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At least 19 recordsLinked to original sources
PubMed1998

Can climacteric women self-adjust therapeutic estrogen doses using symptoms as markers?

OBJECTIVES: To investigate if disappearance of climacteric symptoms during hormone replacement therapy (HRT) also means good therapeutic level of serum estradiol. The study group comprised of 32 postmenopausal women who had frequent climacteric symptoms. METHODS: The women increased the daily treatment doses of percutaneous estradiol every 2 weeks until they felt comfortable with it. Each woman continued at that treatment dose for up to 3 months. Blood samples for estradiol assay were drawn at baseline, every time before the estradiol dosage was increased and at the end of the study. Climacteric symptoms were scored according to the Kupperman menopausal index. RESULTS: Despite the relief of climacteric symptoms, serum estradiol concentration was at a menopausal level (< 50 pg/ml) in 22% of the women. In all, 45% of the subjects showed serum estradiol remaining under 60 pg/ml, 29% of the women showed levels of 60-100 pg/ml and 26% showed serum estradiol concentration more than 100 pg/ml. CONCLUSIONS: The disappearance of climacteric symptoms during HRT does not guarantee that estrogen levels are sufficiently high for obtaining long term benefits of HRT.

Administration, Cutaneous↗
PubMed1993

Inhibition of myelopoiesis by conditioned medium from cultured canine thymic cells exposed to estrogen.

Therapeutic doses of estrogens can cause fatal bone marrow damage in dogs, which are more sensitive than other species to these myelotoxic effects. Investigations with mice indicated that estrogens did not directly damage the bone marrow progenitor cells, but that the thymus responded to estrogen by producing a factor that inhibited bone marrow granulocyte-macrophage progenitor cell replication. A similar estrogen-induced myelopoiesis-inhibitory factor was produced by canine thymic cells in culture. This canine factor was more inhibitory to myelopoiesis than was the murine factor. Canine bone marrow progenitor cell growth was not significantly inhibited by direct estrogen treatment, which supported evidence for indirect thymus mediation of estrogen toxicity in vivo. Estrogen receptors were detected in canine nonlymphoid thymic cells by use of immunocytochemical staining. These findings indicate that the high estrogen sensitivity of dogs may relate to greater estrogen-induced myelopoiesis-inhibition by the thymus.

Animals↗
PubMed1987

[Effects of estrogen and endocrine therapeutic agents on the estrogen receptor, progesterone receptor and DNA synthesis in MCF-7 human breast cancer cells using the whole cell uptake method].

In order to investigate the mechanisms of the endocrine therapeutic agents and the applicability of combined endocrine therapies for breast cancers, we studied the effects of estrogen and the endocrine therapeutic agents on estrogen receptor (ER), progesterone receptor (PgR), and DNA synthesis in MCF-7 human breast cancer cells, which is known to be sensitive to estrogen. ER and PgR of MCF-7 cells were determined by whole cell uptake method. In brief, intact MCF-7 cells cultured in the multi-well plates were incubated with various concentrations of tritiated estradiol (E2) or promegestone (R5020) at 37 degrees C for 1 hour. The characteristics of the hormone binding were analyzed by Scatchard plots. MCF-7 cells had single class of ER (Kd: 2.1 +/- 0.2 X 10(-10) M, MBC: 9.0 +/- 1.5 X 10(3) sites/cell) and PgR (Kd: 7.2 +/- 1.1 X 10(-10) M, MBC: 3.1 +/- 0.5 X 10(4) sites/cell). When cultured in the presence of 10(-8) M or 10(-6) M of E2, tamoxifen (TAM), R5020 or medroxyprogesterone acetate (MPA) for 48 hrs, the numbers of binding sites of ER and PgR altered, but the affinities of either of them did not change. E2(10(-8) or 10(-6) M) increased about twice the number of PgR. Although treatment of 10(-8) M TAM, a non-steroidal antiestrogen, slightly increased the number of PgR, 10(-6) M TAM significantly decreased the number of PgR. Both of R5020 (10(-8) or 10(-6) M) and MPA (10(-8) or 10(-6) M), synthetic progestins, decreased the number of ER dose-dependently. On the other hand, E2 (10(-8) and 10(-6) M) and R5020 (10(-8) M) enhanced DNA synthesis, but 10(-6) M TAM or MPA inhibited DNA synthesis. The effects of single, sequential and coincidental treatment of these agents were compared. The sequential treatment of 10(-8) M E2 for 36 hrs and followed 10(-6) M MPA for 36 hrs ("10(-8) M E2----10(-6) M MPA") and "10(-6) M TAM----10(-6) M MPA" inhibited DNA synthesis of MCF-7 cells more efficiently than 10(-6) M TAM alone or 10(-6) M MPA alone for 72 hrs. However, "10(-6) M MPA----10(-6) M TAM" inhibited DNA synthesis less than "10(-6) M TAM----10(-6) M MPA".(ABSTRACT TRUNCATED AT 400 WORDS)

Breast Neoplasms↗
PubMed1980

The effects of exogenous estrogen replacement therapy of the breast: breast cancer risk and mammographic parenchymal patterns.

A retrospective pilot study was implemented to better define the potential carcinogenic role of conjugated equine estrogen (Premarin) on the breast, and the influence of these hormone analogues on proliferative and atrophic breast parenchyma as determined by high-quality serial xeromammograms. Four hundred and five postmenopausal (spontaneous and surgical) women (mean age 59.7 years) were group matched for the risk factors of age and parity. The dominant parenchymal pattern (N1P1P2DY) as disclosed mammographically was determined for each patient, who was then categorized into one of four groups: Group 1 Asymptomatic-no hormones, 124 patients; Group 2 Symptomatic-no hormones, 75 patients; Group 3 Asymptomatic-hormones; 152 patients; and Group 4 Symptomatic-hormones, 54 patients. Patients in Groups 3 and 4 were treated with therapeutic estrogens a minimum of 18 months (mean 79 months) and follow-up ranged from 39-344 months. In the entire series, 25 carcinomas (6.2%) were detected. In Group 3, five carcinomas (2.4%) were detected, but two cancers (1.0%) were found in symptomatic estrogen users. The occurrence of carcinoma in Group 2 was greater than the remaining categories; however, cancer risk was not statistically greater in any category with regard to hormone replacement therapy. Patients treated with therapeutic estrogens were observed to have an increase of 8.9% in the frequency of a more glandular (P2,DY) mammographic parenchymal pattern and this was noted to be within the range of interpretation error of the mammographer. This suggests a physiologic effect of therapeutic estrogens on atrophic breast parenchyma with conversion to a glandular, proliferative state. This study suggests that long-term replacement estrogen therapy for postmenopausal symptoms does not significantly alter mammographic parenchymal patterns and that the use of these compounds in therapeutic doses does not increase the risk of breast cancer.

Adult↗
PubMed2005

Coregulators in nuclear estrogen receptor action: from concept to therapeutic targeting.

Estrogens are key regulators of growth, differentiation, and the physiological functions of a wide range of target tissues, including the male and female reproductive tracts, breast, and skeletal, nervous, cardiovascular, digestive and immune systems. The majority of these biological activities of estrogens are mediated through two genetically distinct receptors, ERalpha and ERbeta, which function as hormone-inducible transcription factors. Over the past decade, it has become increasingly clear that the recruitment of coregulatory proteins to ERs is required for ER-mediated transcriptional and biological activities. These "coactivator" complexes enable the ERs to respond appropriately: 1) to hormones or pharmacological ligands, 2) interpret extra- and intra-cellular signals, 3) catalyze the process of chromatin condensation and 4) to communicate with the general transcription apparatus at target gene promoters. In addition to activating proteins, the existence of corepressors, proteins that function as negative regulators of ER activity in either physiological or pharmacological contexts, provides an additional level of complexity in ER action. This review also describes current efforts aimed at developing pharmaceutical agents that target ER-cofactor interactions as therapeutics for estrogen-associated pathologies.

Amino Acid Motifs↗
PubMed1999

Early postmenopausal bone loss is prevented by estrogen and partially by 1alpha-OH-vitamin D3: therapeutic effects of estrogen and/or 1alpha-OH-vitamin D3.

A total of 79 Japanese women who were within 5 years of menopause were randomly assigned 1alpha-hydroxyvitamin D3 [1alpha(OH)D3] 1.0 microg/day, conjugated estrogens 0.625 mg/day, a combination of both, or control (no treatment). Lumbar spine and proximal femur bone mineral density (BMD) and biochemical indices were monitored over 2 years. In the 1alpha(OH)D3-treated group, there was a nonsignificant decrease in lumbar spine BMD compared with controls, and no significant loss in the femoral neck compared with controls. In the estrogen-treated group, there was a nonsignificant increase in spine BMD (+2.17% in the first year and +1.71% in the second year), and no loss in femoral neck BMD. The combination of conjugated estrogens +1alpha(OH)D3 was more effective in increasing BMD in the spine (+3. 68% in the first year and +3.63% in the second year) and femur (+2. 56% in the first year and +4.44% in the second year) BMD. There was a significant difference in lumbar spine BMD in both the first and second years between the combination-treated group and the 1alpha(OH)D3-treated and control groups (P < 0.01). Serum osteocalcin (OC) significantly decreased in the combination-treated group (-23.8% in the first year) and the estrogen-treated group (-37. 6% and -41.2% at 6 and 18 months, respectively), and serum alkaline phosphatase (Alp) decreased significantly in the first year in the combination-treated (-31.5%), estrogen-treated (-27.3%), and 1alpha(OH)D3-treated (-7.9%) groups, whereas serum OC increased (+45. 4% in the first year) in women without treatment. The results of this study indicate that early postmenopausal bone loss in the femoral neck is prevented by conjugated estrogens, 1alpha(OH)D3, or both, whereas bone loss in the spine is not prevented by 1alpha(OH)D3. Estrogen proves effective in preventing early postmenopausal bone loss by markedly inhibiting bone turnover. Moreover, a synergistic bone-sparing effect can be expected when estrogen is administered concomitantly with 1alpha(OH)D3 rather than when used alone.

Adult↗