CHANGES IN THE URINARY BLADDER MORPHOLOGY, MAST CELL POPULATION AND ESTROGEN RECEPTOR ALPHA EXPRESSION FOLLOWING OVARECTOMY AND CHRONIC ESTROGEN REPLACEMENT THERAPY IN ALBINO RATS

2013 ◽  
Vol 9 (1) ◽  
pp. 11-21
Author(s):  
L Lucan
Keyword(s):  
Estrogen Receptor ◽  
Mast Cell ◽  
Urinary Bladder ◽  
Replacement Therapy ◽  
Cell Population ◽  
Estrogen Replacement Therapy ◽  
Estrogen Receptor Alpha ◽  
Albino Rats ◽  
Estrogen Replacement ◽  
Mast Cell Population

Estrogen Replacement Therapy After Localized Breast Cancer: Clinical Outcome of 319 Women Followed Prospectively

1999 ◽  
Vol 17 (5) ◽  
pp. 1482-1482 ◽  
Author(s):  
Rena Vassilopoulou-Sellin ◽  
Lina Asmar ◽  
Gabriel N. Hortobagyi ◽  
Mary Jean Klein ◽  
Marsha McNeese ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Replacement Therapy ◽  
Median Time ◽  
Estrogen Replacement Therapy ◽  
Recurrent Breast Cancer ◽  
Estrogen Replacement ◽  
Previously Treated ◽  
Recurrent Breast ◽  
Trial Participants

PURPOSE: To determine whether estrogen replacement therapy (ERT) alters the development of new or recurrent breast cancer in women previously treated for localized breast cancer. PATIENTS AND METHODS: Potential participants (n = 319) in a trial of ERT after breast cancer were observed prospectively for at least 2 years whether they enrolled onto the randomized trial or not. Of 319 women, 39 were given estrogen and 280 were not given hormones. Tumor size, number of lymph nodes, estrogen receptors, menopausal status at diagnosis, and disease-free interval at the initiation of the observation period were comparable for the trial participants (n = 62) versus nonparticipants (n = 257) and for women on ERT (n = 39) versus controls (n = 280). Cancer events were ascertained for both groups. RESULTS: Patient and disease characteristics were comparable for the trial participants versus nonparticipants, as well as for the women on ERT versus the controls. One patient in the ERT group developed a new lobular estrogen receptor–positive breast cancer 72 months after the diagnosis of a ductal estrogen receptor–negative breast cancer and 27 months after initiation of ERT. In the control group, there were 20 cancer events: 14 patients developed new or recurrent breast cancer at a median time of 139.5 months after diagnosis and six patients developed other cancers at a median time of 122 months. CONCLUSION: ERT does not seem to increase breast cancer events in this subset of patients previously treated for localized breast cancer. Results of randomized trials are needed before any changes in current standards of care can be proposed.

The Effects of Transdermal Estradiol and Oral Conjugated Estrogens on Haemostasis Variables

1994 ◽  
Vol 71 (04) ◽  
pp. 420-423 ◽  
Author(s):  
Ulla-Beth Kroon ◽  
G Silfverstolpe ◽  
L Tengborn
Keyword(s):  
Replacement Therapy ◽  
Estrogen Replacement Therapy ◽  
Hormone Replacement ◽  
Plasminogen Activator Inhibitor ◽  
Estrogen Replacement ◽  
Transdermal Administration ◽  
Conjugated Estrogens ◽  
Transdermal Estradiol ◽  
Estrogen Administration ◽  
Activator Inhibitor

SummaryThe effects of oral and transdermal administration of estrogen replacement therapy (ERT) have been fairly well investigated regarding lipoprotein and carbohydrate metabolism, while the effects of different modes of estrogen administration on the haemostatic system have been less well studied.To delineate and compare the effects of perorally administered conjugated estrogens (CE) and transdermally administered estradiol (E2) in doses needed for hormone replacement therapy (HRT) on haemostasis parameters, 23 postmenopausal women were engaged in a study with an open cross-over design. The doses compared (0.625 mg CE and 50 μg E2/24h) are the lowest which, with few exceptions, eliminate climacteric symptoms. Both CE and E2 increased factor VII:C, factor VII:Ag, and the prothrombin fragment1+2. The increase in factor VII:Ag, however, was significantly higher after treatment with CE. These changes were all towards a state of hypercoagulability. Furthermore, CE decreased plasminogen activator inhibitor (PAI) and the thrombin-antithrombin complexes (TAT), as well as antithrombin (ATIII).

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