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

A relationship between exposure to exogenous estrogens and endometrial carcinoma has been reported in numerous studies. The incidence among those so exposed has been estimated to have been increased from 7.5 to 8 times that of those not exposed. Long-term therapy with estrogens for menopausal symptoms has been the usual history. Breast cancer patients treated with estrogens and young women taking sequential oral contraceptives have had increased risks. In this study, the records of Olmsted County, Minnesota, residents with endometrial uterine cancer diagnosed between 1945-1974 at the Mayo Clinic or at other medical facilities were reviewed. There were 122 adenocarcinomas and 23 adenoacanthomas. In 3 instances, adenocarcinomas contained zones of uterine sarcoma. For each of the 146 patients there were 4 age-matched controls. Estrogen use for 6 months or more was recorded for 39 (27%) of the 145 cases and for 163 (28%) of the 580 controls. The controls had more frequent histories of short-term estrogen therapy. Cancer patients had relatively more estrogen use for menopausal symptoms. The relative risk of endometrial cancer tended to increase with the duration of exposure to conjugated estrogens from 2.0 with any exposure to 4.9 (p less than .01) after 6 months or more and to 7.9 after 3 years or more. The risk increased with larger doses (1.25 mg or more) and with continuous administration of conjugated estrogen. Myometrial invasion was superficial in 77 cases and deep in 44 cases. Long-term use of conjugated estrogen was frequently associated with low-stage low-grade superficially invasive endometrial malignancy. The 5-year survival rate of the 145 patients was 85%. Patients with Stage 1 had a 95% relative 5-year survival rate. Those with Stages 2, 3, or 4 had 50% survival rates. Of other risk factors, obesity and nulliparity were noted. Patients had more frequent records of benign cystic adenoma and of adenomatous hyperplasia than controls. The corrected age-specific rate for endometiral cancer increased to a maximum of about 90/100,000 population per year in the group aged 55-64 and then diminished with age. An increase in endometrial cancer among those at risk may have been nullified by an increase in those who have had a hysterectomy. In this study the incidence of endometrial carcinoma in Olmsted County does not show an increase in the last 3 decades. It is noted that the long-term use of conjugated estrogens in this area has been relatively low.
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PMID:Exogenous estrogen and endometrial carcinoma: case-control and incidence study. 19 Aug 87

At the Wilford Hall U.S. Air Force Base Medical Center, Texas, about 4000 postmenopausal women received estrogen replacement therapy during 1975. Of these, 2700 took estrogens only and 1240 were given a progestogen along with estrogen. Hysterectomy had been done previously on 1700 patients (42%), leaving 2300 with intact uteri and a risk of endometrial cancer. Adenocarcinoma of the endometrium was diagnosed in 7 patients. Of these, 6 had received estrogen therapy. There was 1 endometrial malignancy in a patient also receiving a progestogen. Among 510 untreated postmenopausal women with intact uteri, 1 adenocarcinoma of the endometrium was found. Type and dosage of estrogen were unrelated to endometrial malignancy. In addition to the 7 endometrial cancers from the clinic, 22 cases were diagnosed elsewhere and referred for treatment, 11 of these had received no hormones. 10 were taking estrogens and 1 was receiving Oracon for birth control. The incidence of endometrial malignancy in the U.S. is reported to be 21/100,000 women/year. There is a 3-fold to 9-fold increased risk of endometrial cancer associated with obesity alone. The probability that untreated postmenopausal women with intact uteri will develop carcinoma of the endometrium is 1/1000/year. With estrogen users, it is reported to be increased -7.6/1000 women/year. In the author's clinic during 1975, the incidence among those receiving only estrogen was 4.7/1000. Among those also receiving a progestogen the incidence was .8/1000. Unopposed estrogens apparently have a role in the etiology of endometria hyperplasia and neoplasia through incomplete shedding of the endometrium. Progesterone produces more complete sloughing of the endometrium and also converts all degrees of hyperplasia into secretory endometrium. Nulliparity, infertility, and anovulation are predisoposing factors to endometrial carcinoma. Progestogens are palliative therapy for endometrial cancer.
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PMID:Estrogens, progestogens and endometrial cancer. 19 79

A matched pairs analysis of 130 cases of endometrial cancer was undertaken to determine the relationship between post-menopausal estrogen treatment and endometrial cancer. 90% of the cases were in FIGO stage I, 6.9% stage II, and 2.3% stage III. The matching took place according to a wide range of criteria, e.g. age at menopause, age at diagnosis, no. of births, weight, etc., within certain tolerances. After the matching was finished, the information on estrogen use was collated, and the relative risk (RR) for various estrogen preparations was calculated according to the length of estrogen treatment. The number of estrogen users was smaller among the women with endometrial cancer than among the control group (p .01); the RR of endometrial cancer does not increase with estrogen use (RR=.44). The same held true when conjugated estrogens, estriol, estradiol, estrogen-androgen preparations, and ovulation inhibitors were considered separately (.05 p . 05). The RR of endometrial cancer does not increase with the length of estrogen treatment. It was also observed that the RR of endometrial cancer was significantly lower (p .01-.001) among women with predisposing factors such as hypertension, obesity, and nulligravidity. This suggests that the risk of endometrial cancer is not increased by estrogen treatment.
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PMID:[Estrogen therapy and carcinoma of the endometrium (author's transl)]. 21 85

Perimenopausal and postmenopausal substitutive estrogen treatment is valuable if prescribed according to proper indications and in the proper manner. Studies have shown a correlation between menopausal estrogen treatment and endometrial cancer. Siiteri hypothesized that estrone was the estrogen with a specific carcinogenic effect. A study undertaken in California indicates, however, that conjugated estrogens are associated with a lower risk of endometrial cancer. There is also strong indications that certain factors predispose a woman to endometrial cancer during menopausal estrogen treatment: obesity, the Stein-Leventhal syndrone, the Turner syndrome, hirsuitism caused by increased androgen activity, and family history of endometrial cancer. Menopausal estrogen treatment is prescribed in cases of menstrual disturbances, neurovegetative or vaso-motor disturbances, psychological disturbances, atrophy of the urogenital tract, or cases of calcium or fat metabolism disturbances which could lead to osteoporosis or arteriosclerosis.
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PMID:[Estrogen substitution and endometrial carcinoma]. 21 33

A review of the literature concerning the relationship between menopausal estrogen treatment and endometrial carcinoma is presented. Results from animal studies indicate that estrogens may work in conjunction with carcinogenic substances to stimulate proliferation of cancerous growths. Since estrone is produced by fatty tissue, obesity and certain correlated diseases, such as hypertension or diabetes, may be predisposing factors to developing endometrial cancer. Other risk factors are a hereditary predisposition and age. Several American epidemiologica studies showed an increased risk of developing endometrial cancer among women who undergo hormone treatments during menopause. It must be remembered, however, that such studies cannot establish causal relationships. Also, in the American studies, several biases complicate evaluation of the data, e.g. a disregard for social factors, the uncertainty of the state of the endometrium before the beginning of the study, and the inclusion of the problematic "stage 0" into the study. Furthermore, in America there is a tendency to proscribe estrogens alone in high dosages for menopausal treatment over long periods of time. It is concluded that individually determined low-dosage cyclical estrogen therapy during menopause does not increase the risk of endometrial cancer.
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PMID:[Oestrogens during the menopause and the risk of endometrial carcinoma (author's transl)]. 21 69

An increasing incidence of endometrial cancer caused by a higher life expectancy and a number of other facters (i.e. obesity, diabetes, hypertension, lower pregnancy rate) as well as the unfavorable location for early detection when compared with cervical cancer has initiated this review in order to single out women with increased risk. Clinical characteristics of patients with endometrial cancer represented by age, menstrual disorders, reduced fertility, obesity, diabetes, hypertension, hirsutism, hyperplasia of the ovarian stroma or hilus cells in connection with an increased oestrogen effect in the vaginal smear and proliferative changes of the endometrium can be explained by extraglandular respectively peripheral aromatization of androgens to oestrogens, particular by the conversion of androstenedione to oestrone. This is supported by an increased plasma oestrone/oestradiol-ratio and increased conversion rate with age and overweight. In vivo- and in vitro-investigations have demonstrated the participation of adipose tissue in peripheral oestrogene production. The compiled data point towards the importance of the extraglandular oestrone production for the etiology of endometrial cancer by effecting the endometrium over a long period of time. The counter action of the normally cyclic changes of oestradiol and progesterone is lacking. Therefore, a dysoestrogenic effect of oestrone upon the endometrium can be fully effective, depending on the hormone receptor content of the respective endometrium. Based upon these data including recent publications, pre- and postmenopausal oestrogen therapy has to be critically reevaluated.
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PMID:[Endometrial cancer and extraglandular oestrogen biosynthesis (author's transl)]. 32 98

The factors that increase the risk of development of endometrial cancer are reviewed. Many of these conditions are frequently associated with an elevated production of estrone in peripheral (nonendocrine) tissues from circulating androstenedione. Elevated estrone production may occur in young, anovulatory or postmenopausal women whose ovaries secrete higher than normal amounts of androstenedione. Alternatively, conditions such as obesity and liver disease are associated with higher than normal rates of conversion of androstenedione to estrone, resulting in high estrone levels. Neither the exact tissue site(s) of conversion nor the normal function of this process has yet been established. Much less information concerning steroid hormone receptor measurements in endometrial cancer than in breast cancer is available. However, it seems certain that measurement of progesterone receptors will provide a useful guide in the selection of progestational therapy.
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PMID:Steroid hormones and endometrial cancer. 35 36

The purpose of this study was to ascertain if a relationship exists between the transfer constant of conversion of plasma androstenedione to estrone ([rho]AE1BU) and total body weight or excessive body weight in 50 postmenopausal women, of whom 25 had adenocarcinoma of the endometrium and 25 had no endometrial disease. The [rho]AE1BU ranged from 0.015 to 0.129 in these 50 women. The [rho]AE1BU in the women with endometrial cancer was 0.051 +/- 0.006 (mean +/- S.E.), whereas that in the women with no endometrial disease was 0.039 +/- 0.004. These values are not significantly different (p greater than 0.05). The body weights of these 50 women ranged from 104 to 430 pounds. The weight of the patients with endometrial cancer was 234 +/- 16 pounds (mean +/- S.E.), and that for the women with no endometrial disease was 194 +/- 12 pounds. A statistically significant correlation (p less than 0.001) was found between [rho]AE1BU and body weight and between [rho]AE1BU and excessive body weight in both groups of women. Moreover, obesity and aging appear to act in concert to potentiate the conversion of plasma androstenedione to estrone in extraglandular sites since the [rho]AE1BU is considerably greater among obese postmenopausal women than among comparably obese premenopausal women.
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PMID:Effect of obesity on conversion of plasma androstenedione to estrone in postmenopausal women with and without endometrial cancer. 62 89

During a 25 year period in a university hospital gynecology service, 300 obese women, weighing 200 pounds or more, underwent abdominal total hysterectomy. In comparison with nonobese controls, the overweight patients were more likely to have carcinoma of the endometrium, hypertension and diabetes mellitus. Postoperatively, the most striking difference between the obese and nonobese groups was in the incidence of wound complications, with no significant difference in the occurrence of other disorders. The incidence of wound complications was 29 per cent with obesity, seven times that in patients of normal weight, and all types of wound disorders, except evisceration, occurred more frequently in obese patients. Among identifiable factors potentially responsible for wound infection were an increased incidence of diabetes, longer operating time and greater blood loss in overweight patients. The increased incidence of wound infection was responsible for greater febrile morbidity and the more frequent need for prolonged hospitalization. The mortality rate was 1 per cent in the obese group and zero per cent in the control group, a statistically insignificant difference. Since abdominal hysterectomy in obese women is associated with increased risk of morbidity, although not necessarily of mortality, obesity per se should rarely, if ever, contraindicate necessary surgical therapy. In situations in which surgical treatment is more elective, its complications should be borne in mind.
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PMID:Abdominal hysterectomy in obese women. 76 2

There is increasing epidemiological evidence that nutrition plays a dominant role in the pathogenesis of several types of human cancers. There is considerable epidemiological evidence showing that alcoholism in part because of associated nutritional deficiencies, significantly increases the risk of smokers for cancer of the alimentary tract. There is also some suggestion that nutritional deficiencies may relate to cancers of the stomach, cervix, and thyroid. Of particular importance, and based on relatively new concepts, are data indicating that overnutrition significantly affects the development of certain cancers, including cancers of the colon and pancreas, kidney, breast, ovary endometrium, and prostate. Except for cancer of the endometrium, and kidney cancer in women, there is no significant relationship to obesity. Rather, the evidence suggests both epidemiologically and experimentally that the etiological factors relate to a high intake of fats and possibly other variables associated with high fat intake. While we are investigating the mechanistic nature of the epidemiological and experimental observations, the question that needs to be asked is whether it is not prudent for us to associate ourselves with the recommendation of our colleagues in the cardiovascular disease field who call on both individuals and the food industry to practice a "Prudent Diet," i.e., one that is lower in total calories, total fat, saturated fats and cholesterol than is the present American diet.
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PMID:Nutrition and cancer. 77 Feb 4


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