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      Effect of varying doses of tamoxifen on ovarian histopathology, serum VEGF, and endothelin 1 levels in ovarian hyperstimulation syndrome: an experimental study

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          Abstract

          Objective

          To examine the effects of low-to-high doses of tamoxifen on ovarian histopathology, serum VEGF, and endothelin 1 levels in ovarian hyperstimulation syndrome (OHSS) in an experimental setting.

          Materials and methods

          A total of 20 female Wistar albino rats, 22 days of age, were randomly divided into four groups. Follicle-stimulating hormone 10 IU was administered subcutaneously in 15 rats on 4 consecutive days, with OHSS induction on day 5 by 30 IU of human chorionic gonadotropin. Group 1 (n=5) comprised 35-day-old control rats, group 2 (n=5) 35-day-old OHSS rats, group 3 (n=5) 27-day-old OHSS rats receiving 1 mg/kg of oral tamoxifen for 7 days, group 4 (n=5) 27-day-old OHSS rats receiving 3 mg/kg of oral tamoxifen for 7 days. All rats were decapitated on day 35. Serum VEGF, endothelin 1, and ovarian follicular reserve were assessed in all rats. Kruskal–Wallis variance analysis and the Mann–Whitney U-test were used for statistical comparisons. A Bonferroni correction was performed to control the inflation of significance, with a significance level set at a P-value of less than 0.025.

          Results

          Despite higher serum VEGF, endothelin 1, follicular reserve, and angiogenesis and fibrosis of the corpus luteum in the OHSS group compared to controls, these differences were not significant ( P>0.025, Mann–Whitney U-test). There was a significant reduction in the ovarian follicular reserve in tamoxifen groups compared to controls ( P<0.025, Mann–Whitney U-test), while angiogenesis of the corpus luteum, number of atretic follicles, fibrosis, and serum VEGF were significantly higher in rats receiving tamoxifen ( P<0.025, Mann–Whitney U-test). Also, significantly lower follicular reserve and fibrosis were observed among rats in the low-dose tamoxifen group in comparison with rats in the high-dose tamoxifen group ( P<0.025, Mann–Whitney U-test). No groups had a significant change in endothelin 1 levels ( P>0.025, Mann–Whitney U-test).

          Conclusion

          Tamoxifen 1 g and 3 g resulted in a dose-dependent increase in VEGF and endothelin 1 levels, and ovarian follicle reserves were significantly reduced in our experimental model.

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          Most cited references 30

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          Preventing ovarian hyperstimulation syndrome: guidance for the clinician.

          To reevaluate ovarian hyperstimulation syndrome (OHSS) prevention techniques and provide a classification system for grading OHSS and evidence-based treatment strategies for preventing OHSS. A literature search was conducted in PubMed for articles published in the last 5 years using the keywords "controlled ovarian stimulation," "controlled ovarian hyperstimulation," "ovarian hyperstimulation syndrome," "OHSS," "prevention," "chorionic gonadotropin," "hCG," "GnRH agonist," "GnRH antagonist," "coasting," and "cryopreservation." We reviewed randomized controlled trials (RCTs), retrospective studies, pilot studies, case studies, reviews, and meta-analyses. There is a shortage of large, prospective RCTs reporting OHSS prediction and prevention strategies. Our review showed that risk factors such as antral follicle count and baseline anti-Müllerian hormone level may identify women at high OHSS risk. Preventative strategies that appear highly effective at reducing or preventing OHSS include GnRH antagonist protocols and the use of GnRH agonists to trigger final oocyte maturation. Moreover, alternative therapies, such as dopamine receptor agonists (Cabergoline), have also emerged as potential new treatment modalities in the management of this disease. These findings suggest that current treatment guidelines should be updated to incorporate findings from recent literature that show that GnRH antagonist protocols consistently reduce OHSS and that GnRH agonist triggering has considerable promise in preventing OHSS, although further RCTs will be needed to confirm this. Copyright 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
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            The pathophysiology of ovarian hyperstimulation syndrome--views and ideas.

            Ovarian hyperstimulation syndrome (OHSS) is a serious complication affecting ovulation induction. Its most severe manifestation takes the form of massive ovarian enlargement and multiple cysts, haemoconcentration and third-space accumulation of fluid. The full-blown clinical syndrome may be complicated by renal failure and oliguria, hypovolaemic shock, thromboembolic episodes, adult respiratory distress syndrome (ARDS), and death. Although the pathophysiology of this syndrome has not been completely elucidated, it seems likely that the increased capillary permeability triggered by the release of vasoactive substance secreted by the ovaries under human chorionic gonadotrophin (HCG) stimulation plays a key role in this syndrome. Several factors such as histamine, serotonin, prostaglandins, prolactin, and a variety of other substances have been implicated in this process in the past. At present, factors belonging to the renin-angiotensin system, cytokines including the interleukins, tumour necrosis factor alpha, endothelin-1 and vascular endothelial growth factor (VEGF) are thought to be involved in triggering increased vascular permeability after ovulation induction treatment. This manuscript summarizes the current knowledge of the pathophysiology of ovarian hyperstimulation syndrome with emphasis on the correlation of the various factors with the clinical phenomena of this iatrogenic syndrome.
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              Vascular endothelial growth factor as capillary permeability agent in ovarian hyperstimulation syndrome.

              We investigated the role of vascular endothelial growth factor (VEGF) in ovarian hyperstimulation syndrome (OHSS). Two similar peaks of permeability activity were seen in OHSS ascites and liver ascites spiked with recombinant human VEGF (rhVEGF); no activity was seen in control liver ascites. Incubation with rhVEGF antiserum decreased activity in the two OHSS peaks by 79% and 65% and the two spiked liver peaks by 49% and 50%. Control serum produced 24% and 27%, and 17% and 0% reductions, respectively. This is evidence that the major capillary permeability agent in OHSS ascites fluid is VEGF.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Drug Design, Development and Therapy
                Dove Medical Press
                1177-8881
                2015
                24 March 2015
                : 9
                : 1761-1766
                Affiliations
                [1 ]Department of Obstetrics and Gynecology, Fırat University School of Medicine, Elazig, Turkey
                [2 ]Department of Biochemistry, Fırat University School of Medicine, Elazig, Turkey
                [3 ]Department of Pathology, Fırat University School of Medicine, Elazig, Turkey
                Author notes
                Correspondence: Remzi Atilgan, Department of Obstetrics and Gynecology, Fırat University School of Medicine, Elazig 23119, Turkey, Tel +90 4242 233 3555, Email remzi_atilgan@ 123456hotmail.com
                Article
                dddt-9-1761
                10.2147/DDDT.S75266
                4378285
                25848212
                © 2015 Pala et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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