85 resultados para Amenorrhea
Prevalência da baixa densidade mineral óssea em mulheres na pós-menopausa tratadas de câncer de mama
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Background: The aim of this study was to assess clinical and inflammatory markers in nonalcoholic fatty liver disease (NAFLD) in postmenopausal women with metabolic syndrome.Methods: This cross-sectional study included 180 Brazilian women (age >= 45 years and amenorrhea >= 12 months). Metabolic syndrome was diagnosed by the presence of at least three of the following indicators: Waist circumference (WC) > 88 cm, triglycerides (TGs) >= 150 mg/dL, high-density lipoprotein (HDL) < 50 mg/dL; blood pressure >= 130/85 mmHg; and glucose >= 100 mg/dL. NAFLD was diagnosed by abdominal ultrasound. Participants were divided into three groups: Metabolic syndrome alone (n = 53); metabolic syndrome + NAFLD (n = 67); or absence of metabolic syndrome or NAFLD (control, n = 60). Clinical, anthropometric, and biochemical variables were quantified. The inflammatory profile included adiponectin, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). Data were submitted to statistical analysis using a Tukey test, analysis of variance (ANOVA), chi-squared, Pearson correlation, and logistic regression (odds ratio, OR).Results: Women with metabolic syndrome + NAFLD, abdominal obesity, high glucose, and insulin resistance by HOMA-IR were compared to women with metabolic syndrome alone and controls (P < 0.05). High values of IL-6 and TNF-alpha and low values of adiponectin were observed among women with metabolic syndrome alone or metabolic syndrome + NAFLD when compared to controls (P < 0.05). In multivariate analysis, the variables considered as risk of NAFLD development were: High systolic blood pressure (SBP) [(OR 1.02, 95% confidence interval (CI) 1.0-1.04]; large WC (OR 1.07, 95% CI 1.01-1.13); insulin resistance (OR 3.81, 95% CI 2.01-7.13); and metabolic syndrome (OR 8.68, 95% CI 3.3-24.1). Adiponectin levels reduced NAFLD risk (OR 0.88, 95% CI 0.80-0.96).Conclusion: In postmenopausal women, metabolic syndrome, abdominal obesity, and insulin resistance were risk markers for the development of NAFLD, whereas higher adiponectin values indicated a protection marker.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Objective To evaluate the prevalence and risk factors of non-alcoholic fatty liver disease (NAFLD) in postmenopausal women.Methods A cross-sectional study was carried involving 188 women (age >= 45 years and amenorrhea >= 12 months) attending the outpatient unit in south-eastern Brazil. Exclusion criteria were liver disease (hepatitis B and C, cholestatic disease, liver insufficiency), use of drugs that affect liver metabolism; alcoholics; AIDS or cancer history; and morbid obesity. NAFLD was diagnosed by abdominal ultrasound. Clinical, anthropometric (body mass index, waist circumference) and biochemical variables were measured.Results Of the 188 women, 73 (38.8%) had NAFLD. Blood pressure, waist circumference, body mass index, LDL cholesterol, triglycerides and glucose were significantly higher in NAFLD patients when compared with women without NAFLD (control group) (p < 0.05). HOMA-IR values indicated insulin resistance only in the NAFLD group (6.1 +/- 4.6 vs. 2.4 +/- 1.4 in control group, p < 0.05). Metabolic syndrome was detected in 93.1% of the women affected by NAFLD, and 46.1% of the control group (p < 0.05). In multivariate analysis, adjusted for age and weight, the variables considered at risk for the development of NAFLD, were: high waist circumference (odds ratio (OR) 1.07, 95% confidence interval (CI) 1.01-1.13), insulin resistance (OR 3.81, 95% CI 2.01-7.13), and presence of metabolic syndrome (OR 8.68, 95% CI 3.3-24.1).Conclusion NAFLD showed a high prevalence among postmenopausal women. The presence of metabolic syndrome, abdominal obesity and IR were indicators of risk for the development of NAFLD.
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Pós-graduação em Ginecologia, Obstetrícia e Mastologia - FMB
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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The present study investigates the effects of vitamin D on muscle function in postmenopausal women. It has been shown that vitamin D supplementation in postmenopausal women with hypovitaminosis D provides significant protective factor against sarcopenia, with significant increases in muscle strength and control of progressive loss of lean mass. We aimed to evaluate the effect of supplementation of vitamin D (VITD) alone on muscle function in younger postmenopausal women. In this double-blind, placebo-controlled clinical trial, 160 Brazilian postmenopausal women were randomized into two groups: VITD group consisting of patients receiving vitamin D3 1000 IU/day orally (n = 80) or placebo group (n = 80). Women with amenorrhea for more than 12 months and age 50-65 years, with a history of falls (previous 12 months), were included. The intervention time was 9 months, with assessments at two points, start and end. Lean mass was estimated by total-body dual-energy X-ray absorptiometry (DXA) and muscle strength by handgrip strength and chair rising test. The plasma concentrations of 25-hydroxyvitamin D [25(OH)D] were measured by high-performance liquid chromatography (HPLC). Statistical analysis was by intention to treat (ITT), using ANOVA, Student's t test, and Tukey's test. After 9 months, average values of 25(OH)D increased from 15.0 ± 7.5 to 27.5 ± 10.4 ng/ml (+45.4 %) in the VITD group and decreased from 16.9 ± 6.7 to 13.8 ± 6.0 ng/ml (-18.5 %) in the placebo group (p < 0.001). In the VITD group, there was significant increase in muscle strength (+25.3 %) of the lower limbs by chair rising test (p = 0.036). In women in the placebo group, there was considerable loss (-6.8 %) in the lean mass (p = 0.030). The supplementation of vitamin D alone in postmenopausal women provided significant protective factor against the occurrence of sarcopenia, with significant increases in muscle strength and control of progressive loss of lean mass.
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Pós-graduação em Ginecologia, Obstetrícia e Mastologia - FMB
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Pós-graduação em Ciências da Motricidade - IBRC
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The human luteinizing hormone/chorionic gonadotropin receptor (LHCGR) plays a fundamental role in male and female reproductive physiology. Over the past 15 years, several homozygous or compound heterozygous loss-of-function mutations in the LHCGR gene have been described in males and females. In genetic males, mutations in LHCGR were associated with distinct degrees of impairment in pre- and postnatal testosterone secretion resulting in a phenotypic spectrum. Patients with the severe form of LH resistance have predominantly female external genitalia and absence of secondary sex differentiation at puberty. Patients with milder forms have predominantly male external genitalia with micropenis and/or hypospadias or only infertility without ambiguity. The undermasculization is associated with low basal, as well as human CG-stimulated, testosterone levels and elevated LH levels after pubertal age, without abnormal step-up in testosterone biosynthesis precursors. The testes have only slightly reduced size but mature Leydig cells are absent or scarce (Leydig cell hypoplasia). Genetic females with inactivating LHCGR mutations have female external genitalia, spontaneous breast and pubic hair development at puberty, and normal or late menarche followed by oligoamenorrhea and infertility. Estradiol and progesterone levels are normal for the early to midfollicular phase, but do not reach ovulatory or luteal phase levels. Serum LH levels are high whereas follicle-stimulating hormone levels are normal or only slightly increased. Pelvic ultrasound has demonstrated a small or normal uterus and normal or enlarged ovaries with cysts. The inactivating mutations of the LHCGR have provided important insights into distinct physiological roles of LH in reproduction of both sexes.
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We describe a hitherto undocumented variant of dimorphic pituitary neoplasm composed of an admixture of neurosecretory cells and profuse leiomyomatous stroma around intratumoral vessels. Radiologically perceived as a macroadenoma of 3.8 cm in diameter, this pituitary mass developed in an otherwise healthy 43-year-old female. At the term of a yearlong history of amenorrhea and progressive bitemporal visual loss, subtotal resection was performed via transsphenoidal microsurgery. Discounting mild hyperprolactinemia, there was no evidence of excess hormone production. Histologically, solid sheets, nests and cords of epithelial-looking, yet cytokeratin-negative cells were seen growing in a richly vascularized stroma of spindle cells. While strong immunoreactivity for NCAM, Synaptophysin and Chromogranin-A was detected in the former, the latter showed both morphological and immunophenotypic hallmarks of smooth muscle, being positive for vimentin, muscle actin and smooth muscle actin. Architectural patterns varied from monomorphous stroma-dominant zones through biphasic neuroendocrine-leiomyomatous areas, to pseudopapillary fronds along vascular cores. Only endothelia were labeled with CD34. Staining for S100 protein and GFAP, characteristics of sustentacular cells, as well as bcl-2 and c-kit was absent. Except for alpha-subunit, anterior pituitary hormones tested negative in tumor cells, as did a panel of peripheral endocrine markers, including serotonin, somatostatin, calcitonin, parathormone and vasoactive intestinal polypeptide. Mitotic activity was absent and the MIB-1 labeling index low (1-2%). While assignment of this lesion to any established neoplastic entity is not forthcoming, we propose it is being considered as a low-grade neuroendocrine tumor possibly related to null cell adenoma.
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PURPOSE: The value of adjuvant tamoxifen after chemotherapy for premenopausal women with breast cancer has not been adequately assessed. PATIENTS AND METHODS: Between 1993 and 1999, International Breast Cancer Study Group Trial 13-93 enrolled 1,246 assessable premenopausal women with axillary node-positive, operable breast cancer. All patients received chemotherapy (cyclophosphamide plus either doxorubicin or epirubicin for four courses followed by immediate or delayed classical cyclophosphamide, methotrexate, and fluorouracil for three courses), which was followed by either tamoxifen (20 mg daily) for 5 years or no further treatment. The primary end point was disease-free survival (DFS). Tumors were classified as estrogen receptor (ER) -positive (n = 735, 59%) if immunohistochemical (IHC) or ligand-binding assays (LBA) were clearly positive. The ER-negative group included all other tumors (n = 511, 41%). A subset of the ER-negative group was defined as ER absent (n = 108, 9%) if IHC staining was none or if the LBA result was 0 fmol/mg cytosol protein. The median follow-up time was 7 years. RESULTS: Tamoxifen improved DFS in the ER-positive cohort (hazard ratio [HR] for tamoxifen v no tamoxifen = 0.59; 95% CI, 0.46 to 0.75; P < .0001) but not in the ER-negative cohort (HR = 1.02; 95% CI, 0.77 to 1.35; P = .89). Tamoxifen had a detrimental effect on patients with ER-absent tumors compared with no tamoxifen in an unplanned exploratory analysis (HR = 2.10; 95% CI, 1.03 to 4.29; P = .04). Patients with ER-positive tumors who achieved chemotherapy-induced amenorrhea had a significantly improved outcome (HR for amenorrhea v no amenorrhea = 0.61; 95% CI, 0.44 to 0.86; P = .004), whether or not they received tamoxifen. CONCLUSION: Tamoxifen after adjuvant chemotherapy significantly improved treatment outcome in premenopausal patients with endocrine-responsive disease, but its use as adjuvant therapy for patients with ER-negative tumors is not recommended.