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Amnon Brzezinski

Publications and source records attributed to Amnon Brzezinski.

12 recordsLinked to original sources
PubMed2006

Duration not severity of the climacteric syndrome predicts resumption of hormone therapy after discontinuation: a prospective cohort study.

BACKGROUND: Predictive factors of women who are unable to quit prolonged hormonal therapy (HT) are largely unknown. We sought to identify predictors for the resumption of HT after the discontinuation of treatment. METHODS: A cohort prospective study was conducted allocating menopausal women treated with HT for over 3 years. Menopausal symptoms were monitored periodically after HT cessation by the Greene climacteric scale. RESULTS: Eighty-two women participated in the study. Age, the age of menopause, BMI, HT duration, the type of regimen, reasons cited to discontinue HT and the method of discontinuation did not differ between the subjects who successfully discontinued HT and those who failed to quit HT. Only the prevalence of vasomotor symptoms when HT was first prescribed significantly differed between the groups (P = 0.03). Comparable maximal Greene score was recorded in both groups. Over time, the subjects who returned to HT had higher Greene score [Hazard ratio 1.25, confidence interval (CI) 95% (1-1.07)] and significantly higher vasomotor score [Hazard score 1.22, CI 95% (1.02-1.46)]. CONCLUSIONS: The history of hot flashes and the duration of menopausal symptoms upon HT discontinuation predict the resumption of HT. Thus, the return to HT is expected in individuals who are intolerant of prolonged climacteric syndrome.

Aged↗
PubMed2005

Pharmacokinetics of a slow-release formulation of soybean isoflavones in healthy postmenopausal women.

Pharmacokinetic studies of soybean isoflavones have shown that following oral ingestion, the two major isoflavones, daidzin and genistin, are hydrolyzed in the intestine, rapidly absorbed into the peripheral circulation, and eliminated from the body with a terminal half-life of 7-8 h. These characteristics make maintenance of steady-state plasma isoflavone concentrations difficult to attain unless there is repeated daily ingestion of foods or supplements containing isoflavones. In an attempt to sustain more constant plasma isoflavone concentrations, a new slow-release formulation of a soybean isoflavone extract was prepared by microencapsulation with a mixture of hydroxypropylcellulose and ethylcellulose to alter its dissolution characteristics. In vitro experiments confirmed slow aqueous dissolution of isoflavones from this formulation when compared with the conventional isoflavone extract. The pharmacokinetics of this slow-release isoflavone extract was studied in 10 healthy postmenopausal women after oral administration of a single capsule containing the equivalent of 22.3 mg of genistein and 7.47 mg of daidzein expressed as aglycons. A comparison of the key pharmacokinetic parameters obtained in this study with those established in extensive studies performed previously in this laboratory indicated that the mean residence time of genistein and daidzein increased 2-fold with microencapsulation. These findings are indicative of a decreased rate of absorption, consistent with the observed slow in vitro dissolution rate. These findings show that it is feasible to employ polymer matrices that slow the aqueous dissolution for preparing sustained-release formulations of soy isoflavones. Further studies to optimize such formulations are warranted.

Chromatography, High Pressure Liquid↗
PubMed2005

Effects of exogenous melatonin on sleep: a meta-analysis.

Exogenous melatonin reportedly induces drowsiness and sleep, and may ameliorate sleep disturbances, including the nocturnal awakenings associated with old age. However, existing studies on the soporific efficacy of melatonin have been highly heterogeneous in regard to inclusion and exclusion criteria, measures to evaluate insomnia, doses of the medication, and routes of administration. We reviewed and analyzed (by meta-analysis) available information on effects of exogenous melatonin on sleep. A MEDLINE search (1980 to December 2003) provided English-language articles, supplemented by personal files maintained by the authors. The analysis used information derived from 17 different studies (involving 284 subjects) that satisfied inclusion criteria. Sleep onset latency, total sleep duration, and sleep efficiency were selected as the outcome measures. The study effect size was taken to be the difference between the response on placebo and the mean response on melatonin for each outcome measured. Melatonin treatment significantly reduced sleep onset latency by 4.0 min (95% CI 2.5, 5.4); increased sleep efficiency by 2.2% (95% CI 0.2, 4.2), and increased total sleep duration by 12.8 min (95% CI 2.9, 22.8). Since 15 of the 17 studies enrolled healthy subjects or people with no relevant medical condition other than insomnia, the analysis was also done including only these 15 studies. The sleep onset results were changed to 3.9 min (95% CI (2.5, 5.4)); sleep efficiency increased to 3.1% (95% CI (0.7, 5.5)); sleep duration increased to 13.7 min (95% CI (3.1, 24.3)).

Cross-Over Studies↗
PubMed2005

Does postmenopausal hormone replacement therapy affect intraocular pressure?

PURPOSE: To assess the effects of postmenopausal hormone replacement therapy (HRT) on intraocular pressure (IOP). PATIENTS AND METHODS: This was a cross-sectional controlled study, including 107 women aged 60 to 80 years receiving HRT and 107 controls who have never received HRT. All subjects underwent IOP assessment and funduscopic photography for cup-to-disc (C/D) ratios, and completed questionnaires regarding personal and family history of glaucoma, hormone replacement therapy, lifetime estrogen and progesterone exposure, and cardiovascular risk factors. Main Outcome Measures included IOP, prevalence of increased IOP, and C/D ratios. RESULTS: The groups did not differ in mean IOP (15.3 versus 15.3 mm Hg), mean vertical (0.18 versus 0.21) and horizontal (0.17 versus 0.14) C/D ratios, and in prevalence of increased IOP (15% versus 14%), C/D ratio (7% versus 7%), or glaucoma (9% versus 11%). A personal history of ischemic heart disease was the only risk factor associated with increased IOP (O.R. = 4.63, P = 0.003). Lifetime estrogen and progesterone exposure, including pregnancies, deliveries, menstruation years, and the use of oral contraceptives did not significantly affect the risk for increased IOP. CONCLUSION: Hormone replacement therapy and lifetime estrogen and progesterone exposure do not seem to affect IOP or the risk for increased IOP. A personal history of ischemic heart disease may be associated with a higher risk for this disorder.

Aged↗
PubMed2003

Weight control and the management of obesity after menopause: the role of physical activity.

BACKGROUND: Postmenopausal women have an increased tendency for gaining weight. The declines of endogenous estrogen, together with physical inactivity, are probably the major causes of this phenomenon. Postmenopausal overweight and obesity leads to increased rates of hypertension, diabetes mellitus, coronary artery disease, and all cause mortality. Additional consequences may include hormone-dependent cancer, gallstones, nephrolithiasis, and osteoarthritis. Weight loss can reverse many of these complications, reduce the number and dosages of medications used, and improve longevity. This difficult task requires lifestyle modification. OBJECTIVES: To review the current information about the effects of physical activity on postmenopausal weight gain and its consequences and to provide basic strategies to treat obesity during the menopause transition. METHODS: A Medline search together with a manual search of selected articles. CONCLUSION: Several options for weight loss are available, yet lifestyle modification is essential in managing postmenopausal obesity and overweight. While this demands dietary and behavioral changes, a major element of this modification is regular physical activity, which reduces obesity-related morbidity and mortality. The amendment to a healthier lifestyle is achievable at the postmenopausal years. All medical personnel should advocate against overweight and obesity and provide tools for their management.

Female↗
PubMed2002

IUD use and the risk of endometrial cancer.

OBJECTIVE: Although the intrauterine device (IUD) is one of the most widely used forms of contraception throughout the world, its potential long-term effects on the uterus have not been thoroughly evaluated. This paper reports the long-term results of IUD use on the incidence of endometrial cancer. STUDY DESIGN: The data is part of a nationwide case-control, pilot study that was undertaken in order to evaluate the possible influence of ovulation induction drugs on the risk of endometrial cancer. The study included 128 living women 35-64 years old, with a histologically confirmed diagnosis of endometrial carcinoma. The controls were 255 women from the same dialing areas selected by random digit dialing. A multivariate logistic model, controlling for age, was used to assess the independent effects of factors found to be significantly associated with endometrial cancer on univariate analysis. RESULTS: The following parameters were found to be independently associated with endometrial cancer controlling for age: nulliparity OR=2.7 (95% CI 1.1-6.5, P=0.03); history of infertility OR=1.8 (95% CI 1.0-3.3, P=0.05); BMI>/=27 OR=2.3 (95% CI 1.4-3.8, P=0.001). The use of oral contraceptives and IUD were found to be protective; OR=0.29 and 0.37, respectively, (95% CI 0.14-0.61, P=0.001, 0.19-0.70, and 0.003, respectively). CONCLUSIONS: IUD use may have a protective effect on endometrial cancer risk. The protective effect of IUD may be either, through the intense inflammatory response that leads to other lisosomal and inflammatory actions, which may include cells responsible for early elimination of hyperplastic endometrial epithelial cells or, the more complete shedding of the endometrium associated with IUD use may decrease hyperplasia of the endometrium, a known risk factor for endometrial carcinoma.

Adult↗
PubMed2002

Synergistic inhibitory effects of genistein and tamoxifen on human dysplastic and malignant epithelial breast cells in vitro.

OBJECTIVE: Genistein is a phytoestrogen with in vitro anticancerogenic activity. We examined in vitro the effects of genistein alone, or in combination with estradiol and tamoxifen, on the growth of human dysplastic and malignant epithelial breast cell lines. METHODS: Dysplastic breast cell lines (MCF-10A(1), MCF-ANeoT, MCF-T(6)3B) and cell lines of breast cancer (MCF-7, MDA-231, MDA-435) were cultured as monolayers in RPMI 1640 medium supplemented with 10% fetal bovine serum, and L-glutamine. After preincubation of 20 h, genistein (1, 2.5, 5, 7.5 and 10 microg/ml) alone or in combination with estrogen or tamoxifen was added to the cultured cells. The cells were treated continuously for 72 h and then the growth rate was assessed colorimetrically. Stepwise multiple linear regression analysis was used to evaluate the effect of genistein, tamoxifen, and estradiol on cell proliferation. RESULTS: Genistein had a significant (dose-dependent) inhibitory effect on the proliferation of both dysplastic (P<0.0001) and malignant (P<0.0001) cells. The growth inhibition was significantly higher P<0.0001 in dysplastic cells compared to the cancer cells. Addition of tamoxifen to genistein further inhibited the proliferation of both cell types, reflecting a synergistic antiproliferative effect on dysplastic cells P<0.0001 and an additive growth inhibition effect P<0.0003 on malignant cells. Estradiol significantly (P=0.005) stimulated the growth of dysplastic cell lines while a significant (P=0.003) antiproliferative effect on growth of the malignant cells was observed. The concentration of estrogen receptor (ER) had no significant effect on growth rates and did not modulate the effects of genistein or tamoxifen. CONCLUSIONS: Genistein (1-10 microg/ml) inhibits the growth of dysplastic and malignant epithelial breast cancer cells in vitro and the addition of tamoxifen (10(-6), 10(-7)M) has a synergistic/additive inhibitory effect. These effects are not modulated by the presence of ER.

Antineoplastic Agents, Hormonal↗
PubMed2002

Hormonal manipulations and breast cancer.

UNLABELLED: Breast cancer is the most common cancer among women and the leading cause of death in women, 40 to 55 years of age. The lifetime odds of developing breast cancer are apparently up to 1 in 8 women in North America and 1 in 12 in Western Europe. According to the American Cancer Society, some 200,000 women (and 1,500 men) will be diagnosed with breast cancer this year. Although the incidence of breast cancer in women has been rising since the mid-1940s, the mortality has dropped modestly over the past decade, probably due to earlier and improved diagnosis and treatment. Evidence from both epidemiological and experimental studies points to an important role of reproductive variables in the development and promotion of human breast neoplasia. Hormonal manipulations, in the form of contraceptives, hormone replacement therapy, or antiestrogens, affect the incidence and course of breast cancer and may be useful in prevention and treatment of the tumor. In this review we summarize the current status of the use of hormones and antihormones in regard to breast cancer and outline possible areas of additional development and investigation. TARGET AUDIENCE: Obstetricians and Gynecologists, Family Physicians. LEARNING OBJECTIVES: After completion of this article, the reader will be able to summarize the effects of estrogen and progestogens on the breast and to list the effects of other hormonal modulators on the breast.

Antineoplastic Agents↗
PubMedDate not supplied

The effect of hormone therapy on the risk for age-related maculopathy in postmenopausal women.

OBJECTIVE: To evaluate the effect of postmenopausal hormone therapy (HT) as well as the use of oral contraceptives and lifetime endogenous hormone exposure on the risk for age-related maculopathy (ARM) in postmenopausal women. DESIGN: This was a cross-sectional, controlled study. A total of 102 women from 60 to 80 years of age who were receiving HT and 100 controls underwent a detailed clinical funduscopic evaluation and stereoscopic fundus photography for the presence and grading of ARM. All participants completed a standardized questionnaire regarding vascular risk factors, HT, and lifetime exogenous and endogenous estrogen and progesterone exposure. Statistical analysis was performed using Student's t test, chi2 test, and a multivariate logistic regression model. RESULTS: The HT and the non-HT groups did not differ in terms of early (11% v 15%), late (6% v 6%), or wet (2% v 2%) ARM prevalence rates. Women with ARM were significantly older than controls (69 v 66 years; P = 0.001, 95% CI = 0.008 - 0.027) and were more likely to have ischemic heart disease (21% v 9%; OR = 2.86, P = 0.03, 95% CI = 0.020 - 0.360). Lifetime exogenous and endogenous hormone exposures and other cardiovascular risk factors were not significantly different among women with ARM as compared with controls. CONCLUSION: Postmenopausal HT may not affect the risk for either early or late ARM in women aged 60 to 80 years. The risk for both entities is not necessarily affected by either exogenous or endogenous lifetime hormone exposure. A history of ischemic heart disease may be associated with an increased risk for ARM.

Age Factors↗
PubMedDate not supplied

Gradual discontinuation of hormone therapy does not prevent the reappearance of climacteric symptoms: a randomized prospective study.

OBJECTIVE: To investigate the recurrence and severity of climacteric symptoms after two methods of discontinuation of prolonged hormone therapy. DESIGN: Postmenopausal women treated with hormone therapy for more than 3 years and opting to discontinue therapy were randomly assigned to two treatment groups. Hormone therapy was discontinued either abruptly (group 1) or gradually (group 2). Symptoms in both groups were monitored with the Greene climacteric scale at 1, 3, 6, 9, and 12 months. RESULTS: Ninety-one women aged 48 to 73 years (mean age 56.8 +/- 4.2 years) participated in the study. The mean therapy duration was 8.8 +/- 3.8 years. No differences were noted between the two groups regarding age at menopause, body mass index, reasons to start therapy, hormone therapy duration, type of regimen, and reasons cited for hormone treatment discontinuation. After cessation of therapy, a similar percentage of patients in each group resumed hormone therapy. Climacteric syndromes, specifically vasomotor dysfunction, were more severe in group 1 than in group 2 during the first 3 months after hormone therapy withdrawal. However, by 6 months vasomotor symptoms were worse in group 2. By 9 to 12 months, no difference was noted between groups. No differences were observed in the percentage of weight gain, vaginal bleeding, and atrophy after discontinuation of therapy by either method. CONCLUSIONS: Our specific regimen of gradual discontinuation of hormone therapy merely postponed, and neither prevented nor minimized, the reappearance of vasomotor symptoms, mood deterioration, and sexual dysfunction, and the resulting discomfort.

Aged↗