In Vivo Mechanisms of Uterine Myoma Volume Reduction with Ulipristal Acetate Treatment  

Oleh:

Courtoy, Guillaume E. ; Donnez, Jacques ; Marbaix, Etienne ; Dolmans, Marie-Madeleine

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 104 no. 02 (Aug. 2015), page 426–434.
Topik: Uterine Myoma; Ulipristal Acetate; Proliferation; Cell Death; Extracellular Matrix; Matrix Metalloproteinase 2
Fulltext: F02 v104 n2 p426 kelik2016.pdf (3.38MB)

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Objective: To study the in vivo mechanisms of action of ulipristal acetate (UPA) on uterine myomas. Design: Retrospective histologic and immunohistochemical (IHC) study of myomas. Setting: Academic research unit. Patient(s): Among 59 women with symptomatic myomas who underwent myomectomy, 42 were treated preoperatively with UPA, while 17 were not. Intervention(s): Histology and IHC were analyzed on tissue microarrays obtained from surgical specimens. Main Outcome Measure(s): Proliferation, apoptosis, extracellular matrix (ECM) remodeling, and matrix metalloproteinase 2 (MMP-2) expression. Result(s): Proliferation was low in all conditions, with no statistical difference between groups. Terminal deoxynucleotide transferase–mediated dUTP nick-end labeling assay showed an increase in cell death in UPA-treated myomas compared with untreated myomas, but only after short-term treatment; this was not associated with elevated levels of cleaved caspase-3. After long-term treatment, cell density was higher and the ECM volume fraction lower in UPA-treated myomas than in untreated myomas. MMP-2 expression was found to be increased after treatment, showing the highest level after long-term treatment, compared with untreated myomas. Conclusion(s): Regarding sustained clinical volume reduction of myomas, this study strongly points to multifactorial mechanisms of action of UPA, involving: 1) a persistently low cell proliferation rate; 2) a limited period of cell death; and 3) ECM remodeling concomitant with stimulation of MMP-2 expression.

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