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

Cases of endometrial carcinoma reviewed for this study were divided into two groups: 1) Premenopausal, perimenopausal and postmenopausal patients in whom a history of anovulation, obesity, ovarian hyperthecosis (including Stein-Leventhal syndrome) or feminizing tumors, and/or exogenous estrogen intake were found; and 2) post menopausal, elderly patients, without known hormonal or metabolic disturbances and without any history of estrogen therapy. In the first group, frequent associated findings were precursor stages of endometrial carcinoma, such as adenomatous and atypical hyperplasia. In the majority of cases, the cancer was confined to the endometrium, rarely infiltrating the myometrium. In the second group, the cancer was associated most often with an inactive, atrophic endometrium and frequently diffusely infiltrated through the myometrium, with lymphatic and vascular involvement. The lymphatic and plasma-cell infiltrate was evaluated in both groups. It was found to be more abundant in the first group, but at the tumor-host interface and perivascularly, than in the second. As reported in other malignancies of the female reproductive system, the presence or absence of a lymphocytic infiltrate as a morphological expression of local cellular immune response of the host correlates well with the biological behavior of the tumor. A challenging question is the relationship, if any, between hormonal factors and immune mechanisms in tumors arising in tissues such as the endometrium that, even normally, are targets of hormonal stimulation.
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PMID:Morphologic correlates of host response in endometrial carcinoma. 709 92

Although sex steroids have long been known to influence serum concentrations of SHBG, it is now recognized that nutritional factors may be more important in the regulation of SHBG in women. Thus, SHBG concentrations are negatively correlated with body mass index (BMI) and, more particularly, to indices of central adiposity. Polycystic ovary syndrome (PCOS), the most common cause of anovulatory infertility, is associated with truncal obesity, hyperandrogenism and hyperinsulinaemia. There is evidence that insulin may be the humoral mediator of the weight-dependent changes in SHBG. Serum SHBG concentrations are inversely correlated with both fasting and glucose-stimulated insulin levels, and insulin has been shown to have a direct inhibitory effect on SHBG synthesis and secretion by hepatocytes in culture. However, the interrelationship of BMI, insulin and SHBG appears to be different in women with PCOS from that in normal subjects. The clinical importance of the weight-related suppression of SHBG is illustrated by the finding of a greater prevalence of hirsutism in obese women PCOS compared with their lean counterparts. Obese subjects with PCOS have similar total testosterone concentrations to lean PCO women but have lower SHBG and reciprocally higher free testosterone levels. Calorie restriction results in reduction of serum insulin followed by an increase in SHBG and a fall in free testosterone but an isocaloric, low-fat diet has no significant effect on SHBG concentrations. Weight reduction in obese, hyperandrogenaemic women with PCO is an important approach to the management of both anovulation and hirsutism.
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PMID:Sex hormone-binding globulin and female reproductive function. 762 5

Polycystic ovary syndrome (PCOS) is an association of oligomenorrhoea, anovulation, hyperandrogenism, obesity and enlarged polycystic ovaries. It provides a model of loss of cyclic ovarian function. It is classical to distinguish between type I and type II PCOS. In type I, the primary mechanism seems to be hypothalamic dysfunction, which causes an increase in the frequency and amplitude of LH pulses, with diminished FSH release. LH hypersecretion stimulates ovarian stroma hyperplasia while FSH insufficiency results in the failure of folliculare maturation and hence anovulation. Aromatization of androgens to oestrogens is responsible for permanent oestrogen overproduction, which favours LH hypersecretion. Type II PCOS is more frequent and may have multiple causes (local, endocrine, systemic, iatrogenic) that interfere with the gonadotropic axis and alter the FSH/LH ratio. The most efficient treatment of hirsutism is cyproterone acetate which alone has both antiandrogenic and antigonadotropic properties. Clomifene citrate remains the "first choice" treatment of infertility associated with anovulation.
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PMID:[Polycystic ovarian dystrophies. Diagnostic criteria and treatment]. 763 20

Several lines of evidence suggest that a subset of women may be at increased risk of cardiovascular disease because of unfavorable alterations in insulin action and/or production, accompanying altered apolipoprotein metabolism and altered androgenicity and/or estrogenicity. A number of cardiovascular disease risk factors, including central obesity, insulin resistance (with associated hyperinsulinemia), dyslipidemia, and/or diabetes mellitus, tend to cluster in these women. Another common ovarian morphology in women with hyperandrogenism is polycystic ovaries, which cluster with hirsutism, anovulation, infertility, gonadotropin secretion abnormalities, android fat distribution, and many important cardiovascular disease risk factors. Studies indicate that androgen excess may be a signal of increased risk for coronary artery disease, even in younger women. If androgenicity and insulin resistance are early warning signs of increasing risk of morbidity and mortality, these patients are prime candidates for preventive medicine. It is important that primary care providers begin to recognize these androgen disorders as a clue to the existence of a complex, lifelong pattern potentially placing women at risk for premature morbidity and mortality and initiate preventive treatment before irreversible thresholds are crossed.
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PMID:Obesity, lipids, cardiovascular risk, and androgen excess. 782 38

Polycystic ovary syndrome is the most common endocrine disorder in women of reproductive age. Recent prevalence estimates suggest that 5-10% of premenopausal women have the full-blown syndrome of hyperandrogenism, chronic anovulation, and polycystic ovaries. Evidence suggests that women with polycystic ovary syndrome have a unique disorder of insulin action and are at increased risk to develop non-insulin-dependent diabetes mellitus. Further, non-insulin-dependent diabetes mellitus in women with polycystic ovary syndrome has a substantially earlier age of onset (third to fourth decades) than it does in the general population (sixth to seventh decades). Studies assessing whether abnormalities in insulin action are intrinsic or secondary to the hormonal milieu have found that insulin-induced receptor autophosphorylation is markedly diminished in approximately 50% of polycystic ovary syndrome women. This defect is unique to women with polycystic ovary syndrome and is not seen in other common insulin-resistant states of obesity and non-insulin-dependent diabetes mellitus. In polycystic ovary syndrome women who have normal receptor autophosphorylation, it remains likely that signaling mechanisms downstream of the receptor are abnormal, since these women are also insulin resistant. This distinctive post-insulin-binding defect appears to be genetic, since it is present in cells removed from the in vivo environment for generations.
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PMID:Hyperandrogenic anovulation (PCOS): a unique disorder of insulin action associated with an increased risk of non-insulin-dependent diabetes mellitus. 782 39

The endocrinology of the perimenopause--the time between pre- and postmenopause--is characterized by changes in the metabolism of the steroid hormones caused by increasing insufficiency of the ovaries. Until the age of 48 the concentrations of the estrogens are relatively constant with a median level of 120 pg/ml serum for estradiol and of 75 pg/ml for estrone. Between the age of 49 and 54 the levels decrease to concentrations of 35 pg/ml for estrone and 10 pg/ml for estradiol. In the corresponding time, there is a tenfold rise of the level of FSH. The level remains constant until high age. The decrease of the estrogens causes the menopause in an age of 51 to 52. In the postmenopause the ovaries don't play a role for the concentrations of the estrogens. The concentrations are determined by the conversion of the androgens secreted by the adrenal cortex. The serum concentrations of androstenedione are five times higher than those of testosterone. The function of the adrenal cortex remains until high age; there is no 'adrenopause' comparable to the 'menopause'. The suppression of the adrenal cortex by treatment with corticoids (e.g. for asthma) causes a dramatic decrease of the androgens and consecutively for the estrogens. The lack of estrogens play an important role in the induction of osteoporosis and other disturbances of the late postmenopause, e.g. coronary heart disease. Obese women show in the pre- and the perimenopause more often dysfunctional bleedings caused by anovulation or corpus luteum insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Endocrinological changes in pre- and postmenopause]. 783 30

Two long and broad streams of medical literature, from the 1950's to date, have established the existence of two unrelated abnormalities of androgen production in women with breast cancer. One is the genetically determined presence of subnormal production of adrenal androgens (i.e. DHEA and DHEAS) in women with premenopausal breast cancer and their sisters, who are at increased risk for breast cancer. The other is excessive production of testosterone, of ovarian origin, in subsets of women with either premenopausal or postmenopausal breast cancer and women with atypical breast-duct hyperplasia, who are at increased risk for breast cancer; along with the hypertestosteronism, there is frequently chronic anovulation in the premenopausal patients. The combination of ovarian hypertestosteronism and chronic anovulation is characteristic of the polycystic ovary syndrome and is also frequently seen in women with abdominal ("android") obesity; both PCOS and abdominal obesity are known to be characterized by high risk for postmenopausal cancer. The elevated testosterone levels and the increased levels of insulin, IGF-I, and IGF-II that are seen in PCOS and abdominal obesity could favor the development of breast cancer in several ways, all of which have been demonstrated experimentally: binding of testosterone to cancer cells bearing testosterone receptors, with direct stimulation; intratissular aromatization of testosterone to estradiol, with stimulation of estrogen-sensitive cells; stimulation of the production of epithelial growth factor (EGF) by testosterone, with direct mitogenic effect of EGF on cancer cells; stimulation of aromatase by insulin and IGF-I; direct mitogenic stimulation of cancer cells by insulin, IGF-I, and IGF-II; and stimulation by IGF-I and IGF-II of the intratissular reduction of estrone to estradiol. Since PCOS is probably largely genetically determined, and abdominal obesity may also be, the hypertestosteronism of these conditions may represent a second genetically determined hormonal risk factor for breast cancer.
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PMID:Abnormal production of androgens in women with breast cancer. 784 May 9

Concerns about abnormal menstrual bleeding are a common reason for women to consult a primary care physician. The first step in the evaluation is to determine the patient's ovulatory status. Women with heavy bleeding but normal ovulatory cycles should be evaluated for coagulopathies, structural lesions, and hypothyroidism. In the absence of a systemic or structural cause, menorrhagia can be treated with OCPs or NSAIDs. Intermenstrual bleeding in OCP users may be due to noncompliance or the use of low-dose pills. Encouraging patient compliance and adjustment of the estrogen dose can often solve the problem. If the patient is not on OCPs, intermenstrual bleeding is usually due to a structural or inflammatory lesion. The differential diagnosis for anovulatory bleeding is extensive. Pregnancy, systemic illnesses, and structural lesions should be ruled out by history, physical examination, and laboratory evaluation. Endometrial biopsy is indicated in patients over age 35 and younger patients with risk factors for endometrial cancer, such as chronic anovulation and obesity. Dysfunctional uterine bleeding is a nonspecific term for abnormal uterine bleeding in the absence of systemic or structural disease. It is usually associated with anovulation. Adolescents frequently have dysfunctional uterine bleeding owing to immaturity of the hypothalamic-pituitary-ovarian axis. Perimenopausal women have an increased incidence of irregular bleeding secondary to decreased estrogen production by the ovary. Obesity, polycystic ovary syndrome, stress, crash diets, and vigorous exercise can all disrupt normal ovulatory function. Treatment options for dysfunctional uterine bleeding include oral contraceptives, cyclic progesterone, or hormone replacement with estrogen and progesterone. Patients with structural lesions or those who do not resume normal withdrawal bleeding patterns on hormone therapy should be referred to a gynecologist for further evaluation and treatment.
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PMID:Abnormal uterine bleeding. 787 94

Hyperandrogenism, insulin resistance, and obesity are common features of polycystic ovarian syndrome (PCOS). This study was designed to investigate the relationship among these factors and how they might contribute to ovulatory dysfunction in PCOS. Adrenal androgen secretion and insulin resistance were quantified in oligomenorrheic women with PCOS and in three groups of eumenorrheic women: weight-matched hirsute women, obese nonhirsute women, and thin nonhirsute women. Adrenal androgen secretion was defined as the androstenedione response to synthetic corticotropin. Insulin resistance was estimated by calculating the area under the curve for serum insulin levels in response to a 75 g oral glucose load. The mean serum androstenedione response (nmol/L) to corticotropin in PCOS (5.6 +/- 1.3) was greater than that in eumenorrheic hirsute women (3.4 +/- 0.5; P < 0.10), obese nonhirsute women (1.8 +/- 0.8; P < 0.05), and lean nonhirsute women (1.9 +/- 0.5; P < 0.05). The serum androstenedione response was not correlated with body mass index (BMI). The area under the curve for serum insulin (mU/L.min/1000) in PCOS (29.1 +/- 5.3) was greater (P < 0.001) than in eumenorrheic hirsute women (9.1 +/- 1.7), obese nonhirsute women (5.8 +/- 1.0), and lean nonhirsute women (4.5 +/- 0.4). The serum insulin response was highly correlated with BMI (P < 0.001) in the three groups of obese women, but women with PCOS became significantly more insulin resistant with increasing BMI (P < 0.02). There was no correlation between adrenal androgen secretion and insulin resistance in any of the groups. We conclude that adrenal hyperandrogenism and insulin resistance are independent predictors of anovulation in hirsute women. These conditions are present in both oligomenorrheic and eumenorrheic hirsute women, but are present to a greater extent in anovulatory women. Obese women with PCOS also differ from eumenorrheic controls by developing a greater degree of insulin resistance as body mass increases.
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PMID:The role of adrenal hyperandrogenism, insulin resistance, and obesity in the pathogenesis of polycystic ovarian syndrome. 838 5

Endometrial carcinoma is the most frequent malignancy of the female reproductive tract, and irregular vaginal bleeding is its most common symptom. It is most common among postmenopausal women and is associated with obesity, nulliparity, and anovulation. Oral contraceptive (OC) use and tobacco smoking have been reported to protect against it. A 30-year-old nulligravida nulliparous woman presented with menometrorrhagia. She had had normal menses since age 11, she had smoked a pack of cigarettes a day for 15 years, and had been obese since age 15 (weighing 302 pounds). At age 26, she started taking a combination OC containing .1 mg ethynodiol diacetate and 35 mcg ethynyl estradiol (EE). 4 years later she gradually developed menorrhagia which improved upon changing the OC to .3 mg norgestrel and 30 mcg EE. Subsequently she developed early cycle metrorrhagia and was placed on .5 mg norgestrel and 50 mcg EE. She continued having early and midcycle breakthrough bleeding with clots. Physical examination and test results including a PAP smear were normal. She was taken to the emergency department because of continued bleeding. The uterus sounded to 14 cm. Curettings were consistent with grade 1-2, well-differentiated adenocarcinoma of the endometrium. 3 weeks later, she had total abdominal hysterectomy, bilateral salpingo-oophorectomy, and peritoneal biopsy for cytological examination. The pelvis and the abdomen were free of metastasis. Histological examination revealed a superficially invasive, well-differentiated adenocarcinoma consistent with stage IB, grade 1%. Ploidy analysis uncovered 12.5% tetraploid, with 0% aneuploid or hyperploid cells with 8.5% of the cells in S phase and 21% in the proliferative phase. Both estrogen and progesterone receptors were positive. The ploidy analysis and receptor status were consistent with the low-grade nature of the lesions. Postoperative radiation was not recommended, and the patient was well 6 months postoperatively.
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PMID:Menometrorrhagia in an oral contraceptive user. 842 44


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