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NATURE REVIEW: UTERINE FIBROIDS


Abstract

Uterine Fibroids:
Also known as leiomyomas or myomas.
Common clonal neoplasms of the uterus.
Comprise smooth muscle, fibroblast components, and a significant amount of fibrous extracellular matrix.
Heterogeneous in terms of pathophysiology, size, location, and clinical symptomatology.
Some variants display malignant traits but are predominantly benign.
Risk and Prevalence:
Black women have:
Earlier onset.
Higher risk.
More severe forms of fibroids compared to white women.
Clinical Impact:
Account for 33% to 50% of all hysterectomies.
Substantial morbidity and health care costs for reproductive-age women.
Majority of treatments (about 75%) are hysterectomies.
Treatments:
Primarily surgical and interventional.
Emerging innovations in using progesterone receptor modulators for medical therapy.
Genetic Information:
Rapid accumulation of data on genetic subgroups leading to fibroid formation.
Can potentially provide deeper insights into the disease's clinical diversity.
Aims to pave the way for individualized treatments.
Crucial given the current lack of solid evidence for therapeutic decisions.

Introduction

Benign neoplasms of the uterus.
Comprised of smooth muscle cells, fibroblasts, and rich in extracellular matrix (ECM).
Develop and regulate gene expression due to gonadal steroids, especially during menarche and menopause.
Morbidity and Symptoms:
Major morbidity source for reproductive-age women.
Can cause:
Heavy/prolonged menstrual bleeding, leading to social issues and anemia.
Enlargement of the uterus, causing urinary and gastrointestinal symptoms.
Abdominal distention/pain.
Many women remain asymptomatic despite having large fibroids.
Treatments:
Hysterectomy is the primary option, with a lifetime risk of 45% in the U.S.
Contributes to at least 33%-50% of all hysterectomies globally.
Accounts for almost 75% of fibroid-related surgeries in the U.S.
Alternative treatments include:
Myomectomies.
Embolization.
Thermoablative therapies.
Medical therapies: PRMs, tranexamic acid, GnRH agonists, oral contraceptives, levonorgestrel intrauterine device.
Economic and Social Impact:
Indirect costs include lost income, disability, sanitary products, alternative therapies.
Associated with infertility and other pregnancy complications.
Biology and Characteristics:
Interesting yet understudied biology.
Can rapidly increase in volume but have a low mitotic index.
Impressive size (10–20 cm lesions are not uncommon).
Some theories on fibroid-related prolonged/heavy menstrual bleeding but little evidence.
Rare variants display malignant traits but are mainly benign.
Research and Future Perspective:
Fibroids are common, providing ample tissue for research.
Useful as a model for testing minimally invasive therapies.
This review covers epidemiology, pathophysiology, and management of fibroids, highlighting key research questions.

Epidemiology

- **Prevalence of Fibroids:** - Fibroids occur in >70% of women according to ultrasonography and pathology data. - 25–50% of women with fibroids report clinical symptoms. - Self-reported rates for more severe cases range from 12.8 per 1,000 person-years for diagnoses to 2 per 1,000 person-years for hysterectomy-confirmed cases in the U.S. - In Europe, prevalence of diagnosed symptomatic fibroids varies from 11% in France to 24% in Italy. - Women likely experience symptoms for several years before diagnosis.
- **Risk Factors and Demographic Differences:** - **Age:** - Fibroids are not found in prepubertal girls but begin in teenage years. - Incidence rises until menopause. - **Race:** - Incidence of fibroids is 2-3 times greater among black women than white women in the U.S. - Black women develop fibroids about 10 years earlier than white women. - Peak prevalence by 50 years of age: 80% in black women, 70% in white women. - Point prevalence for clinically significant fibroids: 50% for black women, 25% for white women. - Greater severity of symptoms in black women; they also have larger uteri, more and larger fibroids. - Fibroids in black women don't show decelerated growth approaching menopause, unlike in white women. - Mean ages at hysterectomy lower for black women; they are seven times more likely to undergo myomectomy. - In South Africa, black women 20% more likely to have histological evidence of fibroids. - Genetic studies link fibroids to having more African than European ancestry. - Limited data on Asian and Latin American women, but incidence seems closer to white women's rates.
- **Pregnancy and Hormonal Factors:** - **Pregnancy:** - Women with pregnancies longer than 20 weeks have a decreased risk of developing fibroids. - Uterine remodeling post-pregnancy may help shrink or eliminate fibroids. - In women with a solitary fibroid during early pregnancy, 36% were not detectable post-birth, and 80% of remaining tumors were smaller postpartum. - **Hormones:** - Early menarche (before 10 years of age) and exposure to diethylstilbestrol (a non-steroidal estrogen analogue) are risk factors. - Long-acting progestins like depot medroxyprogesterone decrease the risk. - Oral contraceptives generally don't affect development or growth except possibly when used before 16 years of age.
- **Dietary Factors:** - **Red Meat:** Consumption associated with a 70% increased risk. - **Green Vegetables and Fruits:** Intake reduces the risk. - **Dairy:** Decreases risk in a dose-response manner; women consuming ≥4 servings per day had a 33% decrease in risk compared to those consuming <1 serving daily. - **Soy:** Not associated with fibroid risk, often a substitute for dairy. - **Alcohol:** Particularly beer, increases the risk. - **Vitamin D Deficiency:** Associated with increased risk and more common in women of African descent; may explain some differences in prevalence between black and white women.
- **Other Factors:** - **Sexually Transmitted Infections (STIs):** - The SELF trial is investigating associations between STIs and fibroids. - Baseline analysis did not confirm increased risk with pelvic inflammatory disease but supported increased risk with a history of bacterial vaginosis. - Cross-sectional study found no presence of latent Chlamydia spp. or herpes simplex viruses in fixed fibroid tissue. - **Human Papillomavirus (HPV):** - An inverse relationship between fibroids and abnormal pap tests reported in three cohorts, indicating a possible protective effect of HPV on fibroids.

Mechanisms/pathophysiology

Traditional Definition:
Uterine fibroids are clonal smooth muscle cell neoplasms.
They are growth-responsive to gonadal steroids.
Characteristic chromosomal rearrangements underlie their development.
Fibroid Stem Cells and Tissue Constituents:
Myometrium houses smooth muscle stem cells: myometrial stem cells.
These can transform to fibroid progenitor cells under certain conditions.
Myometrial stem cells have low-to-absent levels of sex steroid hormone receptors but need these steroids for growth.
Disease development seems to be a multistep process, dependent on a paracrine mechanism.
WNT–β-catenin pathway, alongside oestrogen and progesterone, mediates this mechanism.
The pathway can stimulate TGFβ3 expression, which further induces fibronectin expression and cell proliferation.
Components and Diversity:
Fibroids consist of:
Smooth muscle cells.
Vascular smooth muscle cells.
Two types of fibroblasts (regular fibroblasts and fibroid-associated fibroblasts).
All these cell types are clonal, derived from the same cell.
Cells exhibit differential expression of genes: CRABP2, PGR, and TGFBR2.
These differences in gene profiles account for the heterogeneity in fibroid biology and clinical types.
Extracellular Matrix (ECM):
ECM secreted by fibroblasts is crucial to fibroid pathophysiology.
Growth factors in the ECM that might regulate fibroid formation include:
FGF2.
VEGF.
HB-EGF.
PDGF.
The quantity and topology of ECM in fibroids differ from the myometrium.
Solid-state signalling might occur in fibroids, converting mechanical stress into biochemical cell signalling.
Fibroblasts, which secrete most ECM components, are key to fibroid pathophysiology.

Genetics:

1. **Identification of Fibroid Genetic Subgroups:** Four key pathogenetic subgroups are identified based on somatic mutations or chromosomal alterations: - **MED12 Group** - **HMGA2 Group** - **FH (Fumarate Hydratase) Group** - **Rare Group with deletion of COL4A5 and COL4A6**
2. **MED12 Mutations:** - MED12 mutations are detected in 50–84% of fibroids and drive their formation. - They occur in racially diverse cohorts and affect the interaction between MED12 and cyclin C, which regulates β-catenin transcriptional activity. - This leads to increased levels of WNT4–β-catenin in fibroids with MED12 mutations. - Oestrogen and the WNT4 pathway interactions might explain enhanced growth in these fibroids. - MED12 mutations are identified in rare fibroid variants but at a lower frequency, suggesting different regulation.
3. **Complex Chromosomal Rearrangements & HMGA2 Dysregulation:** - Chromothripsis, once thought to be limited to malignant tumors, plays a role in fibroid pathogenesis. - Specific karyotypic rearrangements lead to HMGA2 dysregulation, possibly affecting fibroid growth via increased expression of CDKN2A (encodes ARF (p14)). - Interaction between HMGA2 and let-7 (a microRNA precursor) might repress HMGA2, inhibiting cellular proliferation. - Alterations in the let-7–HMGA2–ARF (p14) pathway might increase self-renewal capability and reduce senescence of fibroid progenitor cells. - MED12 and HMGA2 mutations appear to be mutually exclusive.
4. **Inactivating Mutations of FH:** - FH mutations, exclusive to MED12 and HMGA2, include various types that lead to changes in cellular metabolism and activate hypoxia signaling. - Women with these mutations are at high risk of fibroids, with distinct histology akin to lesions in the Eker rat model. - Links between FH and TSC2 mutations include associations with benign skin lesions, hereditary cancer predisposition, and non-malignant lung lesions.
5. **Deletions of Collagen Genes (COL4A5 & COL4A6):** - Associated with diffuse leiomyomatosis with Alport syndrome and rarely with non-syndromic fibroids. - This syndrome includes symptoms in the respiratory, gastrointestinal, genitourinary tracts, and sensorineural hearing loss. - A synergistic effect between the inactivation of these genes and IRS4 underlies the pathogenesis.
6. **Epigenetics of Uterine Fibroids:** - Few studies exist, but epigenetic changes may be involved in silencing tumor suppressor genes in fibroids. - Evidence points to abnormal hypermethylation in some estrogen receptor (ER) response genes and tumor suppressor genes like KLF11, DLEC1, DAPK1, and KRT19.
In conclusion, the genetic factors that contribute to fibroid formation and growth are multi-dimensional and complex. These range from specific gene mutations in MED12, HMGA2, and FH, to chromosomal rearrangements and epigenetic changes.

Nuclear Receptors

Oestrogen and Progesterone Receptors:
Both ERα and ERβ are present in fibroids post-differentiation of fibroid progenitor cells.
Oestrogens binding to ERα mainly have a permissive function, especially through PR induction by progesterone.
Polymorphisms in receptors and elements of their pathways may affect fibroid biology.
Local aromatase expression plays a role in fibroid biology, particularly pronounced in black women.
Progesterone may have a greater regulatory role on fibroid growth than oestrogen. This is evidenced by the efficacy of Progesterone Receptor Modulators (PRMs) in fibroid treatment and findings from rodent xenograft models.
Progestins, antiprogestins, and PRMs might have complex actions in the uterus. The mifepristone–PR complex, for instance, binds to numerous sites in the genome.
KLF11 is essential for PR signaling and fibroid cell proliferation.
Progesterone and its derivatives have non-genomic actions, like activating the AKT pathway, promoting fibroid growth, and inhibiting apoptosis.
Vitamin D Relationship:
Vitamin D deficiency is linked to fibroids.
Single-nucleotide polymorphisms related to vitamin D metabolism are associated with fibroids, such as in ASIP and near DHCR7.
Lower serum concentrations of vitamin D correspond to larger fibroids.
Vitamin D3 has multiple effects on fibroid cells, like inducing apoptosis, modulating TGFβ activity, and regulating other components of the pathway, including MMPs and TIMPs.
Retinoic Acid:
Downregulated in fibroids.
Retinoids and their receptors play crucial roles in fibroid pathogenesis.
They inhibit proliferation and induce apoptosis specifically in fibroid smooth muscle cells.
Retinoic acid regulates many genes with altered expression in fibroids.
Potential racial differences in retinoic acid receptor expression may contribute to fibroid heterogeneity.
Other Nuclear Receptors:
Androgen receptor: Influences fibroid etiology via aromatase overexpression. High testosterone levels correlate with higher fibroid rates.
NR4A subfamily: These receptors are underexpressed in fibroids and are crucial for ECM deposition and cell proliferation.

Other systems

1. Genetic Alterations:
It's still debated whether the numerous genetic alterations identified in uterine fibroids are secondary occurrences or if they play a causal role in fibroid development.
2. Angiogenesis:
This is the process by which new blood vessels form from pre-existing vessels.
There is dysregulation in angiogenesis in fibroid-afflicted uteri.
Some studies suggest fibroids may possess an anti-angiogenic gene expression profile compared to normal myometrium or myometrium adjacent to fibroids.
The roles of myometrium and endometrium are critical, especially in cases where fibroids lead to heavy menstrual bleeding.
3. TGFβ Pathway:
Recognized as a significant regulator in fibroid cell growth.
It works by adjusting tissue remodeling, mediating inflammation, and preventing apoptosis.
TGFβ3, in particular, may also depress the expression of local anticoagulant factors in nearby endometrial cells, contributing to heavy menstrual bleeding.
4. IGF1 System:
This system might preferentially promote mitosis in fibroid cells over standard myometrial cells.
5. Membrane Receptor Systems:
Some have been implicated in fibroid pathogenesis. Notably:
The prolactin-releasing peptide receptor (encoded by PRLHR), which is associated with the mTOR pathway, seems to be abnormally expressed in fibroids.
The loss of RE1-silencing transcription factor (encoded by REST) might also be involved.
Prolactin has been identified as a mitogen in fibroids, and both prolactin and its receptor are found in fibroids, myometrial, and endometrial tissue.
6. Other Significant Genes:
CTNNB1: It's upregulated in fibroids and plays roles in cell adhesion and the WNT signaling pathway. Its upregulation in mice led to fibroid-like lesions.
NR2F2: It's downregulated in fibroids and, when conditionally knocked out, results in abnormal uterine morphology. Both CTNNB1 and NR2F2 have common regulators, including the retinoic acid, progesterone, and Sonic Hedgehog systems.

Animal Models

Eker Rat Model:
Created from retrotransposon insertion in TSC2 gene.
Used for HLRCC and lymphangioleiomyomatosis study.
Limitations:
High maintenance cost.
No comprehensive rat genome map.
Lesions resemble malignancies.
Murine Models:
Human tissue grafted in immunocompromised mice.
Methods:
Subcutaneous xenografts.
Subrenal capsule xenografts.
Other Models:
New mouse models under study.
Domestic hen models being explored.

Diagnosis

Challenges:
Varying fibroid size, location, and number.
Symptoms can be common to other conditions like ovulatory dysfunction, endometriosis, etc.
Some fibroids are asymptomatic.
FIGO Classification:
8-point system for fibroid location related to endometrium.
Helps in clinical trials and understanding heavy menstrual flow linkage.
Symptoms:
Gynecological: Heavy menstrual bleeding, prolonged bleeding, pelvic pressure, pain, and bleeding between periods. Risk of anemia.
Urinary: Frequent urination, incontinence, and hesitancy. Potential ureter obstruction.
Gastrointestinal: Constipation, tenesmus.
Other: Backache, leg pain.
Impact on Pregnancy:
Higher risk of complications like preterm delivery, premature rupture of membranes, and others.
Higher risk of placental abruption, fetal malformation, caesarean section, etc.
Potential association with miscarriage.
Fibroid Location:
Submucosal fibroids affect menstrual bleeding and pregnancy.
Subserosal fibroids grow slowly and cause symptoms when they become bulky.

IMAGING

Clinical Examination:
Identification of firm, multilobular uterus or masses suggests fibroids.
Ultrasonography:
Primary method to identify fibroids.
Diagnosis rate: 17% by palpation vs. 25.8% with transvaginal ultrasonography.
Among those with heavy menstrual bleeding: 73.3% diagnosed with ultrasonography.
Sensitivity: 90%. Specificity: 87%.
Sonohysterography improves sensitivity to 100% and specificity to 98%.
Other Imaging Methods:
Hysterosalpingography: X-ray of uterus and tubes. Sensitivity: 50%. Specificity: 20%. Inferior to ultrasonography.
MRI: Sensitivity & Specificity close to 100%. More expensive than ultrasonography. Useful for complex surgery planning and procedures like uterine artery embolization and magnetic resonance-guided focused ultrasound treatment. Best for cases with larger body habitus, prior surgeries, and intolerance to transvaginal procedures.
Challenges and Limitations:
Differentiating small submucosal fibroids from endometrium is hard with standard transvaginal ultrasonography.
Sonohysterography coupled with ultrasonography can overcome this limitation. Sensitivity: 89.5%. Specificity: 100%.
Transvaginal ultrasonography is limited when the uterus is outside the pelvis. Abdominal ultrasonography or MRI is used in such cases.
MRI can be more accurate than ultrasonography in determining fibroid volume and number.
Special Scenarios:
For infertility cases: Transvaginal ultrasonography identifies myometrium fibroids but not potential tubal obstruction. MRI is used for preoperative mapping of fibroids in these women.

HISTORICAL EVALUATION

Classic Presentation:
Spindle-shaped smooth muscle cells.
Disoriented fascicles separated by substantial ECM.
Well-circumscribed borders, bland cytology, little mitotic activity (≤2 mitoses/10 high power fields).
Nuclei with irregularities but no atypia and small conspicuous nucleoli.
Malignant Potential Assessment:
Based on nuclear grade/atypia, mitoses number, and presence/absence of coagulative necrosis.
10 mitoses/10 high power fields suggest leiomyosarcoma.
Gross degeneration alone doesn't confirm leiomyosarcoma.
Absence of degeneration doesn't guarantee benignity.
Benign Fibroid Variants:
Pathological abnormalities like hyaline degeneration, cellular or atypical leiomyomas

BIOMARKERS

Current serum-based biomarkers don't have high predictive value.
Examined Biomarkers:
Prolactin, HLA-G antigen, VEGF, ghrelin, lactate dehydrogenase, CA125.
Potential Uses:
Identify women at risk of developing rapidly growing fibroids.
Differentiate benign uterine fibroids from other conditions.
Adenomyosis vs. Uterine Fibroids:
Both conditions can cause heavy menstrual bleeding.
Adenomyosis Characteristics:
Ectopic endometrial glands and stroma, associated with pelvic pain.
Unique characteristics due to junctional zone involvement.
Differentiation:
MRI and ultrasonography can sometimes differentiate.
Definitive differentiation via histological examination of surgically removed tissue.

SCREENING

Self-reporting:
A patient suspects and reports symptoms associated with fibroids.
Sensitivity in Black Women: Rises with age - 12% (18-29 years) to 41% (35-45 years).
Specificity in Black vs. White Women: High and nearly equal - 98% vs. 97%.
Factors Influencing Self-reporting:
Ethnicity: Black women show higher sensitivity than white women.
Childbirth: Those with a history have higher sensitivity.
Education: Black women with higher education report more accurately.
Fibroid Size: Sensitivity is 3-4 times higher for fibroids >4cm than for those <2cm.
Clinical Evaluation:
No standard routine screening exists for fibroids, even for high-risk individuals.
Infertility: Imaging screens for fibroids potentially causing infertility.
Related Lesions (Leiomyosarcomas):
Symptomatology, imaging, and biomarkers (like CA125) overlap with fibroids.
Current Challenge: Cannot distinguish fibroids from leiomyosarcomas before surgery.
Screening for Risk Factors:
Age, postmenopausal status, tamoxifen use, HLRCC, abnormal imaging, and biomarkers.
Assessing growth is mainly beneficial for postmenopausal women.
Counseling: Must consider the advantages of minimally invasive surgery for fibroid treatment while being aware of potential risks.

PREVENTION

High lifetime prevalence of uterine fibroids.
Aim: Limit fibroid number and size.
Non-modifiable risk factors: Age, ethnicity, family history.
Modifiable risk factors: Reproductive factors, diet.
Potential Nutritional Supplements for Secondary Prevention:
Vitamin A
Vitamin D
Curcumin
Resveratrol
Isoliquiritigenin
Epigallocatechin Gallate (EGCG)
Euonymus alatus

MANAGEMENT

Current Treatment Guidelines:
Suboptimal due to lack of high-quality evidence.
Few society recommendations based on strong evidence.
Treatment options: Medical, radiological, surgical.
Asymptomatic Fibroids:
Often no intervention.
Recommended follow-up evaluations.
No standard interval for evaluations; some suggest annually.
Some fibroids regress post-menopause or childbirth.
Fibroid growth slows as women approach menopause.
Symptomatic Fibroids:
Consider other possible causes: ovulatory disorders, adenomyosis, endometriosis, etc.
Treatment varies based on symptoms.
Fibroid-related Heavy Menstrual Bleeding:
Hysteroscopic Myomectomy:
Preferred for FIGO type 0 or 1 fibroids.
Same-day surgery, quick recovery.
Suggested even for asymptomatic women desiring future childbearing.
Medical Treatment:
Various therapies available: NSAIDs, antifibrinolytics, contraceptive steroids, levonorgestrel IUD.
Lack of high-quality evidence for most therapies.
NSAIDs:
Reduce painful menses and heavy bleeding.
Available without prescription.
Antifibrinolytics:
Address fibroid-associated heavy menstrual bleeding.
Tranexamic acid as a first-line therapy.
Contraceptives:
Address fibroid-associated heavy menstrual bleeding.
Levonorgestrel IUD decreases heavy bleeding without distorting the endometrial cavity.
Risk of expulsion with fibroids.
Combined oral contraceptives can help control abnormal bleeding.
Surgical Therapy:
Second-line for FIGO type 3+ fibroids with heavy bleeding.
Used post-medical therapy failure.
Procedures:
Endometrial Ablation:
Minimally invasive.
For non-pregnancy seeking women.
Risks: Irreversible, no contraception, extrauterine pregnancies.
Hysterectomy:
For heavy bleeding.
High morbidity.
Myomectomy:
Types: Laparoscopic, robotic, abdominal.
Abdominal for large fibroids.
Fertility:
Evaluate before surgical treatment.
Note: Consult a doctor for advice.
Selective PRMs:
Target bulk symptoms.
Ulipristal acetate (UPA) is standard; reduces fibroid volume and bleeding.
Long-term effect of UPA for 3-12 months observed in some cases.
Some fibroids resistant to UPA.
Other PRMs like mifepristone studied but not approved yet.
GnRH Agonists:
Used preoperatively for 3-6 months.
Initial flare effect, then hypoestrogenic symptoms.
Addback therapy might minimize menopausal symptoms.
GnRH Antagonists:
Rapid onset, no flare effect.
Only licensed for ovulation induction currently.
Other Medical Agents:
Selective ER modulators and aromatase inhibitors show limited effectiveness.
Androgenic steroids also studied but limited evidence on effectiveness.
Interventional and Surgical Therapies:
Myomectomy:
Removes fibroids, preserves uterus.
Laparoscopic and robotic methods available.
FDA warns about morcellation potential to spread cancer.
Laparoscopic Radiofrequency Ablation:
Less blood loss, shorter hospital stays.
Other techniques lack strong evidence.
UAE (Uterine Artery Embolization):
Effective, shorter hospital stays, less post-op pain.
Increased risk of further surgical intervention.
Impact on fertility not entirely clear.
MRgFUS:
Non-invasive, uses ultrasound.
Sustained symptom relief for up to 5 years.
Successful pregnancy outcomes observed.

QUALITY LIFE

1. Impact on Daily Life:
Work and Social Life: Fibroid symptoms can interfere with work performance, social interactions, and daily routines.
Disproportional Effects: The effects of fibroid symptoms seem to be more pronounced in black women compared to white women.
2. Measuring the Impact:
Uterine Fibroid Symptom and Quality of Life (UFS-QOL) Assessment: This is the only validated tool specifically designed for uterine fibroids. It evaluates:
Symptom Severity: Uses an 8-item subscale where higher scores represent greater symptom severity. Symptoms include heavy menstrual bleeding, blood clots, urinary frequency, and fatigue.
Quality of Life: Consists of 29 questions. Higher scores indicate better quality of life. It evaluates concerns, activities, energy or mood, control, self-consciousness, and sexual function.
Limitation of UFS-QOL: Since it focuses on menstrual function, it's not ideal for comparing hysterectomies with other treatments.
Other Instruments: There are other tools that measure specific symptoms related to uterine fibroids, but many don't consider the effect of menses. An exception is the Female Sexual Function Index.
3. Unmet Needs:
Assessment of Bulk-related Symptoms: UFS-QOL does account for symptoms like pelvic tightness and urinary issues. However, it lacks in assessing bowel dysfunction and abdominal protrusion related to fibroids.

Treatment to optimize pregnancy outcomes

1. Controversies and Recommendations:
Potential Role in Infertility: Some reports suggest fibroids can impact fertility and lead to adverse pregnancy outcomes.
Contrary Views: Population-based studies are challenging the direct link between fibroids and infertility.
Treatment Guidelines:
Symptomatic fibroids, specifically FIGO type 0 and type 1, are typically treated using hysteroscopic myomectomy for women wanting to conceive.
Some guidelines even suggest preemptively treating these fibroids even if they are asymptomatic.
Mixed Evidence: Studies on whether removing submucosal fibroids enhances pregnancy outcomes have been contradictory.

OUTLOOK

Need for Modernization: The current treatment methods for fibroids are anticipated to evolve substantially in the upcoming decade.
Paradigm Shift in Treatment: Similar to the shift from radical mastectomy to more conservative breast cancer treatments, there's an expected move from hysterectomy towards other forms of fibroid treatments.
Future Aims:
Identify predictors for fibroid prognosis.
Develop individualized treatments combined with early interventions.
Incorporate primary and secondary prevention strategies.
Emerging Treatments:
Utilizing minimally invasive surgeries or medical therapies.
Novel treatments like hysteroscopic and laparoscopic radiofrequency ablation, and focused ultrasound therapies. These aim at specific fibroids with reduced morbidity.
Use of image-guided or molecularly targeted therapies, which are expected to decrease morbidity associated with traditional surgeries.
Understanding the Disease:
As knowledge on fibroid formation's genetic aspects deepens, it's anticipated that more effective therapies will emerge that can halt growth or even induce regression.
A better understanding of fibroids' biology could lead to improved diagnostics for malignant and pre-malignant uterine diseases.
Fibroids as a Model for Other Diseases:
Due to the prevalence and characteristics of fibroids, they could serve as a model system for treating malignancies.
Their abundant occurrence and larger size compared to malignant tumors, along with the lesser risks associated with incomplete treatment, make them ideal for testing novel therapies.
Conclusion: While the link between fibroids and fertility is still debated, there is consensus on the need to evolve fibroid treatments. With advancements in research and understanding, the next decade is poised to witness a significant transformation in fibroid management, with a strong inclination towards minimally invasive and more targeted treatments.



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