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

The effect of smoking on the development of breast, endometrial, and ovarian cancers is evaluated among cases identified between November 1980 and July 1982 in the Iowa Surveillance, Epidemiology, and End Results Cancer Registry. Population-based, age-frequency matched controls were also evaluated, adjusting for potential confounders: Age, age of menarche, age of menopause, duration of menses, female family reproductive cancer history, obesity, parity, infertility, and lifetime steroid hormone use. Logistic regression analyses of total pack-years of cigarette exposure indicate that smoking is not significantly related to the development of breast cancer [relative risk (RR) = .99; confidence interval (CI) = .97, 1.02] or ovarian cancer (RR = 1.00; CI = 1.00, 1.00). Among women with endometrial cancer, the risk for those who smoke is increased among premenopausal women (RR = 1.27; CI = .65, 2.59) and decreased among postmenopausal women (RR = .41; CI = .16, 1.04).
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PMID:Effects of smoking on the development of female reproductive cancers. 658 29

Much is known about the pathophysiology and pathogenesis of the polycystic ovary syndrome (PCO). The key clinical features are inappropriate gonadotropin secretion, altered production rates, binding and metabolism of steroids and androgen excess, all resulting in defeminization, anovulatory infertility, obesity and endometrial hyperplasia. Management should be based on the patient's reproductive goals. Adjunct measures can control hirsutism.
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PMID:The polycystic ovary syndrome. 668 20

Twenty-three women considered to have polycystic ovarian disease (PCO) were studied in an effort to better understand the mechanism of inappropriate secretion (IGS) which is so characteristic of these women. Criteria for PCO included oligomenorrhea, infertility, an obesity index (ponderal index, PI) < 12, and an LH:FSH ratio > 3. The mean +/- SE weight and PI for this group were 175 +/- 7.5 lbs. and 11.2 +/- 0.2 respectively. Weight was not correlated with steroid levels in PCO or control women. The mean (+/- SE) of serum androgen concentrations (DHEA-S: 2.9 +/- 0.5 micrograms/ml; androstenedione: 2.6 +/- 0.3 ng/ml; and testosterone: 47 +/- 5 ng%) were all significantly higher than those in control women (p < .05). Total serum estradiol (E2) was comparable to those of controls in the follicular phase, while estrone (E1): E2 ratios averaged 2:1. Serum sex hormone binding globulin-binding capacity (SHBG-BC) averaged 56.8 +/- 4.2 nM which was significantly lower than that of controls (p < .05). The percent unbound E2 was significantly elevated in PCO (62% vs 37%). The mass of unbound E2 was also significantly higher in PCO women (40 +/- 3 pg/ml) than in controls (17 +/- 2 pg/ml) (p < .005). Serum LH:FSH ratios had a positive correlation with the relative and absolute concentration of unbound E2. In control women, unbound E2 correlated significantly with LH levels. This suggests that IGS characteristically found in PCO patients and exemplified by elevated LH;FSH ratios, is the result of the feedback response to elevated levels of unbound (i.e., biologically active) E2.
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PMID:Elevations in unbound serum estradiol as a possible mechanism for inappropriate gonadotropin secretion in women with PCO. 677 90

The author presents a hypothesis that the complex of endocrine and metabolic disturbances arising long before the development of endometrial carcinoma determines the biological peculiarities of the tumor, its clinical course, and the prognosis of the disease. On the basis of a prospective study of 366 patients with endometrial carcinoma, the author postulates that there are two different pathogenetic types of endometrial carcinoma. The first pathogenetic type of the disease arises in women with obesity, hyperlipidemia, and signs of hyperestrogenism: anovulatory uterine bleeding, infertility, late onset of the menopause, and hyperplasia of the stroma of the ovaries and endometrium. The second pathogenetic type of the disease arises in women who have no signs stated above or these signs are not clearly defined. The frequency of the first pathogenetic type in the studied group of women was 65%, whereas the frequency of the second type was 35%. The peculiarities outlined above which are characteristic of the first pathogenetic type of the disease determine the development of highly and moderately differentiated tumors (82.3% G1 and G2), superficial invasion of the myometrium (69.4%), high sensitivity to progestogens (80.2%), and favorable prognosis (85.6% 5-year survival rate). In patients who have the second pathogenetic type of endometrial cancer when endocrine and metabolic disturbances are absent or occult, poorly differentiated tumors arise (62.5% G3), a tendency to deep invasion of tumor into the myometrium is observed (65.7%); high frequency of metastatic spread into the pelvic lymph nodes (27.8%); decrease of sensitivity to progestogens (42.5%); and doubtful prognosis (58.8% 5-year survival rate) are noted.
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PMID:Two pathogenetic types of endometrial carcinoma. 682 61

We have carried out a prospective survey of 25 cases of male hypogonadism attending one hospital, and a retrospective study of 73 men attending other endocrine clinics in Manchester. In total, 47 had pituitary disorders, 15 isolated gonadotrophin deficiency (including 4 with Kallmann's syndrome), 10 testicular atrophy of unknown cause, 12 testicular damage, 10 with Klinefelter's syndrome, and 4 had miscellaneous disorders. Our survey emphasises the importance of adequate history and examination. Most patients presented with reduced libido, with marital problems in 62% of married men. Less common problems were facial flushing, osteoporosis and gross obesity. Several patients with pituitary disorders were asymptomatic, even in the presence of visual field defects. Klinefelter's syndrome, and testicular atrophy, may present with infertility or gynaecomastia rather than symptoms of androgen deficiency. On examination, the presence of gynaecomastia or obesity were of no help in differential diagnosis, whereas visual field defects clearly indicated a pituitary cause. Measurement of height/span was of little help. The precise diagnosis was usually established with basal plasma LH, FSH, testosterone and prolactin, with karyotype and pituitary radiology, and without more elaborate dynamic hormone tests. Testosterone esters given by intramuscular injection as "Sustanon 250" was the most commonly used replacement therapy. Improved libido usually resulted. Side-effect occurred in 10%, usually as muscle cramps, pain at the injection sites, acne, or excessive sex drive. One tragic case illustrates the potential dangers of androgen replacement therapy in an unrecognised psychopath, and where doubt exists a psychiatric opinion should be sought before starting therapy.
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PMID:Clinical aspects of androgen deficiency in men. 689 Jul 81

The importance of late-onset congenital adrenal hyperplasia as a cause of hirsutism is controversial. Two of 35 women with a chief complaint of hirsutism met the criteria of 21-hydroxylase deficiency. In one, who presented with hirsutism, oligomenorrhea, obesity, infertility, and enlarged cystic ovaries, the initial diagnosis was polycystic ovarian syndrome. Family data showed that her disorder was autosomal recessive and linked to the histocompatibility leukocyte antigens (HLA), as in the classic form of congenital adrenal hyperplasia. Carriers were thus detectable by HLA typing. Thus late-onset congenital adrenal hyperplasia appears to be an allelic variant of congenital virilizing adrenal hyperplasia with a milder enzymatic defect. The diagnosis cannot be made clinically because the disease has the same presentation as idiopathic hirsutism or polycystic ovarian disease. Basal plasma 17-hydroxyprogesterone levels, unlike in classic congenital adrenal hyperplasia, can be normal, and an ACTH stimulation test or sequential measurements of plasma 17-hydroxyprogesterone throughout the day may be needed to show the abnormality. The incidence among hirsute women is estimated to be 6% to 12%, and the calculated gene frequency for the allele coding for attenuated expression of 21-hydroxylase deficiency is 0.015 to 0.057.
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PMID:Late-onset 21-hydroxylase deficiency mimicking idiopathic hirsutism or polycystic ovarian disease. 697 82

A review of literature, mainly the results of studies conducted in America, shows obesity, diabetes mellitus, hypertension, infertility/nulliparity, late menopause, high endogenous oestrogen production, and the use of oestrogens to be the main factors associated with the development of endometrial carcinoma. Whilst most of these factors undoubtedly apply irrespective of country, doubt in Finland about the use of oestrogens being a risk factor was one of the reasons prompting the study reported here. This study, which was conducted in Turku, Finland, involved 318 endometrial carcinoma patients, 282 of whom could be paired with controls matched for age, height and weight, and social class. The data show the use of oestrogens per se not to be a risk factor. The fact that there appears to be a risk in America, where most of the oestrogenic preparations used are based on conjugated equine oestrogens, but not in Finland, where the preference is for preparations based on oestriol and oestradiol and where conjugated oestrogen preparations are relatively rarely used, supports the hypothesis that the risk depends on the type of oestrogen used.
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PMID:Endometrial carcinoma risk factors, with special reference to the use of oestrogens. 699 4

Cancer prevention as related to the problem of cervical and endometrial cancer involves a great number of factors that are considered contributory to the development of neoplasms in the uterus. Lifestyles encouraging the development of cervical cancer are different from those encouraging endometrial cancer. Cancer of the cervix is a disease of the inner city. It is seen in those staring intercourse in their teens, having multiple partners, having many children, and coming from the low socioeconomic groups. Semen and herpes virus II may have an adverse effect on immature cells, but there are no hard data to confirm these roles. Cancer of the endometrium is a disease of suburbia. The American Cancer Society estimates that there will be 38,000 new cases of endometrial carcinoma in 1980, making it the most common female genital cancer. Women at highest risk for later carcinoma of the endometrium are those who have obesity, diabetes, infertility, irregular menses and failure of ovulation, adenomatous hyperplasia, and/or prolonged estrogen administration. For both cervical and endometrial cancers, it is possible to identify the high-risk patient, to detect changes at an early stage, and, by instituting appropriate therapy, to prevent a more serious problem. It is obvious that prevention, detection, and treatment are all closely intertwined. This paper identifies the patient at high risk and makes suggestions for correcting any imbalance that may predipose to the development of invasive cancer.
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PMID:Uterine cancer (prevention). 723 68

Hirsutism usually results from a subtle excess of androgens. As such, it is a clue to possible endocrine disturbance in addition to presenting cosmetic problems. We use the term hirsutism to mean male-pattern hirsutism--excessive growth of hair in areas where female subjects normally have considerably less than male subjects. An elevation of the plasma free (unbound) testosterone level is the single most consistent endocrinologic finding in hirsutism. The plasma free testosterone level is sometimes elevated when the total level of plasma testosterone is normal because testosterone-estradiol--binding globulin (TEBG) levels are often depressed in hirsute women. Frequent blood sampling is sometimes necessary to demonstrate subtle hyperandrogenic states since androgen levels in the blood are pulsatile and seemingly reflect episodic ovarian and adrenal secretion. The source of hyperandrogenemia can usually be determined from dexamethasone suppression testing. Those patients whose plasma free androgen levels do not suppress normally usually have functional ovarian hyperandrogenism (polycystic ovary syndrome variants). Very high plasma androgen levels or evidence of hypercortisolism, which is not normally suppressible by dexamethasone, should lead to the search for a tumor or Cushing's syndrome. Those patients in whom hyperandrogenemia is suppressed normally by dexamethasone have a form of the adrenogenital syndrome, a prolactinoma, obesity, or idiopathic hyperandrogenemia. In such patients, glucocorticoid therapy may reduce hirsutism and acne and normalize menses. The treatment of hirsutism resulting from functional ovarian hyperandrogenism is not as satisfactory; estrogen-progestin treatment is the most useful adjunct to cosmetic approaches to hirsutism in this country. However, other manifestations of polycystic ovary syndrome, such as infertility, may take precedence over hirsutism when an optimal therapeutic program is designed for many patients.
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PMID:Hirsutism: implications, etiology, and management. 725 62

A reappraisal of endometrial cancer over the past decade reveals: 1) new concepts in its pathologic nature; 2) increase in incidence; 3) acceptance of the theory of hormonal relation; and 4) acceptance of individualization of treatment. Although endometrial carcinoma is still thought of as a predominantly well-differentiated adenocarcinoma, an increase in more virulent tumors has been seen in recent years. These include: adenosquamous carcinoma; adenoacanthoma; mesodermal sarcomas; and adenometous hyperplasia. Women at high risk for these tumors include those suffering from obesity, infertility, failure of ovulation, dysfunctional uterine bleeding, and those on long-term estrogen therapy. These women can be recognized and monitored by means of endometrial biopsy of the aspiration-curettage type. Adenomatous hyperplasia, the precursor of cancer, requires treatment with progestin or hysterectomy according to patient's age and reproductive status. Estrogens should be used only when indications are clear and in the smallest possible dose for the shortest period of time until the therapeutic goal is achieved. Aggressiveness of treatment should correspond to virulence of tumor. Dilatation and curettage under anesthesia should be used for clinical staging of endometrial cancer. Other means of treating endometrial cancers' include: total hysterectomy; bilateral salpingo-oophorectomy; iliac-aortic lymphadenectomy; pelvic irradiation; radical hysterectomy; chemotherapy, and a drug regimen (including cyclophosphamide, doxorubicin, fluorouracil, megestrol acetate).
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PMID:Current concepts in cancer: The changing nature of endometrial cancer. 735 80


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