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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum measurements of bioactive (bio) luteinizing hormone (LH), immunoreactive (i) LH, iLH/follicle-stimulating hormone (FSH) ratios, serum androgens and estradiol (E2) were determined in 20 women with the clinical diagnosis of the polycystic ovary syndrome (PCO), and compared with the levels of 10 women with chronic anovulation (CA) and 10 control subjects in the early follicular phase. Women with CA and control subjects had similar levels of E2, androgens, bioLH, iLH, and iLH/FSH ratios. Fourteen of 20 women with PCO had levels of iLH exceeding 3 standard deviations (SD) of the levels of control women (21 mIU/ml), and 13 of 20 had iLH/FSH ratios above 3.2 (3 SD of control levels). Nineteen of 20 women, however, had bioLH levels above 70 mIU/ml (3 SD of control levels). Mean levels for bioLH were 131 +/- 18 in PCO, 39 +/- 3 in control subjects, and 40 +/- 3 in women with CA. The ratio of bioLH/iLH was 3.5 +/- 0.4 in control subjects and 3.2 +/- 0.3 in women with CA but significantly elevated in PCO (4.6 +/- 0.4, P less than 0.05). There was, however, a significant positive correlation between bioLH and iLH values in PCO (r = 0.64, P less than 0.01). A significant correlation was found between bioLH and serum testosterone as well as between bioLH and serum dehydroepiandrosterone sulfate (DHEA-S) (P less than 0.05), although no correlation was found between iLH and serum DHEA-S. Weight and obesity also did not correlate with either iLH or bioLH in women with PCO and CA. These data suggest that bioLH may be an important hormonal marker in the clinical diagnosis of PCO.
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PMID:Elevated bioactive luteinizing hormone in women with the polycystic ovary syndrome. 622 Sep 24

Polycystic ovarian disease (PCOD) was first described as a single disease by Stein and Leventhal in 1935, but now has been separated into several distinct entities, comprising a symptom complex. The most frequent presenting symptoms associated with PCOD are obesity, hirsutism, amenorrhea or anovulation, dysfunctional uterine bleeding, irregular menses, and infertility. The common finding of hirsutism in PCOD patients is a reflection of the hyperandrogenism resulting from elevation of all the androgens, including testosterone, androstenediol, dehydroepiandrostrone sulfate (DHEA-S), and androstenedione. Some patients with all the clinical features of PCOD can be shown, through appropriate testing, to have an attenuated form of classic congenital adrenal hyperplasia (CAH). Serum follicle stimulating hormone (FSH) levels are usually low or in the normal range, and serum luteinizing hormone (LH) levels are usually elevated in patients with PCOD, resulting in an altered LH/FSH ratio. Treatment for PCOD must be based on the needs and desires of the individual patient, and on the pathophysiology of the patient's particular abnormalities. When pregnancy is desired, ovulation induction with clomiphene is indicated. Clomiphene is a weak estrogen that induces a transient rise in serum LH and FSH, followed by a gonadotropic pattern similar to normal cycles. A 72% ovulation rate and a 41.8% conception rate have been reported after treatment with clomiphene. In patients who do not respond to clomiphene, or clomiphene with added human chorionic gonadotropin (hCG), human menopausal gonadotropin (hMG) can be used to induce ovulation, but the patient should be closely monitored for multiple ovulation, multiple pregnancy, or hyperstimulation syndrome. For patients not interested in conception, regular menstrual cyclicity can be restored and hyperandrogenism reduced with oral contraceptives (OCs).
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PMID:Polycystic ovarian disease. 623 74

Endometrial carcinoma (EC) shows a worlwide trend toward increase in industrialized nations which cannot be explained solely by the longer life expectancy of women although the incidence of EC increases at later age (10-20/100,000 women overall; 1/1000 women in 50-70 year olds). Mortality rate of EC has decreased and 5-year survival rate has increased. Besides age factors and individual disposition, endocrine factors are important in the etiology of EC. Obesity effects estrogen metabolism: in extraglandular aromatization fo androstanedione estrone is formed which, in turn, is metabolized to estradiol in the endometrium. A higher plasma level of estradiol is found in obesity with a correspondingly lower sex hormonebinding globulin capacity. Anovulation, corpus luteum insufficiency (as in the polycystic ovary syndrome) and nulliparity are risk factors because of uninhibited estrogen-induced endometrial proliferation with increased cell-turnover rate. This may lead to precancerous conditions and EC. Whearas estrogens of themselves are not carcinogenic they promote EC; epidemiologic studies have shown an increased risk and incidence of EC in postmenopausal women on longterm estrogen therapy. Although these studies are thus far inconclusive there appears to be a dose and time-dependent risk factor. Continued administration carries a greater risk than cyclic administration. Risk and incidence increase with duration of use; likewise, a 1.25 mg dose of conjugated estrogens carries twice the risk of a smaller dose. On the other had, estrogen-related EC is diagnosed earlier and treated more successfully (92% survival). Progestins inhibit estrogen-induced proliferation; the incidence of endometrial and/or ovarian carcinoma related to the use of hormonal contraceptives has dropped since the advent and use of combination pills with their low estrogen content.
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PMID:[Current views on the epidemiology and etiology of endometrial carcinoma]. 635 Jan 18

10 examine the relationship between obesity and chronic anovulation, we compared basal serum LH, FSH, and PRL levels, determined at 20-min intervals, and basal C21 [progesterone, 17- hydroxyprogesterone , pregnenolone, 17-hydroxypregnenolone ( 17Pe ), and cortisol], C19 [testosterone (T), delta 4-androstenedione (A), and dehydroepiandrosterone] and C18 (estrone and estradiol) steroid hormone concentrations measured at 1- to 2-h intervals for a 24-h period in five normal weight cycling women (NC) and in two groups of weight-matched obese women. Five of the obese women were regularly cycling (OC), and six were amenorrheic (OA). Sex hormone-binding globulin (SHBG) and non-SHBG-bound T and estradiol concentrations were also measured in each woman. Compared to NC women, OC women had normal basal protein and steroid hormone concentrations, except for reduced 17Pe levels (P less than 0.05). Mean SHBG concentrations were reduced by approximately 30%, and non-SHBG-bound T was increased by 70%, although the differences were not significant. In addition, when six precursors of testosterone (pregnenolone, 17Pe , dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, and A) were considered together as a group and the data analyzed by the kappa 2 test, a reduction in basal levels of these precursors was found in OC women relative to those in NC women (P less than 0.005). In OA women, mean concentrations of SHBG were markedly reduced and those of total T, A, estrone, and non-SHBG-bound T were significantly increased compared to those in both NC and OC women. Mean 24-h concentrations of LH tended to be greatest and FSH lowest in this group, but were not significantly different from those in the other groups. The mean LH pulse frequency was significantly greater in OA than in OC women (P less than 0.05). Mean 24-h PRL and cortisol levels were also reduced in OA women relative to those in NC women. These data suggest the possibility of a compensatory decline in total T production in OC women in an attempt to maintain normal hormonal homeostasis; as a consequence, ovulation continues in a cyclic fashion. In OA women, such compensatory mechanisms are no longer operative. Instead, a central and/or peripheral defect, resulting in overproduction of androgen, may also exist and lead to anovulation in OA women. In conclusion, our data imply that obesity is not a primary factor causing chronic anovulation. However, obesity may aggravate an already existing subtle defect in some women and result in amenorrhea.
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PMID:Endocrine comparison of obese menstruating and amenorrheic women. 642 58

The aim of the present study was to determine whether a group of patients selected on the basis of clinical features only is characterized by the typical hormonal findings as discussed in the literature concerning the PCO-syndrome. PCO patients had oligomenorrhea, secondary amenorrhea or otherwise evidence of chronic anovulation, as well as hirsutism and/or obesity. Control women had regular menstrual cycles and a normal body weight. Since androgen and estrogen production in women depends on the stage of follicular development, an effort was made to obtain endocrinological data under standardized conditions. Under well-defined circumstances the PCO group (n = 20) had higher LH levels and lower FSH levels as compared with the control group (n = 10). Consequently the LH/FSH ratio was significantly elevated in the PCO group. Serum estrone and estradiol levels were significantly elevated in the PCO group, as were the serum levels of androstenedione and testosterone. Despite these differences a marked degree of overlap existed in the PCO patients and the control women for gonadotropin, estrogen and androgen levels. It was concluded that although the presence of polycystic ovaries in the investigated PCO group of women was not confirmed by laparoscopy, laparotomy or histological examination of the ovaries, these women had basal endocrinological characteristics similar to those found in well-proven PCO patients reported in the literature.
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PMID:Hormonal characteristics of women with clinical features of the polycystic ovary syndrome. 643 Jul 30

A group of 89 sterile patients with hypothalamic anovulation were subjected to progressive dosages of clomiphene citrate according to a predesigned program. In order to analyze our results, we divided our patients into seven groups, according to the largest dosage of clomiphene citrate received. Clinical features were revised in relation to the ovulatory dose of clomiphene. Significant differences between groups regarding weight, menstrual pattern, age at menarche, and hirsutism were not found. Obesity increased the dose required for ovulation when it was less than 900 mg/cycle, but had no effect at higher doses. The ovulation rate, pregnancies, prenatal wastage, and side effects of treatment were analyzed; and it was found that the scheme for ovulation induction used, without expensive and sophisticated ovarian monitoring resources, improved ovulation and pregnancy rates with few and unimportant deleterious side effects.
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PMID:Progressive dosages of clomiphene in hypothalamic anovulation. 648 38

The association between factors of reproductive life and the occurrence of epithelial ovarian cancer were examined and anovulation and reduced gonadotrophin secretion were considered as mechanisms through which such factors might play their protective roles. All women with newly diagnosed epithelial ovarian cancer and who were resident in 6 counties of Washington and Utah during 1976 through 1979 were interviewed concerning their menstrual, reproductive, and medical histories. For comparison, interviews were also obtained from a random sample of women living in the same counties. To consider adequately the simultaneous effects of multiple relevant and possibly confounding variables, linear logistic regression techniques were used to analyze the data. Women with cancer reported fewer full-term pregnancies, fewer miscarriages, and less total time breastfeeding than controls. Cases in the Washington counties reported fewer exposures to combined oral contraceptive (OC) preparations. The difference between cases and controls was not apparent in the Utah data, possibly because of the low frequency of OC use among Utah residence and the small size of Utah samples. Obesity, defined as more than 20% excess weight at age 30 over the upper limit of ideal for a woman of a given height and medium frame was reported slightly more often by the cases than by the controls. Results obtained for reproduction variables appeared largely consistent with those of previous studies, in that factors associated with suppression of ovulation were generally protective. Histories of childbearing, miscarriages, lactation, and (in Washington) OC use were found to be associated with decreased risk of ovarian cancer. The estimated relative risks were, respectively, 0.88/pregnancy, 0.82/miscarriage, 0.79/year of lactation, and 0.89/year of OC. It was observed that the magnitudes off the diminished risks from these exposures substantially exceeded those which would have been expected solely on the basis of their inhibition of ovulation. The lack of association found between the occurrence of ovarian cancer and either total dose or total time of exposure to noncontraceptive estrogens, or with a history of usage of thyroid medications, suggests that periods of reduced pituitary gonadotrophin secretion fails to reduce risk of ovarian cancer. Pregnancy, lactation, and OC use appear to offer some protection against the development of epithelial ovarian cancer, yet the reasons remain obscure.
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PMID:Events of reproductive life and the incidence of epithelial ovarian cancer. 668 35

To examine the mechanism by which obesity influences ovulation, 55 patients with oligo- or anovulation were studied. Parameters measured in serum were sex steroid-binding globulin (SSBG), testosterone (T), PRL, LH, FSH, and estradiol (E2). The women were divided into 2 groups: an obese group (group 1), greater than 145% of ideal body weight, and a normal weight group, less than 120% ideal body weight. SSBG was measured by saturation analysis T, LH, FSH, PRL, and E2 were measured by RIA. SSBG group 1 levels were 7.14 ng dihydrotestosterone bound/ml compared to 14.7 ng dihydrotestosterone bound/ml in group 2 (P less than 0.05). There were no significant differences in FSH, T, or E2. The correlation of body weight vs. SSBG in all patients was r = -0.62. In these 2 groups, the SSBG was significantly lower in the obese patients compared to that in the normal weight patients, independent of T or E2 levels. SSBG correlated negatively with body weight, suggesting that obesity has an influence on SSBG levels independent of hormonal status. When SSBG is lowered, there may be an increase in free T which, by inhibiting follicular maturation, may begin the sequence of events seen in polycystic ovary syndrome.
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PMID:Obesity and its role in polycystic ovary syndrome. 678 98

Creatinine-adjusted levels of estrone, estradiol, and estriol were determined in luteal phase urine specimens of 200 premenopausal women from rural areas of Greece. The relation of each estrogen to height, weight, obesity index, and serum cholesterol was studied by multiple regression, controlling for age, age at menarche, and ovulation status (ovulation, anovulation, undetermined). No consistent relation between any of the somatometric variables and any of the urine estrogens emerged from the statistical analysis, but among older women (30-40 years old) both estrone and estradiol were positively associated with serum cholesterol (p less than 0.05). The data provide no support for the hypothesis that the relationship between body weight and breast cancer risk is mediated through an influence of body weight on estrogen levels--at least in premenopausal women. On the other hand the data on serum cholesterol levels are consonant with the idea that qualitative aspects of nutrition may affect breast cancer risk among older (e.g., postmenopausal) women.
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PMID:Obesity, serum cholesterol, and estrogens in premenopausal women. 684 49

This review of the connection between unopposed estrogen therapy for climacteric symptoms and the development of endometrial hyperplasia briefly outlines the history of the association, and then concentrates on clinical classification problems which muddy the attempts to come to a clear understanding of the relationship between estrogen replacement therapy (ERT) and endometrial cancer. Little agreement exists about the definition of endometrial pathology and of the malignant potentials of different types of hyperplasia. This paper classifies 4 types of hyperplasia: 1) cystic hyperplasia, which has the risk of malignant change of less than 2%; 2) adenomatous hyperplasia, which has a risk of malignant change from 12-25%; 3) atypical hyperplasia, which has a malignancy potential of 45%; and 4) carcinoma in situ, which is malignant. The following conditions are discussed as they are associated with endometrial hyperplasia and adenocarcinoma: 1) obesity; 2) anovulation; 3) late menopause; 4) Stein-Leventhal syndrome; 5) functioning ovarian tumors; and 6) diabetes history. In addition hypertension and cancers of the breast and ovary occur more often with endometrial cancer than would be expected by chance. The remainder of the paper discusses the administration of exogenous estrogens unopposed, exogenous progestins, and their concurrent use, especially in controlling menopausal symptoms. Prevention, diagnosis, and treatment of hyperplasia are discussed. In terms of prevention, a study showed that low-dose cyclical Premarin (.625 mg) resulted in an incidence of hyperplasia of 7% and with higher doses (1.25 mg) rose to 15%. The addition of d-norgestrel for 7 days to the high dose of Premarin reduced incidences to 3%, whereas estrogen plus low-dose norethindrone resulted in 0% incidence of cystic hyperplasia. It is recommended that the unopposed use of estrogens be avoided if possible, although short-term therapy up to 6 months is probably safe. Longer term therapy must have added progestogen, and endometrial sampling in the form of Vabra curettage should be performed every year in patients taking unopposed estrogens and every 3 years in patients taking combined estrogen therapy.
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PMID:Oestrogens and endometrial hyperplasia. 699 95


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