Hormonal replacement therapy Archives - Revista Brasileira de Ginecologia e Obstetrícia
Summary
Rev Bras Ginecol Obstet. 1998;20(6):303-308
DOI 10.1590/S0100-72031998000600002
Objective: to compare mammographic density changes, case by case, according to image digitization in three consecutive evaluations of users or nonusers of hormonal replacement therapy (HRT). Methods: 59 postmenopausal women were evaluated, 43 being users of cyclic or continuous estro-progestin hormonal replacement therapy, and 16 nonusers. The criteria of inclusion were: amenorrhea for at least 12 months, a normal mammographic examination at the beginning of the HRT (users) or the clinical follow-up without HRT (nonusers), at two incidences (mediolateral and craniocaudal). The following variables were used for the evaluation of mammary density: initial change - the difference between the first mammography after HRT performed in 12 ± 3 months and the mammography performed before HRT-and final change - the difference between the second mammography after HRT performed in 24 ± 3 months and the mammography performed before HRT. Wilcoxon and c² tests were used in order to evaluate the differences in mammographic density changes. Results: more than half (56.3%) of the women, HRT users with initial increase in mammographic density remained with the increase after the final evaluation. This finding was not significant (p=0.617). In the same group, the initial nonincrease was significantly associated with the final nonincrease (p=0.017). Among the nonusers, all breasts that were not totally fat at the initial evaluation presented a mammographic density decrease at the final evaluation. Conclusions: the majority of HRT users presenting mammographic density increase at the first evaluation, after approximately one year of use, remained with the increase at a second evaluation. After some time, the nonusers tended to present a significant mammographic density decrease (p=0.003).
Summary
Rev Bras Ginecol Obstet. 1998;20(6):303-308
DOI 10.1590/S0100-72031998000600002
Objective: to compare mammographic density changes, case by case, according to image digitization in three consecutive evaluations of users or nonusers of hormonal replacement therapy (HRT). Methods: 59 postmenopausal women were evaluated, 43 being users of cyclic or continuous estro-progestin hormonal replacement therapy, and 16 nonusers. The criteria of inclusion were: amenorrhea for at least 12 months, a normal mammographic examination at the beginning of the HRT (users) or the clinical follow-up without HRT (nonusers), at two incidences (mediolateral and craniocaudal). The following variables were used for the evaluation of mammary density: initial change - the difference between the first mammography after HRT performed in 12 ± 3 months and the mammography performed before HRT-and final change - the difference between the second mammography after HRT performed in 24 ± 3 months and the mammography performed before HRT. Wilcoxon and c² tests were used in order to evaluate the differences in mammographic density changes. Results: more than half (56.3%) of the women, HRT users with initial increase in mammographic density remained with the increase after the final evaluation. This finding was not significant (p=0.617). In the same group, the initial nonincrease was significantly associated with the final nonincrease (p=0.017). Among the nonusers, all breasts that were not totally fat at the initial evaluation presented a mammographic density decrease at the final evaluation. Conclusions: the majority of HRT users presenting mammographic density increase at the first evaluation, after approximately one year of use, remained with the increase at a second evaluation. After some time, the nonusers tended to present a significant mammographic density decrease (p=0.003).
Summary
Rev Bras Ginecol Obstet. 2000;22(1):43-48
DOI 10.1590/S0100-72032000000100008
Purpose: to analyze the prevalence of genuine urinary incontinence (GUI) recurrence, after at least two years of follow-up, in different surgical techniques used for its correction. Patients and Methods: fifty-five patients with diagnosis of GUI, submitted to surgery for its repair at the Serviço de Ginecologia e Obstetrícia do Hospital de Clínicas de Porto Alegre from 1992 to 1996 and whose post-surgical follow-up was superior to 2 years were divided into three groups according to the surgical approach: Kelly-Kennedy (n = 24), Burch (n = 23) and Marshall-Marchetti-Krantz (n = 8). Results: there were no differences regarding recurrence rate, age at surgery and at recurrence time, estrogen therapy, number of pregnancies and vaginal delivery (p>0.05). Although posterior perineoplasty was more prevalent in the Kelly-Kennedy group, it did not influence the recurrence rate. The group submitted to the Burch approach had more years of menopause at the time of surgery. Conclusion: the recurrence rates of urinary incontinence comparing the three different techniques (Kelly-Kennedy, Burch and Marshall-Marchetti-Krantz) were, respectively, 29.2, 39.1 and 50%, which did not differ statistically. Considering the potential confusional bias for urinary stress incontinence, they did not differ among the groups. Nevertheless, we noticed that all women who had previous surgery presented recurrence of incontinence.
Summary
Rev Bras Ginecol Obstet. 2000;22(1):43-48
DOI 10.1590/S0100-72032000000100008
Purpose: to analyze the prevalence of genuine urinary incontinence (GUI) recurrence, after at least two years of follow-up, in different surgical techniques used for its correction. Patients and Methods: fifty-five patients with diagnosis of GUI, submitted to surgery for its repair at the Serviço de Ginecologia e Obstetrícia do Hospital de Clínicas de Porto Alegre from 1992 to 1996 and whose post-surgical follow-up was superior to 2 years were divided into three groups according to the surgical approach: Kelly-Kennedy (n = 24), Burch (n = 23) and Marshall-Marchetti-Krantz (n = 8). Results: there were no differences regarding recurrence rate, age at surgery and at recurrence time, estrogen therapy, number of pregnancies and vaginal delivery (p>0.05). Although posterior perineoplasty was more prevalent in the Kelly-Kennedy group, it did not influence the recurrence rate. The group submitted to the Burch approach had more years of menopause at the time of surgery. Conclusion: the recurrence rates of urinary incontinence comparing the three different techniques (Kelly-Kennedy, Burch and Marshall-Marchetti-Krantz) were, respectively, 29.2, 39.1 and 50%, which did not differ statistically. Considering the potential confusional bias for urinary stress incontinence, they did not differ among the groups. Nevertheless, we noticed that all women who had previous surgery presented recurrence of incontinence.
Summary
Rev Bras Ginecol Obstet. 2000;22(1):33-36
DOI 10.1590/S0100-72032000000100006
Purpose: to evaluate the morphologic and morphometric alterations produced by tamoxifen and conjugated estrogens in the mammary epithelium of rats in persistent estrus. Methods: thirty-three adult female rats in persistent estrus induced with 1.25 mg testosterone propionate were divided at random into three groups: GI -- which received only water, control group (n = 12); GII -- treated with 500 mug tamoxifen daily (n = 10); GIII -- treated with 30 mug conjugated estrogens per day (n = 11). The first inguinal-abdominal pair of mammary glands of the animals was extirpated and processed for morphologic and morphometric study. Data were analyzed statistically by the Kruskal-Wallis rank analysis of variance (p < 0.05). Results: the morphologic study revealed signs of epithelial atrophy and the morphometric study showed a statistically significant reduction in the mean number of ducts and alveoli in groups II (10.1 and 1.9, respectively) and III (11.1 and 3.5, respectively) compared to group I (25.0 and 6.6, respectively). There was no significant difference between groups II and III. Conclusions: the results of this study indicate that tamoxifen as well as conjugated estrogens at the tested doses produced mammary epithelial atrophy in rats in persistent estrus.
Summary
Rev Bras Ginecol Obstet. 2000;22(1):33-36
DOI 10.1590/S0100-72032000000100006
Purpose: to evaluate the morphologic and morphometric alterations produced by tamoxifen and conjugated estrogens in the mammary epithelium of rats in persistent estrus. Methods: thirty-three adult female rats in persistent estrus induced with 1.25 mg testosterone propionate were divided at random into three groups: GI -- which received only water, control group (n = 12); GII -- treated with 500 mug tamoxifen daily (n = 10); GIII -- treated with 30 mug conjugated estrogens per day (n = 11). The first inguinal-abdominal pair of mammary glands of the animals was extirpated and processed for morphologic and morphometric study. Data were analyzed statistically by the Kruskal-Wallis rank analysis of variance (p < 0.05). Results: the morphologic study revealed signs of epithelial atrophy and the morphometric study showed a statistically significant reduction in the mean number of ducts and alveoli in groups II (10.1 and 1.9, respectively) and III (11.1 and 3.5, respectively) compared to group I (25.0 and 6.6, respectively). There was no significant difference between groups II and III. Conclusions: the results of this study indicate that tamoxifen as well as conjugated estrogens at the tested doses produced mammary epithelial atrophy in rats in persistent estrus.
Summary
Rev Bras Ginecol Obstet. 2000;22(1):37-41
DOI 10.1590/S0100-72032000000100007
Purpose: to evaluate the effects of tibolone on climacteric symptoms and clinical and metabolic variables. Methods: thirty-four postmenopausal women were treated orally with 2.5 mg tibolone daily for 48 weeks and evaluated as to climacteric complaints, clinical aspects such as weight and blood pressure and lipid profile (total cholesterol, HDL-c, LDL-c, VLDL-c and triglycerides). Results: a significant improvement of climacteric complaints was demonstrated by a significant decrease in the Kupperman index (p<0.001) and the mean number of hot flushes (p<0.001) from the first month of treatment onwards. There was a significant decrease in total cholesterol, triglycerides and VLDL-c (p<0.001). The LDL-c levels presented a slight decrease (not significant). The HDL-c levels showed a significant decrease at week 24. However these levels returned to baseline levels at week 48. With regard to the vital signs no change in body weight and blood pressure was measured. The side effects were mild and temporary, vaginal bleeding, nausea and edema being the most common. Conclusion: tibolone may be considered a safe and efficient option to treat climacteric symptoms in postmenopausal women without significant impact on lipid profile.
Summary
Rev Bras Ginecol Obstet. 2000;22(1):37-41
DOI 10.1590/S0100-72032000000100007
Purpose: to evaluate the effects of tibolone on climacteric symptoms and clinical and metabolic variables. Methods: thirty-four postmenopausal women were treated orally with 2.5 mg tibolone daily for 48 weeks and evaluated as to climacteric complaints, clinical aspects such as weight and blood pressure and lipid profile (total cholesterol, HDL-c, LDL-c, VLDL-c and triglycerides). Results: a significant improvement of climacteric complaints was demonstrated by a significant decrease in the Kupperman index (p<0.001) and the mean number of hot flushes (p<0.001) from the first month of treatment onwards. There was a significant decrease in total cholesterol, triglycerides and VLDL-c (p<0.001). The LDL-c levels presented a slight decrease (not significant). The HDL-c levels showed a significant decrease at week 24. However these levels returned to baseline levels at week 48. With regard to the vital signs no change in body weight and blood pressure was measured. The side effects were mild and temporary, vaginal bleeding, nausea and edema being the most common. Conclusion: tibolone may be considered a safe and efficient option to treat climacteric symptoms in postmenopausal women without significant impact on lipid profile.
Summary
Rev Bras Ginecol Obstet. 2004;26(7):563-571
DOI 10.1590/S0100-72032004000700009
PURPOSE: to measure changes and predictors of changes in mammographic density of climacteric women, before and one year after hormone replacement therapy. METHODS: seventy climacteric women of 45 years or more participated in the study. They were followed-up at a Climacteric Outpatient Service. All of them used regularly either estrogenic or estroprogestative HRT for one year. They were submitted to one basal mammography and another at the end of the first year. HRT schedules could be different from each other, although with the same bioequivalence. Mammographic density was evaluated blindly at the beginning and at the end of the treatment. Age, ovarian function, time since menopause, body mass index, waist/hip ratio, age at menarche, age at first pregnancy, and smoking were evaluated as well. Mammographic density was classified according to the American College of Radiology BI-RADS system into one of the following four parenchymal patterns: A) entirely liposubstituted breasts, B) liposubstituted breasts with disperse glandular parenchyma, C) heterogeneously dense breasts, and D) extremely dense breasts. We proposed a subdivision of each category in to A e A1, B e B1, C and C1, D and D1 in order to identify smaller variations in mammographic density. Therefore, we attributed initial and final scores of 1-8 to each of the patients according to the mammographic density before and after HRT, corresponding to categories A to D1. The proportions of women that presented increase, decrease and no variation in mammographic density after 1 year of HRT were calculated. In addition, we estimated initial to final score variation using the paired t-test of the Statistical Package for Social Sciences (SPSS). RESULTS: mammographic density increased in 22.9%, decreased in 7.1% and did not change in 70% of the studied cases. A significant difference was observed between the score means before (2.2±1.82) and after HRT (2.5±1.9) (p=0.019). The androgenic distribution of body fat was associated with a denser mammographic pattern. CONCLUSIONS: an increase in mammographic density was shown in women undergoing HRT, and was most pronounced in women with androgenic fat distribution. Additional studies must be carried out in order to evaluate if this increment in mammographic density could impair the mammographic screening of breast cancer.
Summary
Rev Bras Ginecol Obstet. 2004;26(7):563-571
DOI 10.1590/S0100-72032004000700009
PURPOSE: to measure changes and predictors of changes in mammographic density of climacteric women, before and one year after hormone replacement therapy. METHODS: seventy climacteric women of 45 years or more participated in the study. They were followed-up at a Climacteric Outpatient Service. All of them used regularly either estrogenic or estroprogestative HRT for one year. They were submitted to one basal mammography and another at the end of the first year. HRT schedules could be different from each other, although with the same bioequivalence. Mammographic density was evaluated blindly at the beginning and at the end of the treatment. Age, ovarian function, time since menopause, body mass index, waist/hip ratio, age at menarche, age at first pregnancy, and smoking were evaluated as well. Mammographic density was classified according to the American College of Radiology BI-RADS system into one of the following four parenchymal patterns: A) entirely liposubstituted breasts, B) liposubstituted breasts with disperse glandular parenchyma, C) heterogeneously dense breasts, and D) extremely dense breasts. We proposed a subdivision of each category in to A e A1, B e B1, C and C1, D and D1 in order to identify smaller variations in mammographic density. Therefore, we attributed initial and final scores of 1-8 to each of the patients according to the mammographic density before and after HRT, corresponding to categories A to D1. The proportions of women that presented increase, decrease and no variation in mammographic density after 1 year of HRT were calculated. In addition, we estimated initial to final score variation using the paired t-test of the Statistical Package for Social Sciences (SPSS). RESULTS: mammographic density increased in 22.9%, decreased in 7.1% and did not change in 70% of the studied cases. A significant difference was observed between the score means before (2.2±1.82) and after HRT (2.5±1.9) (p=0.019). The androgenic distribution of body fat was associated with a denser mammographic pattern. CONCLUSIONS: an increase in mammographic density was shown in women undergoing HRT, and was most pronounced in women with androgenic fat distribution. Additional studies must be carried out in order to evaluate if this increment in mammographic density could impair the mammographic screening of breast cancer.
Summary
Rev Bras Ginecol Obstet. 2001;23(8):507-513
DOI 10.1590/S0100-72032001000800005
Purpose: to evaluate the effect of hormone replacement therapy on breast cell proliferation and on collagen and elastic fiber formation and to analyze the changes occurring in the breast parenchyma as a whole. Method: a total of 61 adult Wistar rats were divided into 5 groups. The standard group (12 rats) represented the normal hormonal ovarian status. The remaining 49 rats were oophorectomized and, starting on the 96th P.O. day, received the specific drug for 30 days. The CEE group received 50 mg/day conjugated equine estrogens (13 rats); the MPA group, 2.0 mg/day medroxyprogesterone acetate (12 rats); the CEE + MPA group, both drugs (12 rats), and the DW group, distilled water (12 rats). On the 31st day of medication, the animals were sacrificed and the inguinal mammary glands were removed for histological analysis. Cell proliferation was assessed at the ductal and acinar levels using anti-PCNA antibody. Mature collagen (type I) and immature collagen (type III) were quantified by Sirius-Red staining, and elastic fiber formation was quantified by Weigert staining. Anatomopathological analysis was performed by hematoxylin-eosin staining, with the determination of number of acini per terminal duct, number of ducts per field, presence of intraductal secretion, and intensity of intracytoplasmic vacuolization. Results: the CEE + MPA group presented a smaller percentage of proliferating ductal cells (46.1%) (p<0.0001) and a greater proliferation of acinar cells (66.3%), similar to those detected in the MPA group (p=0.075) but differing from those detected in the remaining groups (p<0.004). The CEE group showed the largest amount of immature collagen (33.6%) (p<0.01) and the MPA group showed the highest concentration of elastic fibers (11.7%) (p<0.0001). The CEE + MPA and MPA groups showed secretory acinar hyperplasia that was intense (91.7%) in the CEE + MPA group and mild (41.7%) or moderate (58.3%) in the MPA group, but differering in both cases from the remaining groups (p<0,097). Conclusions: conjugated equine estrogens in combination with medroxyprogesterone inhibit ductal cell proliferation and stimulate acinar cell proliferation causing secretory acinar hyperplasia; conjugated horse estrogens intensify the formation of immature (type III) collagen, and medroxyprogesterone acetate increases the formation of elastic fibers.
Summary
Rev Bras Ginecol Obstet. 2001;23(8):507-513
DOI 10.1590/S0100-72032001000800005
Purpose: to evaluate the effect of hormone replacement therapy on breast cell proliferation and on collagen and elastic fiber formation and to analyze the changes occurring in the breast parenchyma as a whole. Method: a total of 61 adult Wistar rats were divided into 5 groups. The standard group (12 rats) represented the normal hormonal ovarian status. The remaining 49 rats were oophorectomized and, starting on the 96th P.O. day, received the specific drug for 30 days. The CEE group received 50 mg/day conjugated equine estrogens (13 rats); the MPA group, 2.0 mg/day medroxyprogesterone acetate (12 rats); the CEE + MPA group, both drugs (12 rats), and the DW group, distilled water (12 rats). On the 31st day of medication, the animals were sacrificed and the inguinal mammary glands were removed for histological analysis. Cell proliferation was assessed at the ductal and acinar levels using anti-PCNA antibody. Mature collagen (type I) and immature collagen (type III) were quantified by Sirius-Red staining, and elastic fiber formation was quantified by Weigert staining. Anatomopathological analysis was performed by hematoxylin-eosin staining, with the determination of number of acini per terminal duct, number of ducts per field, presence of intraductal secretion, and intensity of intracytoplasmic vacuolization. Results: the CEE + MPA group presented a smaller percentage of proliferating ductal cells (46.1%) (p<0.0001) and a greater proliferation of acinar cells (66.3%), similar to those detected in the MPA group (p=0.075) but differing from those detected in the remaining groups (p<0.004). The CEE group showed the largest amount of immature collagen (33.6%) (p<0.01) and the MPA group showed the highest concentration of elastic fibers (11.7%) (p<0.0001). The CEE + MPA and MPA groups showed secretory acinar hyperplasia that was intense (91.7%) in the CEE + MPA group and mild (41.7%) or moderate (58.3%) in the MPA group, but differering in both cases from the remaining groups (p<0,097). Conclusions: conjugated equine estrogens in combination with medroxyprogesterone inhibit ductal cell proliferation and stimulate acinar cell proliferation causing secretory acinar hyperplasia; conjugated horse estrogens intensify the formation of immature (type III) collagen, and medroxyprogesterone acetate increases the formation of elastic fibers.
