Serum leptin concentrations in pre- and postmenopausal women on sex hormone therapy.

AIM: The aim of the present study was to investigate the influence of endogenous estradiol and estrogen and estrogen-progestin therapies on concentration in pre- and postmenopausal women. MATERIALS AND METHODS: The study groups consisted of 26 women with surgical menopause (mean+/-standard deviation (SD): age 51.8+/-2.6 years, body mass index (BMI) 26.45+/-4.56 kg/m(2)), 54 with natural menopause (mean+/-SD: age 50.5+/-3.0 years, BMI 25.75+/-4.09 kg/m(2)) and 40 premenopausal controls (mean+/-SD: age 48.3+/-2.3 years, BMI 26.23+/-4.12 kg/m(2)). The group with surgical menopause received estradiol transdermally (50 microg/day) and those with natural menopause received additionally medroxyprogesterone acetate (5 mg/day) for the last 12 days of the cycle. Before and after 4 months of therapy, body weight, waist and hip circumferences and blood pressure were measured, and BMI and waist-to-hip ratio (WHR) were calculated. Serum leptin, follicle-stimulating hormone (FSH), estradiol (E(2)), testosterone, prolactin and dehydroepiandrosterone sulfate (DHEAS) were measured prior to and after treatment. RESULTS: Leptin concentrations did not differ statistically among the groups. No correlations between leptin and E(2), FSH, prolactin, testosterone and DHEAS concentrations were found in any of the groups before and after treatment. Leptin level correlated positively with body mass, BMI and hip and waist circumferences in all groups. There were no correlations between leptin and WHR in the pre- and postmenopausal groups. In the premenopausal group and in some postmenopausal groups, serum leptin level correlated with blood pressure. CONCLUSIONS: Endogenous E(2) and androgens in premenopausal women and estrogen and estrogen-progestin therapies in postmenopausal subjects do not influence serum leptin concentrations. Leptin level is related to body mass and BMI, but not to sex hormone status. The distribution of adipose tissue and the type of obesity (android or gynoid) have no influence on serum leptin concentration. The correlation between serum leptin level and blood pressure requires further investigation.     

Climacteric obesity: from genesis to clinic.

The etiology of obesity is multifactorial and still unclear. Genetic factors play a significant role and include several gene candidates: polymorphisms of genes for ss(2)-adrenoreceptor, resistin, estrogen receptor-a and peroxisome proliferator-activated receptor-gamma. Moreover, peptides regulating hunger and satiety, e.g. leptin, galanin, cholecystokinin and neuropeptide Y, and altered nutritional patterns have been implicated. Also, factors associated with aging, e.g. decreased levels of growth hormone and dehydroepiandrosterone, and the activity of the sympathetic nervous system (resting metabolism and thermogenesis) cannot be disregarded. Participation of the sex steroids and inflammatory factors has also been postulated in the etiology of obesity. Three phenotypes of obesity are postulated; however, the visceral (abdominal) phenotype is typical of postmenopausal women and is characterized by several metabolic disorders with high risks of diabetes mellitus type 2 and cardiovascular disease. On the basis of personal experience and data from evidence-based medicine, diagnostic-therapeutic algorithms of climacteric obesity are presented.     

筛检对肝癌死亡率影响的研究

5581名HBsAg阳性的男性随机分入周期性筛检组(A组,3712人)及对照组(B组,1869人)。A组(19155.4人年)共发生肝癌257例,B组(9785.5人年)为117例,两组的肝癌发生率分别为1342/10万与1196/10万;两组肝癌死亡分别为218与109例,肝癌死亡率分别为1138/10万与1114/10万。两组中Ⅰ期肝癌病例分别为29.6％与6.0％,差异有非常显著性意义。1、3、5年相对生存率A组为23.7％、7.0％、4.0％,B组为9.7％、4.0％、4.1％。用Poisson回归模型拟合显示,在调正年龄、初筛AFP及入列年份后,筛检对于肝癌的相对危险度为0.83,95％CI为0.68～1.03,有较弱的“保护”作用,Cox回归模型拟合结果显示当临床分期未引入模型时,筛检对于肝癌有显著的“保护”作用:危险率为0.6617,95％CI为0.5234～0.8365;而模型经调整后,危险率即接近“1”,95％CI为0.74～1.26。