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

The clinical records and pathologic specimens from 150 patients with endometrial carcinoma were reviewed to test the hypothesis that constitutionally predisposed patients with evidence of endogenous hyperestrinism (i.e., obesity, hypertension, diabetes, nulliparity, leiomyomata, adenomyosis) have a more benign form of carcinoma than do patients who do not fit this profile. Our results do not support this hypothesis, but do reveal certain other prognostic indicators, in addition to factors relating to the tumor itself, including stage, grade, histologic type, and extent of invasion. These indicators include: (a) age and menopausal status--women over 50 years of age, and more impressively, postmenopausal women of any age, have less favorable histology, staging, and survival; (b) race--black women have higher-grade tumors, higher-stage tumors, and poorer survival rates than white women; (c) hyperplasia--when hyperplasia is found in the biopsy, curettage, or hysterectomy specimen, the accompanying carcinoma is of a much more favorable type and extent, and survival rates are significantly better. The reasons for these correlations are not fully understood, and possible explanations are discussed. There may be two distinct patterns of endometrial carcinoma: a prognostically favorable one arising on a background of hyperplasia predominantly in premenopausal women, and a prognostically unfavorable one, occurring principally in postmenopausal women without hyperplasia. Empirically, we advise pathologists to comment on the presence or absence of hyperplasia in any specimen in which endometrial carcinoma is diagnosed.
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PMID:Endometrial carcinoma: nontumor factors in prognosis. 401 9

It was shown that the risk for endometrial cancer development in uterine myoma increases 43-fold in cases of diabetes mellitus, hypertension and obesity, 20-fold in adnexitis, 15-fold in hyperplastic endometrial lesions and 9.8-fold in the multipara.
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PMID:[Risk factors for the development of endometrial cancer in uterine myoma]. 402 48

The association of endometrial carcinoma (EC) with endocrinopathies manifested by obesity, nulliparity, and/or increased estrogen levels of exogenous or endogenous estrogens is now well-known. EC is also seen in patients without these findings. Are these different cancers? Seventy-four cases of EC were reviewed and classified into two groups: group I, with associated adenomatous hyperplasia (AH), 31 cases; and group II, without associated AH, 43 cases. Group I included more well-differentiated and less invasive carcinomas; histologically, the pattern was glandular in all cases. In Group II, the EC were less well-differentiated, more invasive, and included, besides adenocarcinomas, clear-cell, papillary, and anaplastic carcinomas with giant tumor cells. Squamoid features were found in both groups. The possible existence of two types of EC, a hormonal-dependent EC associated with AH (which is believed to result from hyperestrogenism, and to have a better clinical prognosis), and an "independent" EC, not associated with AH, is discussed.
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PMID:Histologic correlates and virulence implications of endometrial carcinoma associated with adenomatous hyperplasia. 402 79

In a retrospective, epidemiological study of 414 patients with endometrial carcinoma, 73.4 percent were overweight and 55.8 percent were obese. The patients had a significantly greater absolute and relative weight than normal control subjects. A tendency was also apparent for height to be greater than in the controls. The patients had low fertility, early menarche and a tendency to late menopause, as well as a considerable premorbid consumption of estrogen preparations. Another characteristic of the patients was their low social class. The aetiology of endometrial carcinoma is presumably multifactorial. Long-term or increased estrogen stimulation of the endometrium plays a role, possibly potentiated by absence of progesterone influence. Obesity contributes to elevated estrogen level by the conversion of androstenedione to estrone in the fatty tissue. The diet depends on the social background and is significant for the development of obesity. Obesity, together with the amount and the composition of the food consumed, might predispose to endometrial cancer by elevated production of endogenous estrogen.
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PMID:Endometrial carcinoma. A retrospective, epidemiological study. 404 96

In a series of 173 consecutive patients with endometrial cancer treated by a fixed protocol 62 tumors (36%) appear "estrogen independent," i.e. there is no history of estrogen ingestion and no recognized risk factors such as obesity or diabetes mellitus. A high proportion of these tumors are of advanced stage and grade. Prognosis is poorer and mortality higher than for "estrogen-dependent" tumors. Twenty-two tumors were truly occult (no spontaneous vaginal bleeding). Factors which identify this high-risk group are described and the reasons for delay in diagnosis discussed. Spread by intraperitoneal dissemination is considered a major factor in the poorer prognosis. Cytology of peritoneal washings is a useful diagnostic and prognostic aid. An estrogen provocation test is suggested as a means of earlier recognition which could reduce mortality in this group.
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PMID:Occult, high-risk endometrial cancer. 405 14

Many studies indicate that obesity is associated with postmenopausal breast cancer and cancer of the endometrium. The mechanisms by which obesity contributes to cancer risk is not known, although increases in serum estrone from delta 4-androstenedione by the adipose tissue have been implicated in postmenopausal women. Blood estrogens increase with the degree of obesity and aging. In animal experiments the confounding of high fat, low carbohydrate, and high calorie diets needs to be defined. The effects of diet on estrogen metabolism; the relationship of fatty acids from animal, vegetable, and marine sources to tumor formation; and the mechanisms by which energy intake influences cancer risk need to be precisely defined. Any estimate of the contribution of heredity to the burden of human cancer is impossible until we have a better understanding of genetic and environmental interactions.
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PMID:Fat intake, obesity, and cancer of the breast and endometrium. 406 99

This prospective study determines the presence of a consistent endocrine disturbance in patients with endometrial carcinoma. A major requirement of the study was an unbiased control group matched as to age, race, economic status, and primary reason for referral. All patients with untreated endometrial carcinoma or postmenopausal bleeding were studied and grouped into: 1) endometrial carcinoma (n=56), and 2) atrophic endometrium (n=83), or the "bleeding" controls. Average age of patients with carcinoma was 63.9 years and that of controls, 61.3 years. Factors studied were glucose metabolism, estrogenic activity, gonadotropin excretion, obesity, hypertension, time of climacteric, fertility, and menstrual history. By averaging deviations from ideal weight, cancer patients were found to be 13.1 pounds heavier than the control group (49.8 pounds vs. 36.7 for the controls). Analysis of fertility data showed that age at time of marriage in patients who were parous compared with those who were nulliparous was 20.1 and 26.8 years respectively for the carcinoma group, and 20.4 and 27.5 years for the bleeding controls. Of parous cancer patients, 6.3% used contraception vs. 13% of the controls. These data do not suggest that pregnancy prevention by late marriage or contraception plays a significant role in the later development of endometrial carcinoma. Hypertension, time of menopause, diabetes, estrogenic activity, and gonadotropin excretion did not exhibit significant effects in the development of carcinoma. The findings support those of Corscaden, Fertig, and Gusberg that obesity and infertility are statistical concomitants with endometrial carcinoma but contradict current belief that there is direct evidence of abnormal endocrine state (e.g., glucose metabolism, estrogen stimulation, or anterior pituitary activity).
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PMID:Endocrine factors in endometrial carcinoma. A preliminary report. 601 48

Menopausal disorders coincide with the onset of luteal insufficiency and the resulting relative hyperestrogenism. At this stage the risks to be assessed are mainly related to a worsening of the menstrual syndrome (heaviness of the legs, abdominal distention, water retention, mastodynia, depressive syndrome), cycle changes, or various genital types of hemorrhage requiring investigation for detection of a possible fibroma, hyperplasia, endometriosis, or genital cancer. Once the menopause is settled a reduction in estrogen levels comes with reactive increases in FSM and LM levels, and the principal risk is the development of a cancer. The role of endogenous (obesity, diabetes, Stein-Leventhal, adenomatous hyperplasia) or exogenous (prolonged estrogen therapy alone) estrogens has to be evaluated in endometrial cancer. Cancer of the vulva also appears to be more frequent in menopausal women (natural or artificial), as well as cervical cancer and cancer of the breast. There is an apparent increase in cardiovascular risks in untreated menopausal women, but this is still discussed, as to the benefits of estrogen therapy.
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PMID:[Menopausal risk factors (author's transl)]. 625 25

The epidemiologic study of 74 invasive endometrial adenocarcinomas seen over five years confirms the following well-known risk factors: early menarche, disorders of menstruation, hypofertility, and late menopause. Obesity, a positive family history and the presence of another cancer are common findings. Hormone dependent endometrial cancer provides a valuable opportunity for studying hormone and cell receptor concentrations. Hormone dependency has a practical bearing on certain preventive measures and perhaps on a new therapeutic approach to this type of cancer.
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PMID:[The epidemiological study of endometrial adenocarcinoma. From 74 cases seen at the Saint-Antoine Maternity Hospital]. 632 Mar 78

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


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