Journal of South Asian Federation of Obstetrics and Gynaecology

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VOLUME 10 , ISSUE 4S1 ( October-December, 2018 ) > List of Articles


Correlation of Progesterone Receptor B in Endometrial Tissue of Menstrual Blood in Patients with and without Endometriosis

Amy I Soenggono, Zulvayanti, Tita H Madjid, Wiryawan Permadi, Jusuf S Effendi

Keywords : Degree of endometriosis, Endometriosis, Menstrual blood, Progesterone receptor B, Quantitative real-time-polymerase chain reaction

Citation Information : Soenggono AI, Z, Madjid TH, Permadi W, Effendi JS. Correlation of Progesterone Receptor B in Endometrial Tissue of Menstrual Blood in Patients with and without Endometriosis. J South Asian Feder Obs Gynae 2018; 10 (4S1):310-315.

DOI: 10.5005/jp-journals-10006-1614

License: CC BY-NC 4.0

Published Online: 01-01-2018

Copyright Statement:  Copyright © 2018; The Author(s).


Background: Endometriosis is a progressive chronic gynecological disease. There are indications that endometriosis patients have lower progesterone receptor B (PR-B) levels. Menstrual blood contains the same mRNA derived from endometrium cells. The objective of this study was to analyze the different levels of PR-B in the menstrual blood of women with endometriosis compared to nonendometriosis. Materials and methods: A case control study was conducted on 42 women administered to the Gynecology and Reproductive Endocrinology and Fertility Clinic FKUP/Dr Hasan Sadikin Hospital and its networks from December 2016 to January 2017. Through interviews, physical examination and investigation, patients were classified as those with endometriosis and non-endometriosis patients as controls. Surgery was performed to obtain lesion biopsy for endometriosis degree determination and storage. Quantitative RT-PCR for the PR-B mRNA in the menstrual blood samples was performed. Based on the histopathology results and diagnostic confirmation, differences in the PR-B levels in menstrual blood endometrium for endometriosis cases and non-endometriosis women were assessed. Differences in the PR-B levels between endometriosis patients with mild and severe degrees were also investigated. Results: In patients with endometriosis, the mean and median levels of PR-B was significantly lower than non-endometriosis (p <0.05). ROC analysis resulted in a cutoff value of ≤1.1355 μg/dL with 90.5% sensitivity, 81% specificity and 85.7% accuracy for prevalence odds ratio (POR) at 7.85. The PR-B levels strongly inversely correlated with the degree of endometriosis (rs = –0.817; p <0.001). Conclusion: The levels of PR-B in eutopic endometrial tissue of menstrual blood in patients with endometriosis is lower than those in nonendometriosis women. A higher degree of endometriosis is correlated with lower levels of PR-B in patients with endometriosis.

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  1. Hediger ML, Hartnett HJ, et al. Association of endometriosis with body size and figure. Feril Steril 2005;84(5):1366-1374.
  2. Bulun SE. Endometriosis. N Engl J Med 2009;360(3):268-279.
  3. de Ziegler D, Borghese B, et al. Endometriosis and infertility: pathophysiology and management. Lancet (London, England) 2010;376(9742):730-738.
  4. Kennedy S, Bergqvist A, et al. ESHRE guideline for the diagnosis and treatment of endometriosis. Hum Reprod 2005;20(10):2698-2704.
  5. Leyland N, Casper R, et al. Endometriosis: diagnosis and management. JOGC 2010;32(7 Suppl 2):S1-32.
  6. Shinohara A, Kutsukake M, et al. Protease-activated receptor-stimulated interleukin-6 expression in endometriosis-like lesions in an experimental mouse model of endometriosis. J Pharm Sci 2012;119(1):40-51.
  7. Ponce C, Torres M, et al. Nuclear factor kappaB pathway and interleukin-6 are affected in eutopic endometrium of women with endometriosis. Reproduction (Cambridge, England) 2009;137(4):727-737.
  8. Bergqvist A, Bruse C, et al. Interleukin 1β, interleukin-6, and tumor necrosis factor-α in endometriotic tissue and in endometrium. Feril Steril. 2001;75(3):489-495.
  9. A B. Endometriosis. A B, editor. Jakarta: Media Aesculapius Fakultas Kedokteran Universitas Indonesia; 2008. p. 1-31.
  10. Speroff L, Fritz MA. Clinical gynecologic endocrinology and infertility: lippincott Williams & Wilkins; 2005.
  11. Vinatier D, Cosson M, et al. Is endometriosis an endometrial disease? Eur J Obstet Gynecol Reprod Biol 2000;91(2):113-125.
  12. Lessey BA, Metzger DA, et al. Immunohistochemical analysis of estrogen and progesterone receptors in endometriosis: comparison with normal endometrium during the menstrual cycle and the effect of medical therapy. Feril Steril 1989;51(3):409-415.
  13. Casey M, MacDonald P, et al. 17 beta-Hydroxysteroid dehydrogenase type 2: chromosomal assignment and progestin regulation of gene expression in human endometrium. J Clin Invest 1994;94(5):2135.
  14. Mustonen MV, Isomaa VV, et al. Human 17β-hydroxysteroid dehydrogenase type 2 Messenger ribonucleic acid expression and localization in term placenta and in endometrium during the menstrual cycle 1. J Clin Endocrinol Metab 1998;83(4):1319-1324.
  15. Cheng Y-H, Yin P, et al. Retinoic acid (RA) regulates 17β-hydroxysteroid dehydrogenase type 2 expression in end metrium: interaction of RA receptors with specificity protein (SP) 1/SP3 for estradiol metabolism. J Clin Endocrinol Metabb 2008;93(5):1915-1923.
  16. Jiang J, Wu R-f, et al. Effect of mifepristone on estrogen and progesterone receptors in human endometrial and endometriotic cells in vitro. Fertil Sterill 2002;77(5):995-1000.
  17. Halme J, Toma S, et al. A case of severe ovarian hyperstimulation in a healthy oocyte donor. Fertil Sterill 1995;64(4):857-859.
  18. Kaunitz AM. Injectable depot medroxyprogesterone acetate contraception: an update for US clinicians. Int J Fertil Womens Med 1997;43(2):73-83.
  19. Cheng Y-H, Imir A, et al. Stromal cells of endometriosis fail to produce paracrine factors that induce epithelial 17β-hydroxysteroid dehydrogenase type 2 gene and its transcriptional regulator Sp1: a mechanism for defective estradiol metabolism. Am J Obstett Gynecoll 2007;196(4):391. e1-91. e8.
  20. Zeitoun K, Takayama K, et al. Deficient 17β-Hydroxysteroid Dehydrogenase Type 2 Expression in Endometriosis: Failure to Metabolize 17β-Estradiol 1. J Clin Endocrinol Metab. 1998;83(12):4474-4480.
  21. Burney RO, Talbi S, et al. Gene expression analysis of endometrium reveals progesterone resistance and candidate susceptibility genes in women with endometriosis. Endocrinology. 2007;148(8):3814-3826.
  22. Younis A, Hawkins K, et al. Serum tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1 and paraoxonase-1 profiles in women with endometriosis, PCOSs, or unexplained infertility. J Assist Reprod Genet 2014;31(11):1445-1451.
  23. Lebovic DI, Mueller MD, et al. Immunobiology of endometriosis. Feri lSteril 2001;75(1):1-10.
  24. Kastner P, Krust A, et al. Two distinct estrogen-regulated promoters generate transcripts encoding the two functionally different human progesterone receptor forms A and B. EMBO J 1990;9(5):1603.
  25. Sartorius CA, Melville MY, et al. A third transactivation function (AF3) of human progesterone receptors located in the unique N-terminal segment of the B-isoform. Mol Endocrinol 1994;8(10):1347-1360.
  26. Leonhardt SA, Boonyaratanakornkit V, et al. Progesterone receptor transcription and non-transcription signaling mechanisms. Steroids 2003;68(10):761-770.
  27. Evans RM. The steroid and thyroid hormone receptor superfamily. Science 1988;240(4854):889-895.
  28. McEwan IJ. Nuclear receptors: one big family. Methods Mol Biol 2009:3-18.
  29. Escriva H, Bertrand S, et al. The evolution of the nuclear receptor superfamily. Essays Biochem 2004;40:11-26.
  30. Kao L, Germeyer A, et al. Expression profiling of endometrium from women with endometriosis reveals candidate genes for disease-based implantation failure and infertility. Endocrinology 2003;144(7):2870-2881.
  31. Attia GR, Zeitoun K, et al. Progesterone receptor isoform a but not b is expressed in endometriosis 1. J Clin Endocrinol Metabb 2000;85(8):2897-2902.
  32. Misao R, Iwagaki S, et al. Dominant expression of progesterone receptor form B mRNA in ovarian endometriosis. Horm Res 1999;52(1):30-34.
  33. Patel B, Elguero S, et al. Role of nuclear progesterone receptor isoforms in uterine pathophysiology. Hum Reprod 2014:dmu056.
  34. Guo S-W. Epigenetics of endometriosis. Mol Hum Reprod 2009;15(10):587-607.
  35. R R. Hubungankadar estradiol zalir peritoneum, tampilan mRNA Reseptorprogesteron-B dan mRNA DNA metiltransferase-1 sertatingkatmetilasipengajureseptorprogesteron-B Endometrium dengankejadian endometriosis 2014:1-112.
  36. Madjid T, Hernowo B, et al. The relationship of caspase-3, caspase-9, MMP-9 expression and c-1562t mmp-9 gene polymorphism in menstrual blood as the etiopathogenesis marker to clinical endometriosis manifestation. Feri lSteril 2015;3(104):e166.
  37. Leyendecker G, Herbertz M, et al. Endometriosis results from the dislocation of basal endometrium. Hum reprod (Oxford, England) 2002;17(10):2725-2736.
  38. Matalliotakis IM, Cakmak H, et al. Epidemiological characteristics in women with and without endometriosis in the Yale series. Arch Gynecol Obstet 2008;277(5):389-393.
  39. Kitawaki J, Kusuki I, et al. Detection of aromatase cytochrome P-450 in endometrial biopsy specimens as a diagnostic test for endometriosis. Feri lSteril 1999;72(6):1100-1106.
  40. Sharpe-Timms KL. Endometrial anomalies in women with endometriosis. Ann N Y Acad Sci 2001;943(1):131-147.
  41. Girling JE, Rogers PA. Recent advances in endometrial angiogenesis research. Angiogenesis. 2005;8(2):89-99.
  42. Kumar NS, Richer J, et al. Selective down-regulation of progesterone receptor isoform B in poorly differentiated human endometrial cancer cells: implications for unopposed estrogen action. Cancer Res 1998;58(9):1860-1865.
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