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S. Mancuso - One of the best experts on this subject based on the ideXlab platform.
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Polycystic Ovary Disease. A risk factor for gestational diabetes
The Journal of reproductive medicine, 1995Co-Authors: Antonio Lanzone, Anna Maria Fulghesu, Alessandro Caruso, N. Di Simone, S. De Carolis, S. MancusoAbstract:We investigated the impact of pregestationally elevated insulin plasma levels on glycemic control in pregnant women with polycystic Ovary Disease (PCOD). Twelve patients with PCOD who became pregnant within six months following evaluation of their metabolic status were the study subjects. Four were obese and six (two obese) had a hyperinsulinemic response to the oral glucose tolerance test (OGTT). They were tested with the OGTT at 28-30 weeks of gestation. We also tested 12 normal patients and 10 consecutive patients with gestational diabetes; all were at the same gestational age. Plasma levels of insulin and glucose were determined in the samples collected for a period of four hours after glucose load (100 g). All PCOD patients significantly increased their insulin secretion in pregnancy. The hyperinsulinemic PCOD patients developed gestational diabetes (two patients) and impaired gestational glucose tolerance (three patients). The area under the insulin curve was greater in PCOD patients than in control and gestational diabetes patients (P < .01). In spite of their large increase in insulin secretion observed during pregnancy, patients with PCOD may develop a derangement of glycemic control, probably related to their pregestational insulinemic status.
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Polycystic Ovary Disease : a risk factor for gestational diabetes ?
1995Co-Authors: Antonio Lanzone, Anna Maria Fulghesu, Alessandro Caruso, N. Di Simone, S. De Carolis, S. MancusoAbstract:We investigated the impact of pregestationally elevated insulin plasma levels on glycemic control in pregnant women with polycystic Ovary Disease (PCOD). Twelve patients with PCOD who became pregnant within six months following evaluation of their metabolic status were the study subjects. Four were obesse and six (two obese) has a hyperinsulinemic response to he oral glucose tolerance test (OGTT). They were tested with the OGTT at 28-30 weeks of gestation. We also tested 12 normal patients and 10 consecutive patients with gestational diabetes; all were at the same gestational aged. Plasma levels of insulin and glucose were determined in the samples collected for a period of four hours after glucose load (100 g). All PCOD patients significantly increased their insulin secretion in pregnancy. The hyperinsulinemic PCOD patients developed gestational diabetes (two patients) and impaired gestation glucose tolerance (three patients). The area under the insulin curve was greater in PCOD patients than in control and gestational diabetes patients (P
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Effectiveness of a somatostatin analogue in lowering luteinizing hormone and insulin-stimulated secretion in hyperinsulinemic women with polycystic Ovary Disease.
Fertility and sterility, 1995Co-Authors: Anna Maria Fulghesu, Antonio Lanzone, Alessandro Caruso, Cristiana Laura Andreani, E. Pierro, S. MancusoAbstract:Objective To analyze the action of a long-acting somatostatin analogue on circulating insulin levels and on pituitary sensitivity to GnRH in women affected by polycystic Ovary Disease (PCOD). Design Controlled clinical study. Setting Normal human volunteers in the Department of Obstetrics and Gynecology, Universita' Cattolica del Sacro Cuore. Patients Twenty euglycemic women affected by PCOD, aged 19 to 30years, were studied in their early follicular phase. Interventions A long-acting somatostatin analogue (octreotide) was administered SC for 6weeks; an oral glucose tolerance test (OGTT), a GnRH test, and plasma hormone determinations were performed at baseline and repeated after 6weeks of treatment. A glucose load also was performed after 1week of treatment. Main Outcome Measures Insulin and glucose serum concentrations were measured in all samples under the oral glucose stimulus, LH and FSH were measured under GnRH test. Plasma levels of PRL, sex hormone-binding globulin, androstenedione (A), T, 17 β -hydroxyprogesterone, DHEAS, and Cortisol were measured. Steroids also were assayed after the octreotide administration. Results Based on the insulin response to OGTT, subjects were classified as hyperinsulinemic (n=12) and normoinsulinemic (n=8). Octreotide administration did not affect the glycemic levels in both groups. Octreotide significantly reduced insulin and LH exaggerated response to GnRH stimulus, as well as the A and T circulating levels, only in the hyperinsulinemic group. Conclusions A functional linkage exists between exaggerated insulin and LH-stimulated secretion in a group of polycystic Ovary patients. Octreotide may be useful in normalizing these alterations and in reducing ovarian androgen secretion of hyperinsulinemic subjects.
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Long-term naltrexone treatment reduces the exaggerated insulin secretion in patients with polycystic Ovary Disease.
Obstetrics and gynecology, 1993Co-Authors: Anna Maria Fulghesu, Antonio Lanzone, Francesco Cucinelli, Alessandro Caruso, S. MancusoAbstract:OBJECTIVE To evaluate the involvement of endogenous opiates in the pathophysiology of the hyperinsulinism in patients affected by polycystic Ovary Disease by administering naloxone and naltrexone. We also studied the hormonal status following long-term opioid antagonist administration. METHODS Twenty-one women affected by polycystic Ovary Disease participated in the study. An oral glucose tolerance test (GTT) was performed at baseline and repeated after short-term naloxone infusion and after 6 weeks of naltrexone administration. Plasma glucose and insulin levels were evaluated in all samples. Gonadotropins, sex hormone-binding globulin, and androgen levels were determined initially and after the naltrexone treatment. RESULTS None of the patients showed any alteration of glucose tolerance. Based on the insulin response to the GTT, the patients were classified as normo- or hyperinsulinemic. Opioid antagonist administration significantly reduced the insulin response to the GTT in hyperinsulinemic patients, without affecting their glycemic levels. In normoinsulinemic patients, glucose plasma levels were increased whereas insulin levels were not modified by the treatments. Gonadotropin and androgen plasma concentrations were not modified after naltrexone administration. CONCLUSIONS This work supports a role for the endogenous opiates in the regulation of exaggerated insulin secretion in patients with polycystic Ovary Disease. The reduction of insulin secretion failed to demonstrate any hormonal modification in such hyperandrogenized patients.
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Ovulation induction with human menopausal gonadotropin versus follicle-stimulating hormone after pituitary suppression by gonadotropin releasing hormone agonist in polycystic Ovary Disease. A cross-over study.
The Journal of reproductive medicine, 1992Co-Authors: Anna Maria Fulghesu, Antonio Lanzone, Alessandro Caruso, C. Guida, M. C. Nicoletti, P. Rossi, M. Le Donne, S. MancusoAbstract:Ten patients with polycystic Ovary Disease (PCOD) had ovulation induction after pituitary suppression by gonadotropin releasing hormone agonist (GnRHa) with GnRHa plus pure follicle-stimulating hormone (FSH) or plus human menopausal gonadotropin (hMG). Duration of the stimulation period and gonadotropin doses were superimposable. A multifollicular response was observed in both treatments. Bioassay and radioimmunoassay of luteinizing hormone, androstanedione and testosterone plasma levels were higher in hMG cycles compared to FSH-treated cycles. No differences was found in FSH and estradiol (E2) plasma concentrations, whereas in hMG-treated cycles the E2/number of follicles and E2/ovarian volume ratios were greater than in the FSH-treated cycles. Clinical results in terms of percentages of ovulation and pregnancies were the same in the two protocols. We conclude that the presence of luteinizing hormone in induction of ovulation in patients with PCOD does not seem to influence follicular recruitment and development, but it may have a role in the enhancement of steroid production.
Eliezer Shalev - One of the best experts on this subject based on the ideXlab platform.
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Regulation of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of MMP, and progesterone secretion in luteinized granulosa cells from normally ovulating women with polycystic Ovary Disease.
Fertility and sterility, 2003Co-Authors: Izhar Ben-shlomo, Shlomit Goldman, Eliezer ShalevAbstract:To investigate the regulation of MMP-9, TIMP-1, and progesterone via three signal transduction pathways in luteinized granulosa cells from normal ovulatory and PCOD women. In vitro study. Laboratory for Research in Reproductive Sciences, Department of Obstetrics and Gynecology, Ha'Emek Hospital, Afula, Israel. Ten normal ovulatory and 10 women with polycystic Ovary Disease (PCOD) treated in an assisted reproduction program. Cultured cells were exposed to phorbol 12-myristate 13-acetate (TPA), acting via protein kinase C (PKC), to epidermal growth factor (EGF), acting via protein tyrosine kinase (PTK), and to forskolin, acting via protein kinase A (PKA). Secretion of MMP-9, TIMP-1, and progesterone. Phorbol 12-myristate 13-acetate elicited an increase in MMP-9 and TIMP-1 secretion in both groups and apparently did not affect progesterone secretion. Epidermal growth factor did not change significantly neither MMP-9 nor TIMP-1 secretion but dose dependently decreased MMP-9-TIMP-1 ratio and increased progesterone secretion in the PCOD group. Forskolin inhibited MMP-9 activity and increased TIMP-1 and progesterone secretion in both groups. Progesterone production was inversely related to the ratio of MMP-9-TIMP-1 regardless of cell origin. In this preliminary study, similar and divergent patterns have emerged in the regulation of MMP-9 and TIMP-1 in human luteinized granulosa cells. Repressing MMP-9-TIMP-1 ratio may have an important modulatory effect on progesterone secretion.
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Regulation of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of MMP, and progesterone secretion in luteinized granulosa cells from normally ovulating women with polycystic Ovary Disease
Fertility and Sterility, 2003Co-Authors: Izhar Ben-shlomo, Shlomit Goldman, Eliezer ShalevAbstract:Abstract Objective To investigate the regulation of MMP-9, TIMP-1, and progesterone via three signal transduction pathways in luteinized granulosa cells from normal ovulatory and PCOD women. Design In vitro study. Setting Laboratory for Research in Reproductive Sciences, Department of Obstetrics and Gynecology, Ha'Emek Hospital, Afula, Israel. Patient(s) Ten normal ovulatory and 10 women with polycystic Ovary Disease (PCOD) treated in an assisted reproduction program. Intervention(s) Cultured cells were exposed to phorbol 12-myristate 13-acetate (TPA), acting via protein kinase C (PKC), to epidermal growth factor (EGF), acting via protein tyrosine kinase (PTK), and to forskolin, acting via protein kinase A (PKA). Main outcome measure(s) Secretion of MMP-9, TIMP-1, and progesterone. Result(s) Phorbol 12-myristate 13-acetate elicited an increase in MMP-9 and TIMP-1 secretion in both groups and apparently did not affect progesterone secretion. Epidermal growth factor did not change significantly neither MMP-9 nor TIMP-1 secretion but dose dependently decreased MMP-9–TIMP-1 ratio and increased progesterone secretion in the PCOD group. Forskolin inhibited MMP-9 activity and increased TIMP-1 and progesterone secretion in both groups. Progesterone production was inversely related to the ratio of MMP-9–TIMP-1 regardless of cell origin. Conclusion(s) In this preliminary study, similar and divergent patterns have emerged in the regulation of MMP-9 and TIMP-1 in human luteinized granulosa cells. Repressing MMP-9–TIMP-1 ratio may have an important modulatory effect on progesterone secretion.
Krishna B Singh - One of the best experts on this subject based on the ideXlab platform.
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Persistent estrus rat models of polycystic Ovary Disease: an update.
Fertility and sterility, 2005Co-Authors: Krishna B SinghAbstract:To critically review published articles on polycystic Ovary (PCO) Disease in rat models, with a focus on delineating its pathophysiology. Review of the English-language literature published from 1966 to March 2005 was performed through PubMed search. Keywords or phrases used were persistent estrus, chronic anovulation, polycystic Ovary, polycystic Ovary Disease, and polycystic Ovary syndrome. Articles were also located via bibliographies of published literature. University Health Sciences Center. Articles on persistent estrus and PCO in rats were selected and reviewed regarding the methods for induction of PCO Disease. Changes in the reproductive cycle, ovarian morphology, hormonal parameters, and factors associated with the development of PCO Disease in rat models were analyzed. Principal methods for inducing PCO in the rat include exposure to constant light, anterior hypothalamic and amygdaloidal lesions, and the use of androgens, estrogens, antiprogestin, and mifepristone. The validated rat PCO models provide useful information on morphologic and hormonal disturbances in the pathogenesis of chronic anovulation in this condition. These studies have aimed to replicate the morphologic and hormonal characteristics observed in the human PCO syndrome. The implications of these studies to human condition are discussed.
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Persistent estrus rat models of polycystic Ovary Disease: an update.
Fertility and Sterility, 2005Co-Authors: Krishna B SinghAbstract:Objective To critically review published articles on polycystic Ovary (PCO) Disease in rat models, with a focus on delineating its pathophysiology. Design Review of the English-language literature published from 1966 to March 2005 was performed through PubMed search. Keywords or phrases used were persistent estrus, chronic anovulation, polycystic Ovary, polycystic Ovary Disease, and polycystic Ovary syndrome. Articles were also located via bibliographies of published literature. Setting University Health Sciences Center. Intervention(s) Articles on persistent estrus and PCO in rats were selected and reviewed regarding the methods for induction of PCO Disease. Main Outcome Measure(s) Changes in the reproductive cycle, ovarian morphology, hormonal parameters, and factors associated with the development of PCO Disease in rat models were analyzed. Result(s) Principal methods for inducing PCO in the rat include exposure to constant light, anterior hypothalamic and amygdaloidal lesions, and the use of androgens, estrogens, antiprogestin, and mifepristone. Conclusion(s) The validated rat PCO models provide useful information on morphologic and hormonal disturbances in the pathogenesis of chronic anovulation in this condition. These studies have aimed to replicate the morphologic and hormonal characteristics observed in the human PCO syndrome. The implications of these studies to human condition are discussed.
Candeger Yilmaz - One of the best experts on this subject based on the ideXlab platform.
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endocrine and metabolic effects of rosiglitazone in non obese women with polycystic Ovary Disease
Endocrine Journal, 2005Co-Authors: Didem Dereli, Tuğrul Dereli, Firat Bayraktar, Gokhan A Ozgen, Candeger YilmazAbstract:We hypothesized that the administration of rosiglitazone, an insulin-sensitizing agent of the thiazolidinedione class, would improve the ovulatory dysfunction, hirsutism, hyperandrogenemia, and hyperinsulinemia of polycystic Ovary syndrome (PCOS) patients. Forty women with PCOS and impaired glucose tolerance test (IGT) were randomly assigned to the 8-month treatment with rosiglitazone at either 2 mg/day or 4 mg/day. We compared changes in ovulatory function, hirsutism, hormonal levels (total and free testosterone, estradiol, estrone, androstenedione, LH and FSH), and measures of glycemic parameters (fasting and post-challenge levels of glucose and insulin, HOMA-IR, hemoglobin A1c), between the study groups. The patients' baseline characteristics were similar across all treatment arms. Fifteen of 20 women in the 2 mg group and 19 of 20 women in the 4 mg group achieved normal glucose tolerance; 14 of 20 women in the 2 mg group and 17 of 20 women in the 4 mg group achieved ovulatory menses at the end of the study period. The decreases of free testosterone levels were better in the 4 mg group than the 2 mg rosiglitazone group (-1.89+/-0.35 pg/ml vs. -2.21+/-0.39 pg/ml; P<0.01). There were neither any serious adverse events nor any liver enzyme elevations in our study patients during the treatment period. This study demonstrated that rosiglitazone improves the ovulatory dysfunction, hirsutism, hyperandrogenemia, and insulin resistance of PCOS in a dose-related fashion, with minimal adverse effects. This drug may be a good choice for lifetime treatment of patients with PCOS, especially for the ones who failed to show satisfactory results in metformin therapy.
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Endocrine and metabolic effects of rosiglitazone in non-obese women with polycystic Ovary Disease
Endocrine journal, 2005Co-Authors: Didem Dereli, Tuğrul Dereli, Firat Bayraktar, A. Gökhan Özgen, Candeger YilmazAbstract:We hypothesized that the administration of rosiglitazone, an insulin-sensitizing agent of the thiazolidinedione class, would improve the ovulatory dysfunction, hirsutism, hyperandrogenemia, and hyperinsulinemia of polycystic Ovary syndrome (PCOS) patients. Forty women with PCOS and impaired glucose tolerance test (IGT) were randomly assigned to the 8-month treatment with rosiglitazone at either 2 mg/day or 4 mg/day. We compared changes in ovulatory function, hirsutism, hormonal levels (total and free testosterone, estradiol, estrone, androstenedione, LH and FSH), and measures of glycemic parameters (fasting and post-challenge levels of glucose and insulin, HOMA-IR, hemoglobin A1c), between the study groups. The patients' baseline characteristics were similar across all treatment arms. Fifteen of 20 women in the 2 mg group and 19 of 20 women in the 4 mg group achieved normal glucose tolerance; 14 of 20 women in the 2 mg group and 17 of 20 women in the 4 mg group achieved ovulatory menses at the end of the study period. The decreases of free testosterone levels were better in the 4 mg group than the 2 mg rosiglitazone group (-1.89+/-0.35 pg/ml vs. -2.21+/-0.39 pg/ml; P
Anna Maria Fulghesu - One of the best experts on this subject based on the ideXlab platform.
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Polycystic Ovary Disease. A risk factor for gestational diabetes
The Journal of reproductive medicine, 1995Co-Authors: Antonio Lanzone, Anna Maria Fulghesu, Alessandro Caruso, N. Di Simone, S. De Carolis, S. MancusoAbstract:We investigated the impact of pregestationally elevated insulin plasma levels on glycemic control in pregnant women with polycystic Ovary Disease (PCOD). Twelve patients with PCOD who became pregnant within six months following evaluation of their metabolic status were the study subjects. Four were obese and six (two obese) had a hyperinsulinemic response to the oral glucose tolerance test (OGTT). They were tested with the OGTT at 28-30 weeks of gestation. We also tested 12 normal patients and 10 consecutive patients with gestational diabetes; all were at the same gestational age. Plasma levels of insulin and glucose were determined in the samples collected for a period of four hours after glucose load (100 g). All PCOD patients significantly increased their insulin secretion in pregnancy. The hyperinsulinemic PCOD patients developed gestational diabetes (two patients) and impaired gestational glucose tolerance (three patients). The area under the insulin curve was greater in PCOD patients than in control and gestational diabetes patients (P < .01). In spite of their large increase in insulin secretion observed during pregnancy, patients with PCOD may develop a derangement of glycemic control, probably related to their pregestational insulinemic status.
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Polycystic Ovary Disease : a risk factor for gestational diabetes ?
1995Co-Authors: Antonio Lanzone, Anna Maria Fulghesu, Alessandro Caruso, N. Di Simone, S. De Carolis, S. MancusoAbstract:We investigated the impact of pregestationally elevated insulin plasma levels on glycemic control in pregnant women with polycystic Ovary Disease (PCOD). Twelve patients with PCOD who became pregnant within six months following evaluation of their metabolic status were the study subjects. Four were obesse and six (two obese) has a hyperinsulinemic response to he oral glucose tolerance test (OGTT). They were tested with the OGTT at 28-30 weeks of gestation. We also tested 12 normal patients and 10 consecutive patients with gestational diabetes; all were at the same gestational aged. Plasma levels of insulin and glucose were determined in the samples collected for a period of four hours after glucose load (100 g). All PCOD patients significantly increased their insulin secretion in pregnancy. The hyperinsulinemic PCOD patients developed gestational diabetes (two patients) and impaired gestation glucose tolerance (three patients). The area under the insulin curve was greater in PCOD patients than in control and gestational diabetes patients (P
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Effectiveness of a somatostatin analogue in lowering luteinizing hormone and insulin-stimulated secretion in hyperinsulinemic women with polycystic Ovary Disease.
Fertility and sterility, 1995Co-Authors: Anna Maria Fulghesu, Antonio Lanzone, Alessandro Caruso, Cristiana Laura Andreani, E. Pierro, S. MancusoAbstract:Objective To analyze the action of a long-acting somatostatin analogue on circulating insulin levels and on pituitary sensitivity to GnRH in women affected by polycystic Ovary Disease (PCOD). Design Controlled clinical study. Setting Normal human volunteers in the Department of Obstetrics and Gynecology, Universita' Cattolica del Sacro Cuore. Patients Twenty euglycemic women affected by PCOD, aged 19 to 30years, were studied in their early follicular phase. Interventions A long-acting somatostatin analogue (octreotide) was administered SC for 6weeks; an oral glucose tolerance test (OGTT), a GnRH test, and plasma hormone determinations were performed at baseline and repeated after 6weeks of treatment. A glucose load also was performed after 1week of treatment. Main Outcome Measures Insulin and glucose serum concentrations were measured in all samples under the oral glucose stimulus, LH and FSH were measured under GnRH test. Plasma levels of PRL, sex hormone-binding globulin, androstenedione (A), T, 17 β -hydroxyprogesterone, DHEAS, and Cortisol were measured. Steroids also were assayed after the octreotide administration. Results Based on the insulin response to OGTT, subjects were classified as hyperinsulinemic (n=12) and normoinsulinemic (n=8). Octreotide administration did not affect the glycemic levels in both groups. Octreotide significantly reduced insulin and LH exaggerated response to GnRH stimulus, as well as the A and T circulating levels, only in the hyperinsulinemic group. Conclusions A functional linkage exists between exaggerated insulin and LH-stimulated secretion in a group of polycystic Ovary patients. Octreotide may be useful in normalizing these alterations and in reducing ovarian androgen secretion of hyperinsulinemic subjects.
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Long-term naltrexone treatment reduces the exaggerated insulin secretion in patients with polycystic Ovary Disease.
Obstetrics and gynecology, 1993Co-Authors: Anna Maria Fulghesu, Antonio Lanzone, Francesco Cucinelli, Alessandro Caruso, S. MancusoAbstract:OBJECTIVE To evaluate the involvement of endogenous opiates in the pathophysiology of the hyperinsulinism in patients affected by polycystic Ovary Disease by administering naloxone and naltrexone. We also studied the hormonal status following long-term opioid antagonist administration. METHODS Twenty-one women affected by polycystic Ovary Disease participated in the study. An oral glucose tolerance test (GTT) was performed at baseline and repeated after short-term naloxone infusion and after 6 weeks of naltrexone administration. Plasma glucose and insulin levels were evaluated in all samples. Gonadotropins, sex hormone-binding globulin, and androgen levels were determined initially and after the naltrexone treatment. RESULTS None of the patients showed any alteration of glucose tolerance. Based on the insulin response to the GTT, the patients were classified as normo- or hyperinsulinemic. Opioid antagonist administration significantly reduced the insulin response to the GTT in hyperinsulinemic patients, without affecting their glycemic levels. In normoinsulinemic patients, glucose plasma levels were increased whereas insulin levels were not modified by the treatments. Gonadotropin and androgen plasma concentrations were not modified after naltrexone administration. CONCLUSIONS This work supports a role for the endogenous opiates in the regulation of exaggerated insulin secretion in patients with polycystic Ovary Disease. The reduction of insulin secretion failed to demonstrate any hormonal modification in such hyperandrogenized patients.
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Ovulation induction with human menopausal gonadotropin versus follicle-stimulating hormone after pituitary suppression by gonadotropin releasing hormone agonist in polycystic Ovary Disease. A cross-over study.
The Journal of reproductive medicine, 1992Co-Authors: Anna Maria Fulghesu, Antonio Lanzone, Alessandro Caruso, C. Guida, M. C. Nicoletti, P. Rossi, M. Le Donne, S. MancusoAbstract:Ten patients with polycystic Ovary Disease (PCOD) had ovulation induction after pituitary suppression by gonadotropin releasing hormone agonist (GnRHa) with GnRHa plus pure follicle-stimulating hormone (FSH) or plus human menopausal gonadotropin (hMG). Duration of the stimulation period and gonadotropin doses were superimposable. A multifollicular response was observed in both treatments. Bioassay and radioimmunoassay of luteinizing hormone, androstanedione and testosterone plasma levels were higher in hMG cycles compared to FSH-treated cycles. No differences was found in FSH and estradiol (E2) plasma concentrations, whereas in hMG-treated cycles the E2/number of follicles and E2/ovarian volume ratios were greater than in the FSH-treated cycles. Clinical results in terms of percentages of ovulation and pregnancies were the same in the two protocols. We conclude that the presence of luteinizing hormone in induction of ovulation in patients with PCOD does not seem to influence follicular recruitment and development, but it may have a role in the enhancement of steroid production.