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

Tamoxifen is the anti-estrogen the most widely used in breast cancer. The duration of its prescription, as adjuvant treatment, tends to increase (5 years, and even more) and now it is used in chemoprevention. A slight increase of thromboembolic complications was noted in some studies. This article evaluates the frequency of thromboembolic accidents (TEA) in 441 postmenopausal patients treated by an association of conservative radiosurgery, tamoxifen +/- chemotherapy, for a breast carcinoma T0, T1T2 < 4 cm. Nineteen patients (4.3%), all in remission, presented a TEA, between 1 and 44 months after the beginning of the tamoxifen treatment. We observed seven pulmonary embolisms (PE), 11 deep venous thromboses (DVT) and an acute arterial ischemia. Two patients aged 74 and 80 years died, the others had a favourable evolution under anticoagulant treatment. Among these 19 patients, six presented known risks factors (phlebitis, cardiovascular disorders) and ten had a "favouring circumstance" aggravating the risk of TEA (surgical operation, severe infection, fracture). Their median age was 65 years (61 for all the 441 patients). We noted eight cases of breast lobular cancer (42%) among these 19 patients (11% for all the patients). Among postmenopausal patients, the indication of tamoxifen must be evaluated according to the benefits expected in those with high risk factors of TEA (history of heart failure, obesity, spread varix, age > 65 years). In case of DVT and/or PE, this treatment seems contra-indicated. In case of "favouring circumstances", a hypocoagulant or systematic anticoagulant treatment must be proposed. In case of combined chemotherapy, it is better to start tamoxifen at the end of the treatment. These simple prophylactic measures should allow to reduce significantly the risk of TEA in postmenopausal patients with adjuvant anti-estrogenotherapy.
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PMID:[Thromboembolic accidents in postmenopausal patients with adjuvant treatment by tamoxifen. Frequency, risk factors and prevention possibilities]. 774 16

Risk factors for endometrial cancer include obesity, nulligravidity, late menopause, and anovulatory states. Although diabetes is highly associated with endometrial cancer, hypertension is not an independent variable when correction is made for other factors. Exogenous estrogen increases the risk by at least four times, and smoking is a significant factor. Screening of asymptomatic women may be useful among high risk patients. In addition, racial influence on virulence has recently been identified. Most recurrences of endometrial cancer are identified within 3 years of initial diagnosis. Predictors include ploidy, histologic grade, histologic type, receptor status, and stage. Treatment of recurrence is individualized based on tumor location and receptor status and may involve surgery, radiation therapy, hormonal therapy, or cytotoxic chemotherapy. Tamoxifen has been shown to improve survival among subsets of patients with breast cancer in all stages. A comprehensive literature review and meta-analyses, however, verified an increased risk of endometrial cancer among tamoxifen-treated patients compared with control subjects that may equal the cancer risk from exogenous estrogen exposure. Screening techniques include sonographic assessment of endometrial thickening and vascular patterns, hysteroscopy, and endometrial sampling. A subendometrial cystic proliferation can confuse radiographic evaluation of endometrium, leading to unindicated curettage. A disproportionate incidence of high grade lesions has been reported; however, tamoxifen should not be withheld from patients with breast cancer.
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PMID:Endometrial cancer. Management of high risk and recurrence including the tamoxifen controversy. 863 98

Female reproductive hormones cause breast cancer. Long-term use of postmenopausal hormones increases the risk of breast cancer. The apparent survival advantage seen in women diagnosed with breast cancer while taking postmenopausal hormones may be due to the hormone-responsive nature of their tumors, diagnosis at an earlier stage, or other biases. Thus, the data indicating a survival advantage do not specify what the policies were on the use of hormones after diagnosis. Substantial evidence from studies of obesity confirms the association of higher estrogen levels with poorer prognosis. Tamoxifen (Nolvadex), acting as an antiestrogen in breast tissue, increases the likelihood of survival, as does oophorectomy in premenopausal women. Given these data, women diagnosed with breast cancer should use hormones sparingly. Alternatives to hormone therapy should be used for long-term prevention of heart disease and osteoporosis.
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PMID:Estrogen replacement therapy for breast cancer patients. 959 75

We wanted to assess the effect of tamoxifen treated women with breast cancer, as well as to examine patients with diabetes blood hypertension, and obesity. The influence of Tamoxifen was searched over the endometrium in patients treated with it for 3 years. In this research work is assessed the effect of this medicament from this risk group. The second risk group were the women with high blood pressure, obesity and diabetes mellitus. We used transvaginal sonography and the progesterone test to find endometrial pathology and especially endometrial cancer in asymptomatic women-measuring the depth of the endometrium, and using abrasio probatoria separata in order to find endometrial cancer. With these tests we found polyps, hyperplasia, and early endometrial cancer. We wanted with progesteron test and vaginal sonography in these risk groups to find endometrial pathology and especially early endometrial cancer in asymptomatic women.
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PMID:[The progesterone test and transvaginal sonography as methods for the early discovery and screening of endometrial cancer in women in the postmenopause from some risk groups]. 1073 Mar 82

Tamoxifen is a nonsteroidal anti-estrogenic drug used for adjuvant treatment of breast cancer and recently as a chemopreventative agent for breast cancer and, on an investigational basis, for other cancers. To date there are case reports of hypertriglyceridemia and fatty liver disease in tamoxifen users. Fatty liver is associated with visceral obesity and other components of the metabolic syndrome. Here we evaluated steatosis and adipose tissue distribution by CT scan in a cross-sectional study of 32 women on tamoxifen and 39 control women. Tamoxifen users had more visceral adipose tissue (VAT) and more liver fat than controls. This is the first study to demonstrate that fatty liver and intra-abdominal fat accumulation are common in breast cancer patients receiving tamoxifen. Prospective studies of tamoxifen should monitor metabolic changes in obese women with or without breast cancer.
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PMID:Relationships between tamoxifen use, liver fat and body fat distribution in women with breast cancer. 1141 Aug 35

The objective of this paper is to review the published and unpublished knowledge of the effect of selective estrogen receptor modulators on reproductive tissues other than endometrium. Pharmaceutical companies developing or marketing selective estrogen receptor modulators (SERMs) were identified. The investigators at each company responsible for the conduct of investigational trials were contacted and queried about reports of adverse events in any ongoing or completed trials involving SERMs produced by their company. Levormeloxifene and idoxifene trials noted a higher proportion of surgery for pelvic organ prolapse in treated versus untreated women. The development of these pharmaceutical agents was discontinued, primarily for endometrial concerns. However, pelvic organ prolapse was reported to the FDA as an adverse event associated with both drugs. Study weaknesses preclude a definitive association between the agents and pelvic organ prolapse. The treated groups were not necessarily similar for confounding factors such as age, parity, obesity, cigarette smoking, and other risk factors for pelvic organ prolapse. Tamoxifen and raloxifene increase hot flash intensity and frequency. Ovarian cyst formation and uterine fibroid growth have also been reported with some SERMs. The identification and assessment of the impact of current and future SERMs on the pelvic floor and other genital tissues will be important to understanding their potential long-term application in disease treatment and prevention.
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PMID:Effect of selective estrogen receptor modulators on reproductive tissues other than endometrium. 1179 59

Increased risk of breast cancer may result from modifiable factors such as endogenous hormone levels, obesity, HRT, and non-lactation, or non-modifiable factors such as genetic susceptibility or increasing age. Those factors that are easiest to modify may have a limited impact on the totality of breast cancer. The Gail model, based on known factors may be useful for estimating life-time risk in some individuals. Tamoxifen prevention still remains contentious. In the NSABP-P1 study, there was a 49% reduction in risk of breast cancer in women given tamoxifen but in the Italian and Royal Marsden trials, no effect on breast cancer incidence was detected, possibly because of the different case-mix in these studies. Raloxifene, tested in the MORE trial reduced the incidence of breast cancer by 65%. The effect was restricted to ER positive tumours: no reduction in ER negative cancers was seen. Life-style factors such as diet, obesity, exercise, and age of first full term pregnancy and number of pregnancies have a mild to moderate impact on risk and so may have little effect on the incidence of breast cancer. Reduction of alcohol intake could lead to a modest reduction in the risk of breast cancer but possibly adversely affect other diseases. So far, studies of retinoids have not shown a benefit in terms of breast cancer risk reduction. Fat reduction and GnRH analogues reduce mammographic density but have not yet been shown to affect risk.
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PMID:Breast cancer prevention: present and future. 1187 62

Increased risk of breast cancer may result from potentially modifiable causes such as endogenous hormone levels, obesity, HRT, and non-lactation, or non-modifiable factors including genetic susceptibility and increasing age. The Gail model, based on known factors, may be useful for estimating lifetime risk in some individuals, but those risk factors that are easier to modify may have a limited impact on the totality of breast cancer. Tamoxifen prevention still remains contentious, with a significant reduction in risk of breast cancer in women given tamoxifen in the NSABP P1 study but no effect in the Italian and Royal Marsden trials. Raloxifene, tested in the MORE trial, reduced the incidence of breast cancer by 65% but this was restricted to oestrogen receptor positive tumours. Lifestyle factors such as diet, obesity, exercise and age at first full term pregnancy and number of pregnancies have a mild to moderate impact on risk, so may have little effect on the incidence of breast cancer. Reduction of alcohol intake could lead to a modest reduction in the risk of breast cancer but possibly adversely affect other diseases. Fat reduction and GnRH analogue reduce mammographic density but have not yet been shown to affect risk. For women with BRCA1/2 mutation, options include unproven surveillance and prophylactic mastectomy with an unquantified risk reduction. Interesting new candidates for chemoprevention include aromatase inhibitors, new generation SERMs, demethylating agents, non-selective COX inhibitors, tyrosine kinase inhibitors and polyamine synthetic inhibitors.
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PMID:14. Breast cancer prevention. 1266 5

Tamoxifen is a potent antagonist of estrogen, and hepatic steatosis is a frequent complication in adjuvant tamoxifen for breast cancer. Impaired hepatic FA beta-oxidation in peroxisomes, microsomes, and mitochondria results in progression of massive hepatic steatosis in estrogen deficiency. This impairment, although latent, is potentially serious: About 3% of the general population in the United States is now suffering from nonalcoholic steatohepatitis associated with obesity and hyperlipidemia. Therefore, in the present study we tried to restore impaired hepatic FA beta-oxidation by administering a novel statin, pitavastatin, to aromatase-deficient (Ar-/-) mice defective in intrinsic estrogen synthesis. Northern blot analysis of Ar-/- mice liver revealed a significant restoration of mRNA expression of essential enzymes involved in FA beta-oxidation such as very long fatty acyl-CoA synthetase in peroxisome, peroxisomal fatty acyl-CoA oxidase, and medium-chain acyl-CoA dehydrogenase. Severe hepatic steatosis observed in Ar-/- mice substantially regressed. Consistent findings were obtained in the in vitro assays of FA beta-oxidation activity. These findings demonstrate that pitavastatin is capable of restoring impaired FA beta-oxidation in vivo via the peroxisome proliferator-activated receptor-alpha-mediated signaling pathway and is potent enough to ameliorate severe hepatic steatosis in mice deficient in intrinsic estrogen.
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PMID:Pitavastatin ameliorates severe hepatic steatosis in aromatase-deficient (Ar-/-) mice. 1288 Jan 7

The incidence of newly diagnosed breast cancer cases world-wide is expected to double by 2020. Risk-reducing strategies for breast cancer include lifestyle modifications, chemoprevention and surgery (bilateral mastectomy and/or oophorectomy). Lifestyle modifications include avoidance of postmenopausal obesity and hormone replacement therapy (HRT), regular physical activity, and restriction of alcohol and animal fat intake. Tamoxifen is a selective estrogen receptor modulator (SERM) shown in randomized controlled trials to reduce the incidence of estrogen receptor (ER)-positive breast cancer in high-risk healthy women. However, its routine use cannot be recommended for breast cancer prevention in healthy women due to its significant adverse effects, specifically in terms of endometrial carcinoma and thromboembolism. On the other hand, tamoxifen may be used for chemoprevention in women at high risk of developing ER-positive breast cancer and at low risk of developing complications. Raloxifene, another SERM, also appears to be effective in reducing breast cancer risk, and lacks the unwanted stimulatory effect on the uterus. Other promising chemopreventive agents currently under investigation include cyclo-oxygenase 2 (COX-2) inhibitors, fenretinide, aromatase inhibitors, and goserelin. Prophylactic mastectomy can reduce breast cancer risk by 90% in high-risk women. Bilateral oophorectomy has the potential of reducing the risk of both breast and gynecologic cancer in women carrying BRCA-1 or BRCA-2 mutations. Further research is required to identify novel strategies to prevent ER-negative breast cancer, minimize the adverse effects of tamoxifen and other SERMs, and evaluate the role of mammary ductal lavage and ductoscopy in guiding risk-reducing strategies.
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PMID:Risk-reducing strategies for breast cancer--a review of recent literature. 1564 97


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