Effect of Gonadotropin-Releasing Hormone Agonist Treatment upon Angiogenesis in Uterine Leiomyoma
Objective: To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata. Methods: Uterine leiomyomata specimens of 49 consecutive patients who underwent myomectomy or hysterectomy following presurgical treatment with (n = 23) and without (n...
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| Published in | Gynecologic and obstetric investigation Vol. 52; no. 2; pp. 108 - 113 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Basel, Switzerland
Karger
01.01.2001
S. Karger AG |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0378-7346 1423-002X |
| DOI | 10.1159/000052953 |
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| Abstract | Objective: To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata. Methods: Uterine leiomyomata specimens of 49 consecutive patients who underwent myomectomy or hysterectomy following presurgical treatment with (n = 23) and without (n = 26) GnRH agonist were stained immunohistochemically with antibody to factor VIII-related antigen. For each subject, age, parity, number of Lupron treatments, leiomyoma size (cm), and mean microvessel counts calculated from three fields (×400) were recorded. Differences in patient age, parity, microvessel counts and leiomyoma size between GnRH agonist treated and untreated patients were tested by unpaired Student’s t test. Differences among the various number of doses were tested by one-way ANOVA, with Bonferonni and Neuman-Keuls post hoc tests between specific dose-number groups. The relationship between microvessel counts and leiomyoma size was tested by Pearson correlation test. Multivariate stepwise regression tested the relationship between the number of Lupron doses and microvessel counts, correcting for age, parity, and leiomyoma size. p < 0.05 was considered significant. Results: Patient age and parity were similar in GnRH treated and untreated patients (mean 43.3 ± 6.6 versus 43.9 ± 7.5 years and median 2 (range 0–7) versus 1 (range 0–5), p = 0.78 and p = 0.45, respectively). Microvessel counts of leiomyomata specimens treated presurgically with GnRH agonist therapy (median 22.7, range 6.7–65.7) were not significantly different from microvessel counts of specimens without presurgical GnRH agonist treatment (median 19.8, range 6–53; p = 0.77). No correlation between leiomyoma size and microvessel counts was noted (r = 0.06, P = 0.7). Conclusion: Angiogenesis as assessed by microvessel counts in surgically removed leiomyomata is not affected by presurgical medical management with GnRH agonist therapy. |
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| AbstractList | <Objective:< To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata. <Methods:< Uterine leiomyomata specimens of 49 consecutive patients who underwent myomectomy or hysterectomy following presurgical treatment with (n = 23) and without (n = 26) GnRH agonist were stained immunohistochemically with antibody to factor VIII-related antigen. For each subject, age, parity, number of Lupron treatments, leiomyoma size (cm), and mean microvessel counts calculated from three fields (×400) were recorded. Differences in patient age, parity, microvessel counts and leiomyoma size between GnRH agonist treated and untreated patients were tested by unpaired Student's t test. Differences among the various number of doses were tested by one-way ANOVA, with Bonferonni and Neuman-Keuls post hoc tests between specific dose-number groups. The relationship between microvessel counts and leiomyoma size was tested by Pearson correlation test. Multivariate stepwise regression tested the relationship between the number of Lupron doses and microvessel counts, correcting for age, parity, and leiomyoma size. p < 0.05 was considered significant. <Results:< Patient age and parity were similar in GnRH treated and untreated patients (mean 43.3 ± 6.6 versus 43.9 ± 7.5 years and median 2 (range 0-7) versus 1 (range 0-5), p = 0.78 and p = 0.45, respectively). Microvessel counts of leiomyomata specimens treated presurgically with GnRH agonist therapy (median 22.7, range 6.7-65.7) were not significantly different from microvessel counts of specimens without presurgical GnRH agonist treatment (median 19.8, range 6-53; p = 0.77). No correlation between leiomyoma size and microvessel counts was noted (r = 0.06, P = 0.7). <Conclusion:< Angiogenesis as assessed by microvessel counts in surgically removed leiomyomata is not affected by presurgical medical management with GnRH agonist therapy. Copyright © 2001 S. Karger AG, Basel Objective: To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata. Methods: Uterine leiomyomata specimens of 49 consecutive patients who underwent myomectomy or hysterectomy following presurgical treatment with (n = 23) and without (n = 26) GnRH agonist were stained immunohistochemically with antibody to factor VIII-related antigen. For each subject, age, parity, number of Lupron treatments, leiomyoma size (cm), and mean microvessel counts calculated from three fields (×400) were recorded. Differences in patient age, parity, microvessel counts and leiomyoma size between GnRH agonist treated and untreated patients were tested by unpaired Student’s t test. Differences among the various number of doses were tested by one-way ANOVA, with Bonferonni and Neuman-Keuls post hoc tests between specific dose-number groups. The relationship between microvessel counts and leiomyoma size was tested by Pearson correlation test. Multivariate stepwise regression tested the relationship between the number of Lupron doses and microvessel counts, correcting for age, parity, and leiomyoma size. p < 0.05 was considered significant. Results: Patient age and parity were similar in GnRH treated and untreated patients (mean 43.3 ± 6.6 versus 43.9 ± 7.5 years and median 2 (range 0–7) versus 1 (range 0–5), p = 0.78 and p = 0.45, respectively). Microvessel counts of leiomyomata specimens treated presurgically with GnRH agonist therapy (median 22.7, range 6.7–65.7) were not significantly different from microvessel counts of specimens without presurgical GnRH agonist treatment (median 19.8, range 6–53; p = 0.77). No correlation between leiomyoma size and microvessel counts was noted (r = 0.06, P = 0.7). Conclusion: Angiogenesis as assessed by microvessel counts in surgically removed leiomyomata is not affected by presurgical medical management with GnRH agonist therapy. To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata.OBJECTIVETo assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata.Uterine leiomyomata specimens of 49 consecutive patients who underwent myomectomy or hysterectomy following presurgical treatment with (n = 23) and without (n = 26) GnRH agonist were stained immunohistochemically with antibody to factor VIII-related antigen. For each subject, age, parity, number of Lupron treatments, leiomyoma size (cm), and mean microvessel counts calculated from three fields (x400) were recorded. Differences in patient age, parity, microvessel counts and leiomyoma size between GnRH agonist treated and untreated patients were tested by unpaired Student's t test. Differences among the various number of doses were tested by one-way ANOVA, with Bonferonni and Neuman-Keuls post hoc tests between specific dose-number groups. The relationship between microvessel counts and leiomyoma size was tested by Pearson correlation test. Multivariate stepwise regression tested the relationship between the number of Lupron doses and microvessel counts, correcting for age, parity, and leiomyoma size. p < 0.05 was considered significant.METHODSUterine leiomyomata specimens of 49 consecutive patients who underwent myomectomy or hysterectomy following presurgical treatment with (n = 23) and without (n = 26) GnRH agonist were stained immunohistochemically with antibody to factor VIII-related antigen. For each subject, age, parity, number of Lupron treatments, leiomyoma size (cm), and mean microvessel counts calculated from three fields (x400) were recorded. Differences in patient age, parity, microvessel counts and leiomyoma size between GnRH agonist treated and untreated patients were tested by unpaired Student's t test. Differences among the various number of doses were tested by one-way ANOVA, with Bonferonni and Neuman-Keuls post hoc tests between specific dose-number groups. The relationship between microvessel counts and leiomyoma size was tested by Pearson correlation test. Multivariate stepwise regression tested the relationship between the number of Lupron doses and microvessel counts, correcting for age, parity, and leiomyoma size. p < 0.05 was considered significant.Patient age and parity were similar in GnRH treated and untreated patients (mean 43.3 +/- 6.6 versus 43.9 +/- 7.5 years and median 2 (range 0-7) versus 1 (range 0-5), p = 0.78 and p = 0.45, respectively). Microvessel counts of leiomyomata specimens treated presurgically with GnRH agonist therapy (median 22.7, range 6.7-65.7) were not significantly different from microvessel counts of specimens without presurgical GnRH agonist treatment (median 19.8, range 6-53; p = 0.77). No correlation between leiomyoma size and microvessel counts was noted (r = 0.06, P = 0.7).RESULTSPatient age and parity were similar in GnRH treated and untreated patients (mean 43.3 +/- 6.6 versus 43.9 +/- 7.5 years and median 2 (range 0-7) versus 1 (range 0-5), p = 0.78 and p = 0.45, respectively). Microvessel counts of leiomyomata specimens treated presurgically with GnRH agonist therapy (median 22.7, range 6.7-65.7) were not significantly different from microvessel counts of specimens without presurgical GnRH agonist treatment (median 19.8, range 6-53; p = 0.77). No correlation between leiomyoma size and microvessel counts was noted (r = 0.06, P = 0.7).Angiogenesis as assessed by microvessel counts in surgically removed leiomyomata is not affected by presurgical medical management with GnRH agonist therapy.CONCLUSIONAngiogenesis as assessed by microvessel counts in surgically removed leiomyomata is not affected by presurgical medical management with GnRH agonist therapy. To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata. Uterine leiomyomata specimens of 49 consecutive patients who underwent myomectomy or hysterectomy following presurgical treatment with (n = 23) and without (n = 26) GnRH agonist were stained immunohistochemically with antibody to factor VIII-related antigen. For each subject, age, parity, number of Lupron treatments, leiomyoma size (cm), and mean microvessel counts calculated from three fields (x400) were recorded. Differences in patient age, parity, microvessel counts and leiomyoma size between GnRH agonist treated and untreated patients were tested by unpaired Student's t test. Differences among the various number of doses were tested by one-way ANOVA, with Bonferonni and Neuman-Keuls post hoc tests between specific dose-number groups. The relationship between microvessel counts and leiomyoma size was tested by Pearson correlation test. Multivariate stepwise regression tested the relationship between the number of Lupron doses and microvessel counts, correcting for age, parity, and leiomyoma size. p < 0.05 was considered significant. Patient age and parity were similar in GnRH treated and untreated patients (mean 43.3 +/- 6.6 versus 43.9 +/- 7.5 years and median 2 (range 0-7) versus 1 (range 0-5), p = 0.78 and p = 0.45, respectively). Microvessel counts of leiomyomata specimens treated presurgically with GnRH agonist therapy (median 22.7, range 6.7-65.7) were not significantly different from microvessel counts of specimens without presurgical GnRH agonist treatment (median 19.8, range 6-53; p = 0.77). No correlation between leiomyoma size and microvessel counts was noted (r = 0.06, P = 0.7). Angiogenesis as assessed by microvessel counts in surgically removed leiomyomata is not affected by presurgical medical management with GnRH agonist therapy. |
| Author | Lee, Yi-Chun Sherer, David M. Abulafia, Ovadia Kleinhaus, Karine Levi, Gabriel |
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| Keywords | Gonadotropin-releasing hormone agonist therapy Angiogenesis Uterine leiomyoma Human Leiomyoma Agonist Treatment efficiency Gonadotropin RH Intramuscular administration Female genital diseases Chemotherapy Treatment Uterus Uterine diseases Adult Female Benign neoplasm |
| Language | English |
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| References | Kiltz RJ, Rutgers J, Phillips J, Murugesapillai ML, Kletzky OA: Absence of a dose-response effect of leuprolide acetate on leiomyoma uteri size. Fertil Steril 1994;61:1021-1026.8194611 Demopoulous RI, Jones KY, Mittal KR, Vamavakas EC: Histology of leiomyomata in patients treated with leuprolide acetate. Int J Gynaecol Pathol 1997;16:131-137. Folkman J: Tumor angiogenesis. Adv Cancer Res 1985;43:175-203.2581424 Wilcox LS, Koonin LM, Pokras R, Struss LT, Xia Z, Peterson HB: Hysterectomy in the United States, 1988-1990. Obstet Gynecol 1994;83:549-555.8134065 Friedman AJ, Barbieri RL: Leuprolide acetate: Application in gynecology. Curr Prob Obstet Gynecol Fertil 1988;11:209-244. Abulafia O, Sherer DM: Angiogenesis of the ovary. Am Obstet Gynecol 2000;182:240-246. Folkman J: How is blood vessel growth regulated in normal and neoplastic tissue? Cancer Res 1986;46:467-473.2416426 Gokdeniz R, Oren S, Mizrak B, Bazoglu N: GnRH agonist decreases endothelial nitric oxide synthase (eNOS) expression in leiomyoma. Int J Gynaecol Obstet 2000;70:347-352.10967169 Rein MS, Barbieri RL, Friedman AJ: Progesterone: A critical role in the pathogenesis of uterine myomas. Am J Obstet Gynecol 1995;172:14-18.784752410.1016/0002-9378(95)90077-2 Friedman AJ, Hoffman DI, Comite F, Browneller RW, Miller JD: Treatment of leiomyomata uteri with leupolide acetate depot: A double-blind, placebo-controlled, multicenter study. Obstet Gynecol 1991;77:720-725.1901638 Rutgers JL. Spong CY, Sinow R, Heiner J: Leupride acetate treatment and myoma arterial size. Obstet Gynecol 1995;86:386-388.7651647 Abulafia O, Sherer DM: Angiogenesis of the endometrium. Obstet Gynecol 1999;94:148-153.10389738 Anania CA, Stewart EA, Quade BJ, Hill JA, Nowak RA: Expression of the fibroblast growth factor receptor in women with leiomyomas and abnormal bleeding. Mol Hum Reprod 1997;3:685-691.9294852 Mizutani T, Sugihara A, Nakamuro K, Terada N: Suppression of cell proliferation and induction of apoptosis in uterine leiomyoma by gonadotropin-releasing hormone agonist (leuprolide acetate). J Clin Endocrinol Metab 1998;83:1253-1255.954315110.1210/jc.83.4.1253 Colgan TJ, Pendergast S, LeBlanc M: The histopathology of uterine leiomyomas following treatment with gonadotropin releasing hormone analoques. Hum Pathol 1993;24:1073-1077.8406417 Huang SC, Chou CY, Lin YS, Tsai YC, Hsu KF, Liu CH, Huang KE: Enhanced deoxyribonucleic acid damage and repair but unchanged apoptosis in uterine leiomyomas treated with gonadotropin-releasing hormone agonist. Am Obstet Gynecol 1997;177:417-424. Huang SC, Yu CH, Huang RT, Hsu KF, Tsai YC, Chou CY: Intratumoral blood flow in uterine myoma correlated with a lower tumor size and volume, but not correlated with cell proliferation or angiogenesis. Obstet Gynecol 1996;87:1019-1024.8649683 Vollenhoven BJ, Lawrence AS, Healy DL: Uterine fibroids: A clinical review. Br J Obstet Gynaecol 1990;97:258-298. Crow J, Gardner RL, McSweeny G, Shaw RW: Morphological changes in uterine leiomyomas treated by GnRH agonist Goserrelin. Int J Gynecol Pathol 1995;14:235-242.8600075 Upadhyaya NB, Doody MC, Googe PB: Histopathology changes in leuprolide acetate. Fertil Steril 1990;54:811-814.2121550 Dou Q, Zhao Y, Tarnuzzer RW, Rong H, Williams RS, Schultz GS, Chegini N: Supression of transforming growth factor-β (TGFβ) and TGFβ receptor messenger ribonucleic acid and protein expression in leiomyomata in women receiving gonadotropin-releasing hormone agonist therapy. J Clin Endocrinol Metab 1996;81:3222-3230.8784073 Buttram VC, Reiter RC: Uterine leiomyomata: Etiology, symptomatology and management. Fertil Steril 1981;36:433-445.7026295 Shaw RW: Mechanism of LHRH analogue in uterine fibroids. Horm Res 1989;32:150-153.2533145 Dou Q, Tarnuzzer RW, Williams RS, Schultz GS, Chegini N: Differential expression of matrix metalloproteinase and their tissue inhibitors in leiomyomata: A mechanism for gonadotropin releasing hormone agonist-induced tumour regression. Mol Hum Reprod 1997;3:1005-1014.9433928 Knighton DR, Silver IA, Hunt TK: Regulation of wound healing angiogenesis: effects of oxygen gradients in inspired oxygen concentration. Surgery 1981;90:262-270.6166996 Mietinnen M, Lindenmeyer AE, Chaubal A: Endothelial cell marker CD31, CD34, BNH9 antibody to H- and Y- antigen: Evaluation of their specificity and sensitivity in the diagnosis of vascular tumors and comparison with von Willenbrand factor. Mod Pathol 1994;7:82-90.7512718 Sidky Y, Auerbach R: Lymphocyte induced angiogenesis: A quantitative and sensitive assays of graft versus host reaction. J Exp Med 1975;141:1084-1100.236355 ref2 ref1 |
| References_xml | – reference: Demopoulous RI, Jones KY, Mittal KR, Vamavakas EC: Histology of leiomyomata in patients treated with leuprolide acetate. Int J Gynaecol Pathol 1997;16:131-137. – reference: Shaw RW: Mechanism of LHRH analogue in uterine fibroids. Horm Res 1989;32:150-153.2533145 – reference: Vollenhoven BJ, Lawrence AS, Healy DL: Uterine fibroids: A clinical review. Br J Obstet Gynaecol 1990;97:258-298. – reference: Folkman J: How is blood vessel growth regulated in normal and neoplastic tissue? Cancer Res 1986;46:467-473.2416426 – reference: Upadhyaya NB, Doody MC, Googe PB: Histopathology changes in leuprolide acetate. Fertil Steril 1990;54:811-814.2121550 – reference: Folkman J: Tumor angiogenesis. Adv Cancer Res 1985;43:175-203.2581424 – reference: Sidky Y, Auerbach R: Lymphocyte induced angiogenesis: A quantitative and sensitive assays of graft versus host reaction. J Exp Med 1975;141:1084-1100.236355 – reference: Mizutani T, Sugihara A, Nakamuro K, Terada N: Suppression of cell proliferation and induction of apoptosis in uterine leiomyoma by gonadotropin-releasing hormone agonist (leuprolide acetate). J Clin Endocrinol Metab 1998;83:1253-1255.954315110.1210/jc.83.4.1253 – reference: Anania CA, Stewart EA, Quade BJ, Hill JA, Nowak RA: Expression of the fibroblast growth factor receptor in women with leiomyomas and abnormal bleeding. Mol Hum Reprod 1997;3:685-691.9294852 – reference: Mietinnen M, Lindenmeyer AE, Chaubal A: Endothelial cell marker CD31, CD34, BNH9 antibody to H- and Y- antigen: Evaluation of their specificity and sensitivity in the diagnosis of vascular tumors and comparison with von Willenbrand factor. Mod Pathol 1994;7:82-90.7512718 – reference: Abulafia O, Sherer DM: Angiogenesis of the ovary. Am Obstet Gynecol 2000;182:240-246. – reference: Dou Q, Tarnuzzer RW, Williams RS, Schultz GS, Chegini N: Differential expression of matrix metalloproteinase and their tissue inhibitors in leiomyomata: A mechanism for gonadotropin releasing hormone agonist-induced tumour regression. Mol Hum Reprod 1997;3:1005-1014.9433928 – reference: Gokdeniz R, Oren S, Mizrak B, Bazoglu N: GnRH agonist decreases endothelial nitric oxide synthase (eNOS) expression in leiomyoma. Int J Gynaecol Obstet 2000;70:347-352.10967169 – reference: Crow J, Gardner RL, McSweeny G, Shaw RW: Morphological changes in uterine leiomyomas treated by GnRH agonist Goserrelin. Int J Gynecol Pathol 1995;14:235-242.8600075 – reference: Friedman AJ, Barbieri RL: Leuprolide acetate: Application in gynecology. Curr Prob Obstet Gynecol Fertil 1988;11:209-244. – reference: Kiltz RJ, Rutgers J, Phillips J, Murugesapillai ML, Kletzky OA: Absence of a dose-response effect of leuprolide acetate on leiomyoma uteri size. 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| Snippet | Objective: To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata. Methods: Uterine... To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata. Uterine leiomyomata specimens of 49... <Objective:< To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata. <Methods:< Uterine... To assess the effect of gonadotropin-releasing hormone (GnRH) agonist treatment upon angiogenesis in uterine leiomyomata.OBJECTIVETo assess the effect of... |
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| SubjectTerms | Analysis of Variance Antineoplastic Agents, Hormonal - therapeutic use Biological and medical sciences Female Genital system. Reproduction Gonadotropin-Releasing Hormone - agonists Gonadotropin-Releasing Hormone - therapeutic use Humans Hysterectomy Immunohistochemistry Leiomyoma - complications Leiomyoma - pathology Leiomyoma - surgery Leuprolide - therapeutic use Medical sciences Neovascularization, Pathologic - complications Neovascularization, Pathologic - drug therapy Neovascularization, Pathologic - pathology Original Paper Paraffin Embedding Pharmacology. Drug treatments Preoperative Care Regression Analysis Uterine Neoplasms - complications Uterine Neoplasms - pathology Uterine Neoplasms - surgery Uterus - blood supply Uterus - drug effects Uterus - surgery |
| Title | Effect of Gonadotropin-Releasing Hormone Agonist Treatment upon Angiogenesis in Uterine Leiomyoma |
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