Abstract

Objectives: Uterine lyomyomata are the most common benign tumours during reproductive life. GnRH-agonists have become a useful tool in the management of benign fibroids. The aim of this study was to investigate if treatment with GnRH-agonists is able to modify the proliferation rate and cell biological markers of uterine fibroids and enhance therapy of this benign disease. Patients and methods: Sixty-seven myoma and in 22 cases the corresponding myometrium were investigated in this study. Twenty patients with fibroids underwent a GnRH-agonist treatment for 3–6 months (Enantone®-Gyn) whereas the remaining 20 patients had regular menstrual cyclings or were postmenopausal. The proliferation marker Ki-67 and the differentiation markers desmin, vimentin and M-cadherin and were analyzed. Results: Independent of the hormonal situation at time of biopsy no differences concerning the cell biological differentiation markers between the GnRH-agonist treated group and the not treated group could be observed ( p>0.05). GnRH-agonist treatment leads to a significant ( p<0.05) reduction of the cell proliferation rate of uterine myoma but not to changes in uterine differentiation. Discussion: GnRH-agonists are potent drugs in the treatment of benign gynaecological diseases. This is one of the first investigations that describe the potency of GnRH-agonist to reduce, statistically significantly, the proliferation rate of uterine myoma. By the same way, it could be demonstrated that GnRH-agonists do not lead to differentiations of smooth muscle cells, so that the use of GnRH-agonists in the treatment of uterine fibroids can be seen as useful for reduction of lyomyomata volume, but it is not able to change significantly differentiation parameters of these benign smooth muscle cell tumours.

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