Progestogens or progestogen-releasing intrauterine systems for uterine fibroids (other than preoperative medical therapy).
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ABSTRACT:
SUBMITTER: Sangkomkamhang US
PROVIDER: S-EPMC8094271 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature
Publications
Progestogens or progestogen-releasing intrauterine systems for uterine fibroids (other than preoperative medical therapy).
Sangkomkamhang Ussanee S US Lumbiganon Pisake P Pattanittum Porjai P
The Cochrane database of systematic reviews 20201123
<h4>Background</h4>Uterine fibroids can cause heavy menstrual bleeding. Medical treatments are considered to preserve fertility. It is unclear whether progestogens or progestogen-releasing intrauterine systems can reduce fibroid-related symptoms. This is the first update of a Cochrane Review published in 2013.<h4>Objectives</h4>To determine the effectiveness of progestogens or progestogen-releasing intrauterine systems in treating premenopausal women with uterine fibroids.<h4>Search methods</h4> ...[more]
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| S-EPMC9939308 | biostudies-literature
Project description:ObjectiveTo investigate the association of non-cavity-distorting uterine fibroids and pregnancy outcomes after ovarian stimulation-intrauterine insemination (OS-IUI) in couples with unexplained infertility.DesignSecondary analysis from a prospective, randomized, multicenter clinical trial investigating fertility outcomes after OS-IUI.SettingReproductive Medicine Network clinical sites.Patient(s)Nine hundred couples with unexplained infertility who participated in the Assessment of Multiple Intrauterine Gestations from Ovarian Stimulation (AMIGOS) clinical trial.Intervention(s)Participants were randomized to one of three arms (clomiphene citrate, letrozole, or gonadotropins), and treatment was continued for up to four cycles or until pregnancy was achieved.Main outcomes measure(s)Conception (serum hCG increase), clinical pregnancy (fetal cardiac activity), and live birth rates.Result(s)A total of 102/900 participants (11.3%) had at least one documented fibroid and a normal uterine cavity. Women with fibroids were older, more likely to be African American, had a greater uterine volume, lower serum antimüllerian hormone levels, and fewer antral follicles than women without fibroids. In conception cycles, clinical pregnancy rates were significantly lower in participants with fibroids than in those without uterine fibroids. Pregnancy loss before 12 weeks was more likely in African American women with fibroids compared with non-African American women with fibroids. There was no difference in conception and live birth rates in subjects with and without fibroids.Conclusion(s)No differences were observed in conception and live birth rates in women with non-cavity-distorting fibroids and those without fibroids. These findings provide reassurance that pregnancy success is not impacted in couples with non-cavity-distorting fibroids undergoing OS-IUI for unexplained infertility.Clinical trial registration numberNCT01044862.
| S-EPMC5472203 | biostudies-literature
Project description:Purpose of reviewThis article provides the current evidence related to transcervical radiofrequency ablation of uterine fibroids under integrated intrauterine sonography guidance (the Sonata System).Recent findingsPublished data on the treatment of fibroids with the Sonata System has demonstrated significant median reductions in total (73.3%) and perfused (73.3%) uterine fibroid volume, menstrual bleeding (72.3%), symptom severity (62.5%), and improvements in health-related quality of life (127%) at 12 months post-ablation. A clinical trial under an FDA Investigational Device Exemption is in progress.SummaryThe Sonata System is a promising treatment modality for uterine fibroids. As an incisionless, minimally invasive treatment that does not require general anesthesia or hospitalization, it has the potential for redefining the current paradigm for management of symptomatic fibroids.
| S-EPMC5350207 | biostudies-literature
Project description:Uterine fibroids are benign tumours affecting up to 80% of women of reproductive age, with 30% of patients suffering severe symptoms including abnormal uterine bleeding, pain and infertility. Several studies have identified mutations in MED12 or HMGA2 that account for the vast majority of genomic abnormalities in uterine fibroids, however, the processes by which these lead to UFs and HMB remain poorly understood. To systematically correlate genetic, transcriptional and proteomic phenotypes we collected fibroid, myometrium and endometrium tissues from 137 donors undergoing hysterectomy, myomectomy, or transcervical resection. Donors were profiled by genome-wide SNP arrays and their fibroids were genotyped for known mutations using a targeted sequencing approach. Tissues were analysed by RNA-sequencing and proteomics followed by a systems level approach using multiomics factor analysis. Whilst genotyping revealed 39.7% of common MED12 UF mutations, we observe multiple novel exonic and intronic variants of previously known mutated genes like COL4A5 and COL4A6. Systems level analysis of genotype, transcriptomic, and proteomic data between myometrium and fibroid donors identified multiple interrelated gene sets involved in UF pathophysiology, including extracellular matrix deposition and remodelling, protein glycosylation and sulphate biology. Equivalent analysis of endometrium stratified by donor HMB status revealed gene sets implicated in the condition, in particular RNA splicing in MED12 mutant fibroids. A paradigm is proposed, supported by a mouse model of HMB, whereby aberrant production of signalling molecules by MED12 mutant fibroids influences RNA transcript isoform expression in the endometrium, associated with abnormal bleeding. By merging clinical, genetic, transcriptomic, and proteomic information, we highlight multiple pathways which may underlie the pathomechanisms of UF biology and may facilitate the development of novel therapeutic strategies to treat heavy menstrual bleeding
2025-08-25 | PXD051220 | Pride
Project description:BackgroundUterine fibroids are the most common benign uterine tumours present in women of reproductive age. Mifepristone (RU-486) competitively binds and inhibits progesterone receptors. Studies have suggested that fibroid growth depends on the sexual steroids. Mifepristone has been shown to decrease fibroid size. This review summarises the effects of mifepristone treatment on fibroids and the associated adverse effects as described in randomised controlled trials.ObjectivesTo determine the efficacy and safety of mifepristone for the management of uterine fibroids in pre-menopausal women.Search methodsWe searched the specialised register of the Cochrane Menstrual Disorders and Subfertility (Cochrane Menstrual Disorders and subfertility Review Group), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2011, Issue 4), MEDLINE, EMBASE, PsycINFO, and CINAHL (to November 2011). We handsearched a number of journals, and searched reference lists, databases of ongoing trials and the Internet. There were no language restrictions.Selection criteriaOnly truly randomised controlled trials of mifepristone versus other forms of medical therapy or placebo in pre-menopausal women with confirmed uterine fibroids were included.Data collection and analysisFour authors independently extracted data and assessed trial quality. Data were analysed using the Peto odds ratios (OR) for dichotomous data and the weighted mean differences for continuous data, with 95% confidence intervals (CI). Meta-analyses were performed using the fixed-effect model.Main resultsThree studies involving 112 participants were included. Comparison interventions included different dosages of mifepristone, placebo and vitamin B tablets. There is evidence that treatment with mifepristone relieves heavy menstrual bleeding compared with placebo (Peto OR 17.84; 95% CI 6.72 to 47.38; 2 RCTs, 77 women, I(2) = 0%). Three studies (Bagaria 2009; Engman 2009; Fiscella 2006) were included in the meta-analysis of this comparison. There was no evidence of an effect of mifepristone on the fibroid volume (standardised mean difference (SMD) -0.02; 95% CI -0.38 to 0.41; 99 women). Two studies (Bagaria 2009; Fiscella 2006) were included in the meta-analysis of this comparison. There was no evidence of an effect of mifepristone on uterine volume (mean difference (MD) -77.24; 95% CI -240.62 to 86.14; 72 women). The pooled data suggest an increased adverse event (abnormal endometrial histology) in the mifepristone group compared to placebo (OR 31.65; 95% CI 4.83 to 207.35; 2 RCTs; 54 women; I(2) = 0%). Only one study (Bagaria 2009) reported endometrial hyperplasia at the end of the therapy (12/19 women in the mifepristone group versus 0/16 in the placebo group; OR 55.0; 95% CI 2.86 to 105.67). Engman 2009 found a significantly higher rate of cystic glandular dilatation in women in the mifepristone group (5/8 women biopsied) compared with the placebo group (1/11 women biopsied) (OR 16.67; 95% CI 1.36 to 204.03). One study (Fiscella 2006) suggested significant improvements (P < 0.001) for specific quality of life outcomes.Authors' conclusionsMifepristone reduced heavy menstrual bleeding and improved fibroid-specific quality of life. However, it was not found to reduce fibroid volume. Further well-designed, adequately powered RCTs are needed before a recommendation can be made on the use of mifepristone for the treatment of uterine fibroids.
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Project description:We review recent studies dealing with the molecular genetics and basic results of omics analysis of uterine leiomyoma (LM)-a common benign muscle tumor of the uterus. Whole genome studies of LM resulted in the discovery of many new gene nets and biological pathways, including its origin, transcriptomic, and epigenetic profiles, as well as the impact of the inter-cell matrix in LM growth and involvement of microRNA in its regulation. New data on somatic cell mutations ultimately involved in the origin, distribution and growth of LM are reviewed. Putative identification of LM progenitor SC (stem cells) giving rise to maternal fibroid nodes and junctional zones provide a new clue for hypotheses on the pathogenomics of LM. The reviewed data are consistent with at least two different but probably intimately interacted molecular mechanisms of LM. One of them (the genetic hypothesis) is focused primarily on the MED12 gene mutations and suggests its onset in the side population of embryonic myoblasts of the female reproductive system, which later gave rise to multiple small and medium fibroids. The single and usually large-size fibroids are induced by predominantly epigenetic disorders in LM SC, provoked by enhanced expression of the HMGA2 gene caused by its hypomethylation and epigenetic deregulation enhanced by hypoxia, muscle tension, or chromosome instability/aberrations. The pathogenomics of both genetic and epigenetic programs of LM with many peculiarities at the beginning later became rather similar and partly overlapped due to the proximity of their gene nets and epigenetic landscape. Pathogenomic studies of LM open ways for elaboration of novel strategies of prevention and treatment of this common disease.
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