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

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

Corticosteroids inhibit the differentiation of adipocyte precursor cells in the presence of fetal calf serum. This inhibition is more pronounced in serum-free media or in the presence of serum, extracted free from steroid hormones. Progesterone antagonized this inhibition in serum-free media and in media with extracted serum, and caused an increased differentiation in media with sera where corticosteroids had not been removed. Corticosteroid hormones bind specifically to these cells. The binding is saturable and has a Kd in the order of circulating hormonal concentrations. Progesterone competes effectively with this binding at physiological concentrations. Progesterone is also bound to these cells but 17-beta-estradiol, is not. Neither of these hormones shows effects alone or in combination with each other on the development of new adipocytes in the system in question. It was speculated that the effect of progesterone to release corticosteroid inhibition of adipose precursor cell differentiation might be of importance during pregnancy, and contribute to the risk of development of hyperplastic obesity.
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PMID:The effects of steroid hormones on adipocyte development. 208 10

As a second line therapy after failure to previous therapies, a combination therapy with MPA 1,200 mg po and 5'DFUR 1,200 mg po daily was given to 31 patients with recurrent breast cancer. At a median follow up period of 18 months, the overall response rate was 42%. The response rates for bone and visceral lesions were still good for the second line therapy. Patients previously exposed to tamoxifen (24 patients), 5-FU or its derivatives (21) and/or adriamycin (18) had response rates of 42%, 33%, 33%, respectively. The median duration of response in responders was 10 months. The overall median survival for the entire series was 9 months after start of the treatment. Thirteen (81%) of 16 patients with bone lesions were relieved from their bone pain. It is of special interest that the pain relief was also obtained in 7 out of 10 NC/PD patients with bone lesions, resulting in much improvement of their performance status. Side effects included obesity 52%, edema of the leg 35%, diarrhea 16% and so on. One patient developed venous thrombosis of her lower extremities and 4 were suspected to have the same condition. Fifty-five % of the patients underwent dose reduction of MPA at the 5th month of treatment in a median. This combination therapy is useful for recurrent disease even in late stages, so long as close observation is made for the occurrence of thrombosis.
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PMID:[Combination therapy with 5'DFUR and MPA as a second line treatment for advanced/recurrent breast cancer]. 214 Oct 52

Ninety-five patients diagnosed as having stage I endometrial carcinoma (EC) were divided into two groups, one with associated adenomatous hyperplasia (AH; group 1) and the other without (group 2). Adenomatous hyperplasia results from estrogenic stimulation of the endometrium. Therefore, patients in group 1 are considered to have an estrogen-related EC. Group 1 included 49 patients with an average age of 59; group 2 included 46 patients with an average age of 65. Review of the histologic characteristics of EC showed that group 1 tumors are better differentiated and less invasive and that their morphology is closer to the normal glandular structure of the endometrium. Group 2 tumors are less well differentiated, more often invade the myometrium, and include histologic variants such as papillary, clear cell, and anaplastic carcinoma that are dissimilar from the glandular structure of the normal endometrium. Mucinous adenocarcinomas and the presence of stromal foam cells were found to be associated with group 1 EC. Progesterone receptors (PR) were measured in a sample of 30 patients. They were present in all cases of group 1 ranging from 50 to 2,400 fmol/mg protein and absent or very low (30-190 fmol/mg protein) in group 2. All EC with stromal foam cells had high PR (380-2,400 fmol/mg protein). This study confirms that estrogen-related EC is generally a better differentiated and less aggressive tumor and suggests that there are two types of EC. The tumors not related to estrogens, which are histologically more malignant, were seen in an older age group of patients. In addition to the currently accepted methods of clinical evaluation of EC patients, defining the morphologic and biochemical characteristics of two types of EC may contribute to the management of EC, now the most prevalent cancer of the female pelvis. The patients known to be at risk for endometrial carcinoma, identifiable by abnormal hormonal manifestations (obesity, infertility, and other conditions related to hyperestrogenism) as well as those receiving exogenous estrogens are likely to develop a better differentiated and less aggressive form of neoplasia. It would be important to elaborate a system of early detection of EC in the group of elderly patients with no signs of hyperestrogenism prone to develop the less differentiated and biologically more aggressive tumors.
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PMID:Endometrial carcinoma: two diseases? 356 22

Synthetic progestins derived from nortestosterone provide a promising contraceptive alternative for women with contraindications for estrogens. Progesterone and synthetic progestins reduce vasodilatation and edema induced by estrogens and stop estrogen-dependent cellular multiplication in target tissue. Progestins have 2 kinds of contraceptive affect: antigonadotropic action at sufficient doses, and peripheral action at lower doses. The cervical mucus is modified in composition and volume, becoming hostile to sperm; the endometrial mucus atrophies; and tubal motility is slowed. High dose progestins are administered from the 5th or 10th to the 25th cycle day, with the earlier date preferred for women with shorter cycles. They are an ideal method for women with endometrial hyperplasia or benign breast disease or histories of breast or uterine cancer, as well as for women over 40 with dysovulatory cycles. Contraindications to high dose progestins include obesity, hypertension, lipid metabolic anomalies, and diabetes. Low dose progestin-only pills are administered at the exact same time each day including during menstruation. They are attractive for some women because they contain no estrogen, a reduced progestin dose causing fewer headaches and less somnolence, and fewer metabolic effects. Low dose progestins are indicated for lactating women, those with contraindications to estrogens such as obesity, hypertension, hyperlipidemia, and diabetes, and those with renal or cardiac insufficiency with valvulopathy. Low dose progestins are also indicated for nulliparas and other women for whom IUDS are contraindicated. Women using low dose progestins should never take drugs that act as enzymatic inductors, which speed hepatic degradation of steroids and reduce their efficiency. A resulting pregnancy is likely to be extrauterine because of slowed tubal transport. The failure rate of low dose progestins ranges from .9-3%, with higher failure rates among younger women. About 30% of users initially experience spotting, which despite its usual disappearance after 2-3 months of use is the most common reason for discontinuing the method. Low dose progestins have no metabolic or vascular effects, but they may cause a relative hyperestrogenism is some users. Other modes of administration of progestin contraception include continuous high doses, never justified solely for contraception. Trimonthly injections of medroxyprogesterone acetate of norethindrone enanthate provide contraception through a long lasting antigonadotropic effect. Metrorrhagia and amenorrhea are among possible side effects. The method is used primarily in developing countries where its ease of use is a major advantage. Subcutaneous implants releasing continuous doses of levonorgestrel provide contraceptive protection for over 5 years. The cumulative failure rate is 1.7 at 5 years. Metabolic tolerance is good. The major side effect is menstrual irregularity.
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PMID:[Progestational contraception]. 365 94

In order to study the effect of obesity or underweight on gonadotropins and steroid hormone levels, serum concentrations of FSH, LH. Testosterone, Estradiol, Estrone, 17-OH-Progesterone and SHBG were measured by RIA in obese, underweight and control women, all menstruating in the follicular phase. Serum concentrations of all parameters measured did not differ significantly in the underweight and control groups. All obese women had higher levels of estrone than the control group, and only obese patients with a body mass index above 39 showed a lower SHBG level than that of the control group. The data suggest that the increased levels of estrone could play a role in the amenorrhea of obese women.
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PMID:[Influence of body weight on gonadotrophins and steroid hormone levels in menstruating women]. 379 88

The presence of obesity, defined as weight 20 per cent or more above ideal body weight or increased body fat content, significantly increases risk of pulmonary, cardiovascular, metabolic, and gastrointestinal problems. Obesity is a major cause of shortened life expectancy. While obesity is not essential for the development of the obstructive sleep apnea syndrome, a significant percentage of patients with obstructive sleep apnea are obese. When evaluating these patients who have obstructive sleep apnea, it is important to search diligently for medical problems that are commonly found among the obese. While there is an increased incidence of obese patients among those who have obstructive sleep apnea, the exact reason for this is uncertain. The study of endorphins and enkephalins may expand our understanding of obesity, ventilatory regulation, and obstructive sleep apnea. This may, in fact, enable us to understand better the interrelationship between obesity and obstructive sleep apnea. The role that thyroid hormone, testosterone, and progesterone play in obstructive sleep apnea has also been reviewed. Patients who have obstructive sleep apnea should not be treated with testosterone. All patients given testosterone should be observed quite closely for the possible signs and symptoms of obstructive sleep apnea. Progesterone seems to be of some help in patients who have obesity hypoventilation syndrome. Its effectiveness in patients with obstructive sleep apnea is less clear. The obesity hypoventilation syndrome as described by Burwell is relatively uncommon. Many of the manifestations of the obesity hypoventilation syndrome, however, are found in patients with obstructive sleep apnea. The recognition that the symptoms stem from underlying obstructive sleep apnea offers great potential for therapy. Weight reduction is valuable therapy for patients with obesity and pulmonary dysfunction, obesity and obstructive sleep apnea, and obesity hypoventilation syndrome. Weight reduction and weight maintenance, while difficult, are essential in patients with obesity, obesity and obstructive sleep apnea, and the hypoventilation syndrome. Obesity should be viewed as a medical problem deserving medical attention and long-term medical follow-up.
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PMID:Obesity and hormonal factors in sleep and sleep apnea. 390 3

Epidemiologic studies suggest that ovarian hormones contribute to the development of breast cancer at all stages. Early menopause and premenopausal obesity reduces the risk while postmenopausal obesity and menopausal estrogen replacement therapy increases the risk. Combined oral contraceptives and Depo-Provera do not reduce the risk. It appears that estrogens and progestogens act through and with proto-oncogenes and growth factors to affect breast cell proliferation and breast cancer etiology. Animal studies suggest that estrogen causes interlobular ductal cell division and progesterone causes increased terminal duct lobular unit cell division in the luteal phase. Most breast carcinomas originate from terminal duct lobular unit cells. During pregnancy, these cells fully multiply. Their reproduction is also increased during the luteal phase. Yet, there is considerable interpersonal variation. No studies examining breast cell division have compared cell division rates with serum hormone concentrations, however. The peak of mitosis occurs about 3 days before breast cell death in the late luteal and very early follicular phases. Other research suggests that breast stem cell proliferation is linked to breast cancer development. Endocrine therapy reduces mitotic activity, indicating the estrogen and progesterone receptor content of breast cancers. Hormone-dependent breast cancer cell lines are all estrogen-dependent. Progesterone can block the estrogen-dependent cell lines which act like endometrial cells. The results of the various breast cell proliferation studies in relation to breast cancer are unclear and research identifying a molecular explanation would help in understanding the different findings.
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PMID:Estrogens, progestogens, normal breast cell proliferation, and breast cancer risk. 840 1

In 22 patients with endometrial carcinoma, Stage I-III (mean age 57.8 years) with obesity, initial and reactive hyperinsulinemia (during glucose load) was revealed. Significant correlations between values of "peak" and field-square of the insulin secretion curve and cytoplasmatic receptors to Estradiol and Progesterone in the tumor were found. In a group of the patients with high values of reactive hyperinsulinemia significantly larger amounts of steroid hormone receptors in the tumor were determined as compared to the group of the patients who had low insulinemia values. On considering these data a possible conclusion was reached as to the modifying influence of hyperinsulinemia on sensitivity of endometrial carcinoma to hormone receptor synthesis in the tumor by insulin.
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PMID:Hyperinsulinemia as a factor modifying sensitivity of endometrial carcinoma to hormonal influences. 850 Apr 94

The two types of endometrial carcinomas are preceded by precancerous lesions. Type I endometrial carcinomas are most commonly encountered in perimenopausal women with the classical risk factors associated with estrogen exposure: obesity, multiparity, diabetes, estrogen treatment, ... Hyperplasia (simple, followed by complex forms without cellular atypias and subsequently by complex hyperplasias with cellular transformation) precede such cancers. Estrogens exert a promoting effect on these lesions but do not initiate them. Progesterone and progestins exert a preventive and protective effect. However, the progressive loss of steroidal receptors is correlated to the progression of tissular anomalies and to the onset of cytogenetic anomalies and to mutations of p53 anti-oncogene. The preventive role of progestin is well established, but their curative beneficial effect on atypical precursors forms of endometrial cancers and on endometrial carcinomas remains controversial. The second type of endometrial cancer appears during the postmenopause and is characterized by an increased invasiveness and a poor prognosis, devoid of identifiable risks factors, these aggressive cancers are not preceded by hormone-sensitive precancerous lesions, but by an intra-epithelial endometrial carcinoma. This lesion appears most often in an atrophic endometrium. Finally, the two types of precancerous states are characterized by distinct gene anomalies suggesting two different pathogenic mechanisms of cancerisation.
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PMID:[Precancerous states of the endometrium: hormonal aspects]. 952 83


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