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PubMed2004

Idiopathic osteoporosis in premenopausal women.

Although osteoporosis predominantly affects older postmenopausal women, low bone mineral density also occurs in men and younger women. In men, it is often unexplained by recognized secondary causes. These men with idiopathic osteoporosis have reductions in serum IGF-I as well as indices of reduced bone formation. Younger women also experience bone loss of unknown etiology (IOP). Whether premenopausal women with IOP have similar decreases in IGF-I levels and reduced indices of bone formation is unknown. We prospectively evaluated a group of premenopausal women with unexplained low bone mass and compared them to normal premenopausal women with respect to serum concentrations of IGF-I. Thirteen premenopausal women (34.2+/-2.3 years) with low bone density (mean lumbar spine T-score -2.26+/-0.20) were compared with 13 premenopausal women (35.7+/-1.7 years) with normal bone density of similar age, height and ethnic composition. Body mass index (BMI) was lower in subjects than controls (20.5+/-0.7 versus 25.2+/-1.1 kg/m(2), P<0.01). A family history of osteoporosis and a history of fragility fractures were found more frequently in subjects than controls (P< or =0.05). Calciotropic hormones did not differ between the two groups. In contrast to our observations in men with idiopathic osteoporosis, mean serum IGF-I concentrations did not differ between subjects and controls (subjects: 22.5+/-2.2 nmol/l versus controls: 20.8+/-1.6 nmol/l; NS). Moreover, serum IGF-I levels did not correlate significantly with serum estradiol or with BMD at either the lumbar spine or femoral neck. However, lower follicular phase serum estradiol levels among non-oral contraceptive users were found in subjects as compared to controls (subjects: 124.1+/-13 pmol/l versus controls 194.9+/-24 pmol/l, P=0.06). Calculated free, bioavailable estradiol levels were significantly lower overall in subjects than controls (0.6+/-0.1 versus 1.2+/-0.2 pmol/l, P<0.05). Total serum estradiol levels correlated with BMD at the femoral neck (r=+0.50; P<0.05). Free, bioavailable estradiol correlated with BMD and BMAD at the lumbar spine (r=+0.54, P<0.01 and r=+0.54, P<0.05, respectively) and femoral neck (r=+0.60 and r=+0.55 respectively, both P<0.01). Urinary NTX excretion, although within the normal premenopausal range, was 45% higher in subjects than controls (41.6+/-5.9 nmol BCE/l versus 28.3+/-2.4 nmol BCE/l; P<0.05). Bone-specific alkaline phosphatase activity was also higher (17.4+/-1.6 ng/ml versus 14.7+/-0.8 ng/ml), although the difference was not statistically significant. These results suggest differences in the pathogenesis of idiopathic osteoporosis in women as compared to men with IOP.

Adult↗
PubMed2003

[Acute myocardial infarction in premenopausal women].

UNLABELLED: Prospective, systematic studies of the pathophysiology and prognosis of premenopausal women vs young men who suffer an acute myocardial infarction (MI) and are treated with direct angioplasty are scarce. METHODS AND RESULTS: A total of 782 consecutive and unselected patients who presented with an acute ST-elevation MI within 12 h of symptom onset underwent immediate angiography to guide direct angioplasty. Using this therapeutic approach clinical characteristics, angiographic observations, and short- and long-term prognosis were analyzed in a sub-group of 31 premenopausal women and compared to 192 young men with acute MI. Premenopausal women account for 4% of individuals with acute MI and for 15% (31/205) of all women. Men of the same age range make up 25% (192/782) of all MI patients (p<0.001). Three or more classic risk factors were present in 20/31 women. Young women presented later than men. Angiography demonstrated a coronary occlusion in 27/31 women (88%) but in 98% of young men (p<0.02). Direct PTCA was successful in all premenopausal women and in 179/185 men (97%, p=ns). Predischarge EF was 57% in women and 54% in men (p=ns). After 4 years of follow-up, all women had survived as compared to a 95% survival in young men. Major cardiac events had occurred in 50% of persons of either gender. CONCLUSION: Premenopausal women account for 4% of individuals and for 1/6 of all female patients who presented with acute MI within 12 h of onset. Hospital admittance is delayed in young women. MI was caused by (atherosclerotic) coronary occlusion in most young women and in virtually all young men. Short- and long-term survival of premenopausal women is favorable after direct PTCA for acute MI and not different than men from the same age group.

Adult↗
PubMed2001

Disease activity during the premenopausal and postmenopausal periods in women with systemic lupus erythematosus.

PURPOSE: Cyclophosphamide-induced ovarian failure has been reported to be protective against flares of systemic lupus erythematosus (SLE). We studied whether patients with SLE experience a decrease in disease activity after natural menopause. SUBJECTS AND METHODS: We studied 30 SLE patients with natural menopause who had been observed at least 2 years before and after menopause and who did not receive hormone replacement therapy or danazol. Menopause was defined as the date of the last self-reported menstrual period. Disease activity was assessed retrospectively by medical chart review using standard measures (the SLE disease activity index) during the immediate premenopausal and postmenopausal periods, and 2 (n = 30 patients), 3 (n = 19), and 4 (n = 13) years before and after menopause. We also compared the use of health services and medications. RESULTS: Patients were studied for a mean (+/- SD) of 6.4 +/- 1.7 years (premenopausal, 3.3 +/- 0.9 years; postmenopausal, 3.2 +/- 0.9 years). During the premenopausal periods, the mean disease activity score was 2.3 +/- 2.3 (range, 0 to 9 on a 0 to 105 scale), compared with 2.3 +/- 2.9 (range, 0 to 12; P = 0.37) after menopause. The maximum disease activity score was somewhat greater in the premenopausal period (7.9 +/- 6.0 [range, 0 to 22] vs. 5.8 +/- 5.1 [range, 0 to 22]; P = 0.04). The incidence rates of flares (0.56 per year vs. 0.43 per year, P = 0.20) and severe flares (0.17 per year vs. 0.12 per year, P = 0.33) were similar in the premenopausal and postmenopausal periods. Differences in disease activity scores (mean and maximum) and the number of visits to a rheumatologist's office were only significant when the fourth year before menopause was compared with the fourth year after menopause. CONCLUSIONS: Disease activity is mild during the premenopausal and postmenopausal periods in women with SLE. A modest decrease, especially in the maximum disease activity, is seen after natural menopause.

Anti-Inflammatory Agents↗
PubMed2003

Expression of estrogen receptor alpha and beta in myometrium of premenopausal and postmenopausal women.

Although a clear role for estrogen receptor (ER) alpha has been established, the contribution of ERbeta in estrogen-dependent development, growth and functions of the myometrium is not understood. As a first step towards understanding the role of ERbeta, we have examined the expression of ERalpha and ERbeta in the human myometrium. With competitive RT-PCR assays, the level of ERbeta mRNA was 10-200 times lower than that of ERalpha mRNA in both premenopausal and postmenopausal myometrium. In premenopausal myometrium, the expression pattern of ERbeta mRNA during the menstrual cycle was similar to that of ERalpha mRNA, with highest levels in peri-ovulatory phase. In postmenopausal myometrium, ERbeta mRNA was significantly higher than it was in premenopausal myometrium, while the level of ERalpha mRNA was lower. The net result was a change in the ratio of ERbeta to ERalpha mRNA expression. The ratio changed from 0.6-1.5 in premenopausal to 2.5-7.6 in postmenopausal myometrium. In premenopausal women, the gonadotropin releasing hormone analogue, leuprorelin acetate, elicited a decrease in ERalpha and an increase in ERbeta mRNA expression to cause a postmenopausal receptor phenotype. Estradiol, on the other hand, reversed ERalpha and ERbeta mRNA expression and their ratio in postmenopausal myometrium to those of premenopausal myometrium. Immunohistochemical staining and Western blot analysis of ERalpha and ERbeta with semiquantitative analysis showed good agreement between mRNA and protein levels. The data indicate that coordinated expression of ERalpha and ERbeta might be necessary for normal estrogen action in myometrium. Furthermore, estrogen appears a dominant regulator of both receptors in the myometrium.

Adult↗
PubMed2003

Hypoestrogenemia of hypothalamic origin and coronary artery disease in premenopausal women: a report from the NHLBI-sponsored WISE study.

OBJECTIVES: We sought to evaluate hypoestrogenemia of hypothalamic origin and its association with angiographic coronary artery disease (CAD) in premenopausal women. BACKGROUND: Coronary artery disease in premenopausal women appears to have a particularly poor prognosis. Primate animal data suggest that premenopausal CAD is strongly determined by psychosocial stress-induced central disruption of ovulatory cycling and resulting hypoestrogenemia. METHODS: We assessed reproductive hormone blood levels and angiographic CAD using core laboratories in 95 premenopausal women with coronary risk factors who were enrolled in the National Heart, Lung, and Blood Institute-sponsored Women's Ischemia Syndrome Evaluation and were undergoing coronary angiography for evaluation for suspected ischemia. RESULTS: Premenopausal women with angiographic CAD (n = 13) had significantly lower estradiol, bioavailable estradiol, and follicle-stimulating hormone (FSH) (all p < 0.05) than women without angiographic CAD (n = 82), even after controlling for age. Hypoestrogenemia of hypothalamic origin, defined as estradiol <184 pmol/l (50 pg/ml), FSH <10 IU/l, and luteinizing hormone <10 IU/l, was significantly more prevalent among the women with CAD than those without CAD (9/13 [69%] vs. 24/82 [29%], respectively, p = 0.01). Hypoestrogenemia of hypothalamic origin was the most powerful predictor of angiographic CAD in a multivariate model (odds ratio [OR] 7.4 [confidence interval (CI) 1.7 to 33.3], p = 0.008). Anxiolytic/sedative/hypnotic and antidepressant medication use were independent predictors of hypoestrogenemia of hypothalamic origin in a multivariate model (OR 4.6 [CI 1.3 to 15.7], p = 0.02, OR 0.10 [CI 0.01 to 0.92], p = 0.04, respectively). CONCLUSIONS: Among premenopausal women undergoing coronary angiography for suspected myocardial ischemia, disruption of ovulatory cycling characterized by hypoestrogenemia of hypothalamic origin appears to be associated with angiographic CAD.

Adult↗
PubMed2000

Variation of lipids and lipoproteins in premenopausal women compared with men and postmenopausal women. DELTA (Dietary Effects on Lipoproteins and Thrombogenic Activity) Investigators.

Numerous studies have reported cyclic fluctuations in lipids and lipoproteins as a function of the phase of the menstrual cycle. However, the reported patterns are quite variable and have led to an unclear picture of the influence of the menstrual cycle on the variability of lipids, and hence of the role of the menstrual cycle phase in the interpretation of serum lipids for premenopausal women. As part of the DELTA Study (Dietary Effects on Lipoproteins and Thrombogenic Activity), we evaluated the cyclic variation of circulating lipids and lipoproteins in 39 premenopausal women and compared intraindividual variances in these women, 18 postmenopausal women, and 46 men under conditions of tight dietary control. Cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, triglyceride, apolipoproteins A-1 (apo A-1) and B-100 (apo B-100), and lipoprotein (a) [Lp(a)] all demonstrated cycling in the premenopausal women. However, the observed cycling accounts for only a small fraction of the total biologic variability of lipids in premenopausal women. The magnitude of total intraindividual variability based on coefficient of variation (CV) for these lipids in premenopausal women (CV, 4% to 8.1%) was similar to that found for men (CV, 4.3% to 9.1%) and for postmenopausal women (CV, 3.7% to 6.7%). These results suggest that protocols for screening and monitoring of serum lipids in premenopausal women need not differ from those used for men or postmenopausal women.

Adult↗
PubMed2006

Plasma enterolactone and genistein and the risk of premenopausal breast cancer.

BACKGROUND: The scientific debate on the role of dietary phytoestrogens for prevention of breast cancer is still ongoing. We previously reported an inverse association between dietary phytoestrogen intake and premenopausal breast cancer risk and now examine the relationship with plasma phytoestrogen concentrations. METHODS: We measured enterolactone (mammalian lignan) and genistein (isoflavone) concentrations in plasma samples of 220 premenopausal cases and 237 age-matched controls from a population-based case-control study in Germany. RESULTS: Median plasma enterolactone concentrations in cases and controls were 6.3 and 9.7 nmol/l, respectively, and median genistein concentrations were 4.5 and 3.7 nmol/l, respectively. Premenopausal breast cancer risk decreased with increasing plasma enterolactone concentrations. Adjusted odds ratios (95% confidence intervals) were 0.42 (0.20-0.90) and 0.38 (0.17-0.85) (P for trend 0.007) for women in the third and fourth quartile of plasma enterolactone compared to those in the lowest quartile. There was no significant association between plasma genistein concentration and premenopausal breast cancer risk. CONCLUSION: Using biomarkers of phytoestrogen intake, we confirmed the strong inverse association between enterolactone and premenopausal breast cancer risk as found with dietary intake estimates. This result gives support to the potential role of mammalian lignans for breast cancer prevention among premenopausal women in Western populations.

4-Butyrolactone↗
PubMed2006

The insulin-like growth factor system and mammographic features in premenopausal and postmenopausal women.

High levels of circulating insulin-like growth factor-I (IGF-I) and its major binding protein (IGFBP-3) at premenopausal ages have been associated with an increased breast cancer risk. We conducted a cross-sectional study (215 premenopausal women and 241 after natural menopause) nested within the Guernsey prospective studies to examine the relationship between the IGF system and mammographic features of the breast. The mammographically dense area in the breast increased with increasing serum levels of IGF-I (P for linear trend, P(t) = 0.05), IGF-II (P(t) = 0.08), and IGFBP-3 (P(t) = 0.01) only in premenopausal women. IGF-II and IGFBP-3 serum levels were associated with increases in the mammographically lucent area in both premenopausal (P(t) = 0.01 and 0.04, respectively) and postmenopausal women (P(t) < 0.001 for both), but these associations were no longer statistically significant after adjustment for body mass index and waist circumference. Neither the IGF-I/IGFBP-3 nor the IGF-II/IGFBP-3 molar ratio was associated with any of these mammographic features. The number of A alleles at a polymorphic locus in the promoter region of the IGFBP-3 gene was associated with increasing mean IGFBP-3 levels in both premenopausal (P(t) = 0.01) and postmenopausal (P(t) <0.001) women but not with mammographically dense area. These results support the hypothesis that the IGF system may affect the amount of mammographically dense tissue in premenopausal women, possibly by promoting cell proliferation and inhibiting apoptosis in the fibroglandular tissue. The findings also show strong relations between IGF-II and IGFBP-3 levels and the amount of mammographically lucent tissue, reflecting the associations between body adiposity and amount of fat tissue in the breast and between body adiposity and circulating levels of these growth factors.

Adult↗
PubMed1998

Carotid atherosclerosis in premenopausal and postmenopausal women and its association with risk factors measured after menopause.

BACKGROUND AND PURPOSE: In women, symptoms of coronary artery disease are delayed by 10 to 15 years in comparison with men, most likely because of the protective effect of ovarian hormones. This report compares the prevalence and degree of carotid atherosclerosis between 292 premenopausal women and 294 women at 5 to 8 years after menopause. METHODS: Scans were performed in the same laboratory over the same time period for both groups. Intima-media thickness (IMT) was averaged across the common, bulb, and internal carotids. The plaque index summarized degree of focal plaque based on the size and number of plaques throughout both carotid systems. RESULTS: Mean IMT was 0.69 mm for premenopausal women and 0.77 mm for postmenopausal women (P < 0.001). Prevalence of plaque was 25% among premenopausal women and 54% among postmenopausal women (P < 0.001). In both premenopausal and postmenopausal women, risk factors measured before menopause were associated with carotid atherosclerosis. Premenopausal risk factors independently associated with IMT were higher pulse pressure (P < 0.001), triglycerides (P = 0.002), body mass index (P < 0.001), and study group (a surrogate for both age and menopausal status; P < 0.001). Premenopausal risk factors independently associated with focal plaque were ever smoking (P = 0.002), higher pulse pressure (P = 0.028), higher LDL (P = 0.003), age at baseline (P = 0.050), and study group (P < 0.001). CONCLUSIONS: Subclinical carotid atherosclerosis can be observed in middle-aged women. Risk factors measured before menopause are clearly associated with subclinical disease measured both concurrently and at 5 to 8 years after menopause.

Adult↗
PubMed2001

Blood growth hormone-binding protein levels in premenopausal and postmenopausal women: roles of body weight and estrogen levels.

A substantial proportion of GH circulates bound to high affinity GH-binding protein (GHBP), which corresponds to the extracellular domain of the GH receptor. Current evidence indicates that nutritional status has an important role in regulating plasma GHBP levels in humans. In the present study the relationship among plasma GHBP levels, body composition [by bioelectrical impedance analysis (BIA) and dual energy x-ray absorptiometry (DEXA)] and serum estradiol (E(2)) was evaluated in premenopausal (n = 92) and postmenopausal (n = 118) healthy women with different body weight [three groups according to body mass index (BMI): normal, 18.5-24.99; overweight, 25-29.99; obese, 30-39.99 kg/m(2)]. Plasma GHBP levels were measured by high pressure liquid chromatography gel filtration. GH and insulin-like growth factor I levels were determined by immunoradiometric assay and RIA, respectively. GHBP levels were significantly higher in premenopausal women with BMI above 25 kg/m(2) (overweight, 3.789 +/- 0.306 nmol/L; obese, 4.372 +/- 0.431 nmol/L) than those observed in postmenopausal women (overweight, 1.425 +/- 0.09 nmol/L; obese, 1.506 +/- 0.177 nmol/L). No significant differences were found between normal weight premenopausal (1.741 +/- 0.104 nmol/L) and postmenopausal (1.524 +/- 0.202 nmol/L) women. In premenopausal women GHBP levels correlated positively with BMI (r = 0.675; P < 0.001), fat mass (FM; r = 0.782; P < 0.001; by BIA; r = 0.776; P < 0.001; by DEXA), truncal fat (TF; r = 0.682; P < 0.001), waist to hip circumference ratio (WHR; r = 0.551; P < 0.001), and E(2) (r = 0.298; P < 0.05), whereas no significant correlation was found in postmenopausal women between GHBP levels and BMI, FM, TF, WHR, or E(2). In normal weight pre- and postmenopausal women GHBP levels did not change between the ages of 20 and 69 yr. No statistically significant correlation was found between GHBP and age for all groups studied. Moreover, in two distinct subgroups of pre- and postmenopausal women, aged 40-49 yr, the direct relationship between GHBP levels and all indexes of adiposity were only observed in premenopausal women [BMI: r = 0.836; P < 0.001; FM: r = 0.745 (BIA) and r = 0.832 (DEXA); P < 0.001; TF: r = 0.782; P < 0.001; WHR: r = 0.551; P < 0.05], but not in postmenopausal women. In conclusion, the present data indicate a strong direct correlation between GHBP and body fat in premenopausal, but not in postmenopausal women, whereas they failed to detect a relationship between GHBP and age. Therefore, these results suggest that endogenous estrogen status may be an important determinant of the changes in GHBP levels in women with different body weights.

Adult↗
PubMed2004

Bone densitometry in premenopausal women: synthesis and review.

Bone loss prior to menopause is being increasingly identified in women. Clearly, low bone mineral density (BMD) is a significant risk factor for fracture in the estrogen-deficient female postmenopause. The significance of low bone density prior to menopause needs to be addressed. Low bone density in the premenopausal female may reflect attainment of a lower peak bone mass. It may also be secondary to progressive bone loss following achievement of peak bone density. The etiology of low bone density in the premenopausal female needs to be clarified with meticulous exclusion of secondary causes of bone loss. Menstrual status is an important determinant of peak bone mass as well as the development of bone loss in women prior to the onset of menopause. Subclinical decreases in circulating gonadal steroids may be associated with a lower peak bone mass as well as progressive bone loss in otherwise reproductively normal women. Elevations of follicle-stimulating hormone (FSH) of greater than 20 miu/L are associated with evidence of increased bone turnover marker activity and correlate with progressive bone loss in perimenopausal women. This transitional period requires further study with respect to the magnitude of bone loss experienced and the potential benefits of antiresorptive therapy. Detailed assessment of menstrual status is necessary in the evaluation of low bone density in premenopausal women. The majority of the cross-sectional and longitudinal studies completed evaluating BMD in the premenopausal years suggest that minimal bone loss does occur prior to menopause after attainment of peak bone mass. The magnitude of premenopausal bone loss, however, is controversial and may be site-dependent. More rapid rates of bone loss are seen in the transitional period beginning 2-3 yr prior to the onset of menopause. Prospective data are needed to understand further the relationship between BMD and fracture in the premenopausal period. Women with steroid-induced bone loss as well as other secondary causes of osteoporosis respond to antiresorptive therapy with documented improvements in BMD. Biomarkers can identify perimenopausal women with increased bone turnover. Lifestyle modification can improve BMD in the pre- and the perimenopausal period. Antiresorptive therapy has not been evaluated in pre- or perimenopausal women with low BMD in the absence of secondary causes of osteoporosis. As new treatment options are evaluated and become available, biomarker assessment may be of value in identifying women at risk of fracture.

Bone Density↗
PubMed2002

Relation between fat distributions and several plasma adipocytokines after exercise training in premenopausal and postmenopausal women.

Circulating concentrations of adipocytokines, such as leptin, tumor necrosis factor-alpha (TNF-alpha), and plasminogen activator inhibitor-1 (PAI-1), vary with exercise training, menopause, or regional variations in adipose tissues. In the present study, the relationships between body fat distributions and some adipocytokines were compared in premenopausal (N = 9) and postmenopausal women (N = 9), before and after exercise training. The training for 10 weeks (that is, 3 days/week) consisted of aqua exercise plus resistance exercise. The training reduced percent fat, body mass index, total fat mass (TFM), subcutaneous fat mass (SFM), and plasma levels of leptin and PAI-1 in both women. Mean value of plasma TNF-alpha tended to increase after training in both women. Plasma leptin levels were lower in postmenopausal than in premenopausal women, independently of training. In premenopausal women, plasma leptin levels correlated well with either TFM or SFM before and after training. Regression analysis of decreases in plasma leptin with a reduced amount of SFM revealed that decreases in plasma leptin depended to a greater extent on a loss of SFM. In postmenopausal women, no significant correlation was found between leptin levels and any of the fat depots. Plasma TNF-alpha levels correlated well with visceral fat mass (VFM) in premenopausal but not in postmenopausal women. Changes in TNF-alpha levels after training correlated well with reduced amount of VFM in premenopausal but not in postmenopausal women. Plasma PAI-1 levels were not different between groups. Moreover, no significant correlation was found between PAI-1 levels and any of the fat depots in both women. Thus, in premenopausal but not in postmenopausal women, changes in plasma concentrations of leptin and TNF-alpha correlate well with specific alterations in relative amount of SFM and VFM after training, respectively. However, no significant relationship between PAI-1 and any of the fat depots was found independently of either menopause or training.

Adipose Tissue↗
PubMed2002

Coronary vascular dysfunction in premenopausal women with diabetes mellitus.

BACKGROUND: Diabetes mellitus abolishes the sex differential in coronary artery disease morbidity and mortality in premenopausal women. This finding is independent of other diabetes-associated risk factors, suggesting that other mechanisms such as impaired coronary vascular function may contribute to the increased cardiovascular risk in women with diabetes. The objective of this study was to investigate the effect of diabetes on coronary vascular function in premenopausal women. METHODS: We studied 13 premenopausal women with diabetes (aged 41 +/- 10 years) who were free of overt cardiovascular complications, and 21 control women (12 age-matched and 9 postmenopausal [aged 56 +/- 8 years]). We used [13N]-ammonia as the flow tracer and positron emission testing to measure myocardial blood flow (MBF) at rest, during maximal hyperemia, and in response to cold pressor testing. RESULTS: Baseline MBF was lower in the postmenopausal controls, reflecting the differences in cardiac work and oxygen demand as assessed by the rate-pressure product. However, baseline MBFs were similar in the 3 groups after normalization for differences in the rate-pressure product. During hyperemia, MBF increased and coronary vascular resistance decreased significantly in the 3 groups. However, the increase (from baseline) in MBF in the women with diabetes (164% +/- 58%) was less than in the premenopausal controls (258% +/- 81%, P =.021), but not significantly different from the postmenopausal control women (204% +/- 104%, P =.51). Likewise, the increase in MBF in response to cold pressor testing in the women with diabetes (24% +/- 19%) was significantly lower than in the premenopausal controls (60% +/- 39%, P =.013), but similar to that in postmenopausal control women (27% +/- 15%, P =.97). These differences persisted after adjusting for age and diabetes-associated metabolic abnormalities. CONCLUSIONS: These results demonstrate reduced coronary vasodilator function and impaired response of resistance vessels to increased sympathetic stimulation in premenopausal women with diabetes, similar to those observed in healthy postmenopausal women in whom the sex differential in coronary artery disease morbidity and mortality is no longer present.

Adult↗
PubMed2004

A prospective study of body size in different periods of life and risk of premenopausal breast cancer.

The prevalence of obesity at all ages is increasing epidemically worldwide. Information on the association between premenopausal breast cancer and body size during childhood and teenage years is scarce. In 1991 to 1992, a prospective cohort study was assembled in Norway and Sweden. We included in the analysis presented here 99,717 premenopausal women. During the follow-up period, which ended in December 1999, 733 of these women developed a primary invasive breast cancer. Overweight and obesity [body mass index (BMI) > 25 kg/m(2)] at enrollment was associated with a decreased risk of premenopausal breast cancer (P for linear trend = 0.007). Apparent associations between perceived body shape at age 7 and BMI at age 18, with heavier builds at both ages seemingly being protective for premenopausal breast cancer risk, lost their statistical significance after adjustment for BMI at cohort enrollment. Body size at age 7 was correlated with BMI at age 18 (r = 0.43); BMI at age 18 was correlated with adult BMI (r = 0.48). Changes in body size from age 7 or 18 to adulthood did not affect per se risk of premenopausal breast cancer risk. Height was related to risk, with a statistically significantly 30% reduced risk only in women shorter than 160 cm as compared with taller ones. The decreased risk of premenopausal breast cancer was observed in overweight and obese women without, but not in those with, a family history of breast cancer.

Adult↗
PubMed1995

[The significance of bone mineral density measurement of premenopausal women].

We examined the starting age for measuring bone mineral density (BMD) in premenopausal women to detect osteopenia as soon as possible. BMD of the second to fourth lumbar spine vertebrae was measured by dual-energy X-ray absorptiometry to determine normal values for 500 healthy premenopausal women (aged from 17 to 55). We found the rate for low BMD premenopausal women, whose BMD was under the peak bone mass-2SD. And we compared normal BMD women with low BMD women with reference to menstrual history, obstetrical history, and life style, by means of a questionnaire. The peak bone mass of premenopausal women was reached between 35 and 39 years of age (1.059 +/- 0.097g/cm2). The low BMD rate was 7% in all premenopausal women, and increased to 13.5% at from 45 to 49 years. On the other hand, it was only from 5.7 to 7.4% even at from 20 to 29 years. There was the positive correlation between BMD and the body mass index (BMI). There was no statistically significant difference between the low BMD women and the normal BMD women in menstrual history, obstetrical history or life style (parity was 1.7 +/- 1.6 and 1.1 +/- 1.2, respectively, p < 0.05). We concluded that premenopausal women should have their BMD measured after aged 45, and be measured once from 20 to 40 years of age if possible.

Absorptiometry, Photon↗
PubMed1994

Histopathologic adequacy of office endometrial biopsies taken with the Z-sampler and Novak curette in premenopausal and postmenopausal women.

This study compared the adequacy of office endometrial biopsies taken with the Novak curette and a disposable, flexible polypropylene biopsy device, the Z-sampler, in premenopausal and postmenopausal women. Between September 1988 and November 1991, 407 women had paired office endometrial biopsies with the Z-sampler followed by the Novak curette. Overall, 83.0% of endometrial biopsies obtained with the Z-sampler were adequate for histopathologic diagnosis as compared to 84.5% obtained with the Novak curette (P = .53). In 181 (44.5%) premenopausal women, 94.5% of Z-sampler biopsies were adequate as compared to 95.6% of Novak curette biopsies (P = .80). In 226 (55.6%) post-menopausal women, 73.9% of Z-sampler biopsies were adequate as compared to 75.7% of Novak curette biopsies (P = .66). The Z-sampler biopsies were adequate in 94.5% of premenopausal women as compared to 73.9% of postmenopausal women (P < .0001). The Novak curette biopsies were adequate in 95.6% of premenopausal women as compared to 75.7% of post-menopausal women (P < .001). While we did not demonstrate a significant difference in the adequacy of endometrial samples taken with the Z-sampler and Novak curette in premenopausal and postmenopausal women, postmenopausal women had a significantly lower rate of adequate samples obtained with either device as compared to premenopausal women.

Adult↗
PubMedDate not supplied

Estradiol concentrations in premenopausal women with coronary heart disease.

BACKGROUND: Because of the beneficial effects of estrogen, premenopausal women are normally protected against coronary heart disease (CHD) and are at lower risk for myocardial infarction; consequently, CHD occurs very rarely in menstrually active women. Given this background, the aim of the present study was to test the hypothesis that decreased concentrations of estrogen are associated with CHD in premenopausal women. METHODS: Fourteen premenopausal women with CHD were investigated and compared with a healthy control group comparable for age and cardiovascular risk factors. Relevant characteristics of patients and controls were assessed: age, blood pressure, body mass index, total cholesterol and high-density lipoprotein cholesterol, triglycerides, former pregnancies, ovariectomy and related surgical interventions, smoking history and former use of oral contraceptives. To ensure the premenopausal status of the participants, the regularity of the menstrual cycle and the follicle-stimulating hormone concentrations were also assessed. Plasma estradiol and progesterone and urine estrone concentrations (24 h urine collection) were measured at day 6 after estimated ovulation to assess the relative increase in plasma estradiol and progesterone during the second half of the menstrual cycle. RESULTS: Compared with the control group, premenopausal women with CHD had significantly lower concentrations of plasma estradiol (408.9 +/- 141 pmol/l and 287.8 +/- 109 pmol/l respectively; P = 0.0228) and total estrogen (2061 +/- 693 pg/mumol creatinine and 1607 +/- 448 pg/mumol creatinine respectively; P = 0.025) in the urine. However, the progesterone concentrations were not significantly different between the groups. These findings might be explained by a partial ovarian dysfunction, as the patient group had a significantly higher number of tubal sterilizations (eight compared with one). CONCLUSION: Our data provide support for the hypothesis that decreased concentrations of estradiol might be an additional pathogenetic factor for the development of CHD in menstrually active premenopausal women.

Adult↗
PubMed1984

A case-control study of risk indicators among women with premenopausal and early postmenopausal breast cancer.

Among 714 premenopausal and 130 postmenopausal breast cancer cases matched with 8440 controls for age in years and menopausal status, risk indicators for breast cancer were similar, although most associations were stronger in the premenopausal women. Compared with nulliparous women, the relative risk (RR) for those with first birth before age 25 years was 0.7 (95% confidence limits [CL] from 0.5 to 0.9) among premenopausal women, and 0.7 (0.4-1.4) for postmenopausal women. In the premenopausal cases, a history of breast cancer in a sister gave a RR of 3.0 (2.1-4.1) and in a mother 1.9 (1.4-2.5), whereas for the postmenopausal women the RRs were 1.4 (0.6-3.1) and 1.3 (0.6-2.6), respectively. Fibrocystic breast disease was also a significant predictor of subsequent breast cancer in the premenopausal and postmenopausal women. In relation to women having a single birth, premenopausal women with six or more births had a risk of breast cancer of 0.6 (0.4-1.0), which was present even after adjustment for age at first birth.

Age Factors↗