion of a microwave antenna to induce thermal coagulation necrosis. Fewer data are available compared to TVRFA but, in a prospective study of 123 patients, MWA achieved a 37% reduction in symptom severity score (SSS) and 74% improvement in health-related quality of life (UFS-QoL) at 6 months post-treatment (P < 0.001), alongside 38% decreased menstrual blood loss, according to a pictorial bleeding assessment chart (PBAC).78 Median fibroid volume shrinkage reached 64% for the three largest treated fibroids, with submucosal types showing superior (82%) reduction compared to 66% intramural and 55% in subserosal cases. The procedure involved real-time ultrasound monitoring, with power settings of 50–100W for 10–30 minutes per fibroid, often under sedation; 97% of patients were discharged on the same day, reporting mild or moderate pain (VAS median not exceeding 4). The safety profile was favorable, with only 0.8% Clavien-Dindo Grade 3 adverse events (one bowel injury requiring resection) and high acceptability.78 A 2021 meta-analysis of 671 cases confirmed 66% symptom relief, 72% quality-of-life gain, and 85% volume reduction, with minor complications in 21%.79
Uterine artery embolization (UAE)
Uterine artery embolization (UAE) is a minimally invasive, uterus-sparing procedure widely employed for the treatment of symptomatic uterine fibroids. The technique involves catheter-directed occlusion of the uterine arteries, reducing blood flow to fibroids and inducing ischemic infarction, which results in significant fibroid volume reduction and symptom relief.80
Indications and patient selection
UAE is primarily indicated for women with symptomatic fibroids causing heavy menstrual bleeding, pelvic pain or bulk-related symptoms. It is particularly beneficial for patients who wish to avoid hysterectomy or those with contraindications to surgery. Ideal candidates have fibroids confirmed by imaging, without suspicion of malignancy, and no desire for immediate future pregnancy, as the impact on fertility is still debated.81
Procedure and outcomes
The procedure is performed under local anesthesia and guided by fluoroscopy. Embolic agents, typically polyvinyl alcohol particles, are introduced bilaterally to achieve vessel occlusion. UAE effectively reduces fibroid size by 40–60% and alleviates symptoms in approximately 85–90% of patients, with durable results over long-term follow-up. Complications are uncommon but may include post-embolization syndrome characterized by pain, fever and nausea, which is generally self-limiting. Rarely, non-target embolization, infection or premature ovarian failure can occur.81
Impact on fertility
The effect of UAE on fertility remains controversial. While some studies report successful pregnancies post-UAE, others suggest a higher risk of miscarriage and adverse obstetric outcomes compared to myomectomy. Hence, UAE is generally reserved for women who have completed childbearing or have contraindications to surgery.80
High-intensity focused ultrasound
Magnetic resonance-guided high-intensity focused ultrasound (MR-HIFU) provides an outpatient treatment for symptomatic uterine fibroids, using focused ultrasound waves under real-time MRI to induce thermal coagulation necrosis.82
In a 2025 prospective study (n = 175), symptom severity scores (SSS, UFS-QoL) decreased significantly from baseline to 28 at 12 months (P < 0.001), with quality-of-life (QoL) scores rising to 73, approaching healthy controls. Fibroid volume reductions averaged 50–70% at 12 months, sustained with 2% reintervention rate;83 meta-analyses confirm 40–60% SSS improvement and superior short-term QoL gains over surgery.
However, the technique has in recent years largely been replaced by other ablation techniques due to its unfavorable cost and complication profile.
CONCLUSION
Most women with uterine fibroids remain asymptomatic throughout their lives, with only approximately 30% developing clinically relevant symptoms that justify active intervention. Optimal medical management strategies require a nuanced understanding of the molecular and cellular mechanisms underlying fibroid growth, the role of ovarian steroid hormones and other modulators, as well as the safety profile and pharmacodynamics of each therapeutic agent.
The management of women with uterine fibroids should be individualized, ensuring that therapeutic decisions are driven by the predominant symptomatology (abnormal uterine bleeding, bulk-related symptoms, pain, infertility) and by clearly defined reproductive and clinical objectives. Appropriately selected, targeted medical and minimally invasive techniques can postpone or, in some cases, avoid the need for invasive surgical procedures, which is particularly relevant for patients with a strong desire for uterine preservation or for those who are poor surgical candidates.
Moreover, availability, reimbursement policies and overall affordability of medical treatments and access to alternative and minimally invasive approaches significantly influence real-world management pathways and treatment adherence. These health-system and socioeconomic factors underscore the importance of promoting equitable access to evidence-based therapies, especially in populations disproportionately affected by a higher fibroid burden, including many women of African and Afro-Caribbean ancestry.
PRACTICE RECOMMENDATIONS
- Individualize treatment: tailor therapy based on symptoms, fibroid size, number, location, patient’s age, reproductive goals and comorbidities to optimize outcomes and align with patient preferences.
- First-line medical management: utilize hormonal agents such as GnRH antagonists for symptom control and volume reduction, particularly in patients desiring fertility preservation or as a bridge to invasive therapies.
- Minimally invasive techniques: consider uterus-sparing procedures like ablation techniques and uterine artery embolization, balancing efficacy, recovery time and fertility considerations.
- Surgical approach: reserve myomectomy for symptomatic fibroids in women wishing to maintain fertility or when minimally invasive options are unsuitable or ineffective.
- Multidisciplinary decision-making: engage gynecologists, interventional radiologists and reproductive specialists in shared decision-making to enhance individualized care plans and address complex cases.
- Fertility counseling: provide detailed counseling on the reproductive implications and available fertility-sparing treatments, considering emerging evidence on the safety of minimally invasive ablation techniques.
CONFLICTS OF INTEREST
The author(s) of this chapter declare that they have no interests that conflict with the contents of the chapter.
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