Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cholesterol and triglycerides were measured in plasma samples from patient with cancer of the prostate before and after 3 months treatment with either Premarin, Provera, Provera and diethylstilbestrol, or diethylstilbestrol alone. Cholesterol was also measured before and after one of three doses of diethylstilbestrol or placebo. Pretreatment cholesterol levels at 196 +/- 1.3 mg per 100 ml (X +/- SE, N = 1093) were significantly lower than these reported for similar age group noncancer controls. Significant increases occurred with some of the estrogen treatments. Pretreatment cholesterol levels showed a significant negative correlation with age in Stage III and IV patients of both studies and a positive correlation with hemoglobin in Stage III patients of both studies. Pretreatment triglyceride levels at 120 +/- 1.9 mg per 100 ml (X +/- SE, N = 1089) were similar to levels reported for noncancer controls of similar age. Estrogen treatment produced a significant increase in triglyceride levels. Serum triglycerides were significantly correlated with hemoglobin, weight, and cholesterol and negatively correlated with age, Analysis of covariance for both cholesterol and triglycerides showed highly significant treatment effects, but no stage effects and no stage-treatment interactions. It showed that the pretreatment value is of extreme importance for predicting or explaining the 3-month value. Death rates were calculated by level of pretreatment cholesterol or pretreatment triglycerides for all Stage II and IV patients, all treatments combined, and for Study 2 and Study 3 separately. No consistent trends were evident for cholesterol. Spearman correlation coefficients between category of initial triglyceride value and rank of death rate were computed to test for a quadratic effect. When the absolute values of the initial triglyceride values minus the overall mean were correlated with the death rate, a significant negative correlation was found for all causes of death and for deaths due to cardiovascular disease and prostatic cancer. These results indicate that the death rate is highest near the overal mean for initial triglyceride values and decreases as the initial values deviate above or below the mean. Initial triglyceride levels appear to have potential as indicators of risk of death in patients with prostatic cancer. The percentage of patients dead at 1 year by initial triglyceride levels, measured only in Study 3, revealed a pattern similar to that observed for the death rate, that is, the highest percentages were associated with values near the overall mean.
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PMID:Response of serum cholesterol and triglycerides to hormone treatment and the relation of pretreatment values to mortality in patients with prostatic cancer. 18 47

Fibrinogen and plasminogen were measured in plasma samples from prostatic cancer patients before and after 3 months of treatment with either Premarin, Provera, Provera and diethylstilbestrol, one of three doses of diethylstilbestrol, or placebo. Plasminogen levels generally were increased significantly with the estrogens but were unchanged following placebo or Provera treatment. Pretreatment plasminogen levels in Study 3 were significantly lower (p less than .001) than in Study 2. Plasminogen pretreatment levels were significantly correlated with age, hemoglobin, body weight, and blood pressure. Fibrinogen pretreatment levels were significantly elevated above normal. They were not significantly with age, hemoglobin, body weight, or blood pressure. Fibrinogen levels generally were significantly decreased by the estrogens. Comparisons of means of pretreatment fibrinogen and plasminogen levels from patients dying during the first year of the study with the mean pretreatment levels of the patient group alive after 1 year on study yielded no significant differences. Death rates were calculated by pretreatment plasminogen or fibrinogen for all treatments of all Stage III and Stage IV patients combined for Study 2 and Study 3 separately. Such rates were calculated for all causes combined and for deaths from prostatic cancer or cardiovascular disease separately. The levels of plasminogen were significnatly negatively correlated with death rate from all causes combined and with cardiovascular disease considered separately, but not with death from prostatic cancer. The levels of fibrinogen were signigicantly positively correlated with death rates from all cuses and nearly significantly with prostatic cancer, but not cardiovascular disease. Elvated pretreatment fibrinogen levels were associated with an increased proportion of deaths at 1 year from all causes and from cancer of the prostate.
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PMID:Response of plasma fibrinogen and plasminogen to hormone treatment and the relation of pretreatment values to mortality in patients with prostatic cancer. 18 48

The cardiovascular risk induced by oestrogen treatment appears to be minimal when oestrogens are prescribed at low doses (daily dose less than 3 mg/day) and when this drug is not prescribed in patients with a history of cardiovascular disease. The Prostatic Cancer Cooperative Study Group compared the course of 137 patients treated by oestrogens with a French male population matched for age: ten accidents were observed versus nine expected and one death was observed versus 3 expected. By selecting patients, oestrogens can therefore still be part of the range of treatments available for advanced prostatic cancer.
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PMID:[Cardiovascular risks induced by estrogens prescribed at low doses. 208 years of observation--137 patients]. 184 29

From 1966 to 1979, 360 patients with clinical stages A2, B and C1 prostate cancer underwent staging pelvic lymphadenectomy, and completed a course of combined interstitial radioactive gold seeds and external beam radiotherapy. All patients had a normal serum prostatic acid phosphatase level and a bone scan negative for metastases. All patients were followed until death or for a mean of 7.3 years (range 1.2 to 18.25 years) for those alive at analysis. To determine the risk of dying of prostate cancer we reviewed the records of the 142 patients (39%) who died. At analysis 21% of the patients had died of prostate cancer and 17% of other known causes. The cause of death could not be determined in 4 patients (1%). Cardiovascular disease accounted for a fifth of all deaths. The actuarial risk of death of prostate cancer for all patients was 8 +/- 3% (+/- 2 standard errors) at 5 years and 30 +/- 7% at 10 years. The risk of death of all causes was 16 +/- 4% at 5 years and 46 +/- 7% at 10 years. An increased risk of cancer death was associated with established risk factors, including advanced local disease, poorly differentiated histology, pelvic nodal metastases and distant recurrence. We also noted a substantial risk of cancer death in patients who had local tumor recurrence. While previous studies have reported a relatively low incidence of cancer deaths (4 to 17%) in patients initially diagnosed with localized disease, our data suggest that prostate cancer is the major cause of mortality in such patients. Aggressive curative therapy, regardless of treatment modality, should be considered for localized prostate cancer in men with a life expectancy of 10 or more years.
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PMID:The risk of dying of prostate cancer in patients with clinically localized disease. 189 20

The therapeutic management of early prostatic cancer is discussed with background of recent reports and trials. For an old patient with localized, well differentiated cancer deferred treatment can be the best alternative especially if he has significant cardiovascular disease. Advantages and disadvantages of the different local treatment methods (radical prostatectomy, external beam irradiation, interstitial irradiation) are discussed. The author concludes that present information does not permit any recommendations regarding the most effective treatment. The physician should carefully explain all the risks and benefits of each option and then help the patient decide which therapy he would be most willing to accept.
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PMID:Treatment of early prostatic cancer. 202 15

The aim of this study was to predict cardiovascular complications in patients with prostatic cancer treated with oestrogen. A randomised prospective study of oestrogen therapy versus orchiectomy was performed. Patients with pre-existing cardiovascular morbidity were excluded (16%). Prior to the initiation of therapy, patients were subjected to exercise stress tests, physiological evaluation of peripheral circulation, blood volume estimation, chest X-ray, blood test, including hormones, lipoproteins, and antithrombin III, and a physical examination and history by a cardiologist. The oestrogen treatment and the orchiectomy group did not differ with regard to these pretreatment variables; 25% of the patients given oestrogen therapy had cardiovascular complications during the initial treatment year compared with none in the orchiectomy group. Three statistical discriminating techniques were employed and they allowed us to identify 2 strong discriminating variables for cardiovascular complications if oestrogen therapy is instituted in patients with prostatic cancer but without overt clinical cardiovascular disease. These 2 discriminators were luteinising hormone (LH) and ST-segment depression during exercise. This means that a patient with ST-segment depression during an exercise test and/or a high luteinising hormone concentration should not be treated with oestrogen.
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PMID:Patients at high risk of cardiovascular complications in oestrogen treatment of prostatic cancer. 264 97

Anabolic steroids are used therapeutically for various disorders and as ergogenic aids by athletes to augment strength, muscular development, and to enhance performance. There is a wide range of concomitant temporary and permanent adverse effects with steroid administration. Several well-documented adverse actions of these hormones may develop rapidly within several weeks or less (i.e. altered reproductive function) or require up to several years of steroid intake (i.e. liver carcinoma). More recent studies indicate that glucose intolerance, insulin resistance, increased cardiovascular disease risk profiles, cerebral dangers, musculoskeletal injuries, prostate cancer, psychosis and schizophrenic episodes, among others, accompany anabolic steroid intake. There is, at present, no evidence to support the claim that athletes are less susceptible to adverse effects than those individuals receiving hormone treatment in a clinical setting. Based on the available information which has accumulated primarily from cross-sectional, short term longitudinal, and case studies, there is a need: (a) to develop a comprehensive battery of specific and sensitive markers of adverse effects, particularly those that would be able to detect the onset of adverse actions; and (b) to conduct controlled long term longitudinal studies in order to fully understand the extensiveness and mechanisms involved in the occurrence of adverse effects.
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PMID:Adverse effects of anabolic steroids. 2942 77

The rationale of the combination of a nonsteroid antiandrogen with an LH-RH analogue (LH-RH-A) in the treatment of prostate cancer is discussed. Whereas the LH-RH-A depresses testosterone (T) levels via an action on the hypothalamus-pituitary-gonad axis, the antiandrogen counters the effect of any residual T, from the testes or adrenals, on the target organ, the prostate. Although bilateral orchiectomy and administration of estrogen or LH-RH-A give equivalent low T levels over long-term treatment, the manner and rate at which T suppression is achieved vary and each treatment presents characteristic disadvantages. Orchiectomy is irreversible, and it is known that approximately 20% of patients will not benefit from such endocrine manipulation, estrogen use is associated with cardiovascular disease, and LH-RH analogues produce an early surge in T. None of these treatments has any significant effect on adrenal androgen levels, which may contribute toward the progression of disease. Nonsteroid antiandrogens such as anandron and flutamide inhibit the uptake of androgen by the prostate by an action that probably involves the androgen receptor. They do not possess the progestational and glucocorticoid component of steroid antiandrogens or their pituitary inhibitory activity but do exert some inhibition of the 17 alpha-hydroxylase and 17,20-lyase enzyme systems. Unlike steroids, the nonsteroid antiandrogens potentiate the activity of LH-RH-A at the central level in the rat. The inhibitory action of the combined treatment of "anandron + buserelin" on the prostate is greater than that of each compound alone. Clinical pharmacology studies have demonstrated that both steroid and nonsteroid antiandrogens can help to control the effect of increased T levels (disease flare) that occur on initiating LH-RH-A administration. Prostatic acid phosphatase (PAP) levels decrease immediately in spite of the increase in T. The decrease appears faster when nonsteroid antiandrogens are used. Nonsteroid antiandrogens sensitize the pituitary to stimulation by LH-RH in eugonadal volunteers. The results of randomized clinical studies with the combination of "nonsteroid antiandrogen + LH-RH-A" have established a definite trend toward greater efficacy of the combined treatment over monotherapy. Further data are needed to confirm this trend. In particular, further dose-ranging studies are warranted since the need for LH-RH-A doses that reduce T down to castration levels may not be justified in the presence of a potent antiandrogen.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antiandrogens in combination with LH-RH agonists in prostate cancer. 307 51

One hundred consecutive patients aged up to 75 with newly diagnosed cancer of the prostate suitable for hormonal treatment were included in a controlled study of the cardiovascular effects of oestrogen versus orchidectomy. In all cases pre-existing cardiovascular morbidity was excluded. Of the 100 patients, 91 were strictly randomised to receive either oestrogen (n = 47) or orchidectomy (n = 44) and 9 (6 given oestrogen, 3 orchidectomy) either chose their own treatment (five cases) or had it selected for them by the urologist (four). Oestrogen was given in the lowest recommended dosage in Sweden--namely, as 160 mg polyestradiol phosphate intramuscularly every month for the first three months, then 80 mg monthly, plus ethinyloestradiol 1 mg by mouth daily for the first two weeks, then 150 micrograms daily. At entry to the study the two treatment groups showed no difference in demographic characteristics or conventional risk factors for cardiovascular disease. During the first year, however, 13 (25%) of the patients given oestrogen suffered major cardiovascular events as compared with none of the patients after orchidectomy. Patients in the oestrogen treatment group who did not have minor signs of atherosclerosis at entry to the study suffered a similar incidence of cardiovascular complications to those who did have these signs at entry. The substantially increased risk of cardiovascular complications in patients given oestrogen for prostatic cancer warrants careful consideration when choosing treatment for this disorder.
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PMID:Orchidectomy versus oestrogen for prostatic cancer: cardiovascular effects. 309 Nov 38

Cardiovascular complications are a well recognized side-effect of antihormonal therapy in men with prostatic carcinoma. We studied changes in plasma lipoproteins in patients with prostate cancer during treatment with several androgen suppression therapies. Estrogen, orchiectomy, and a combination of LHRH agonist and antiandrogen (flutamide) reduced plasma testosterone concentrations (89-92%) and plasma estradiol decreased by 85%, 44%, and 54%, respectively. Estrogen induced hypertriglyceridemia and elevation of plasma HDL cholesterol, phospholipid, and apolipoprotein A-I and A-II concentrations. Low density lipoprotein (LDL) cholesterol decreased but LDL apolipoprotein B did not. These results suggest that the cardiovascular complications that occur during estrogen administration are not mediated through changes in lipoprotein profile, other than the hypertriglyceridemic effect. Orchiectomy caused hypercholesterolemia and an increase in both total and LDL apolipoprotein B, all of which are strong determinants of cardiovascular disease. The high density lipoprotein (HDL) concentration was not affected despite a reduction in plasma testosterone, perhaps due to a simultaneous decrease in estradiol. Combination therapy had no effect on plasma lipid and apolipoprotein B concentrations, but very low density lipoprotein (VLDL) apolipoprotein B decreased, and LDL apolipoprotein B increased. The HDL cholesterol and apolipoprotein A-I concentrations increased but A-II and phospholipids did not. These results suggest enhanced lipoprotein lipase activity, consistent with the reciprocal changes in VLDL and LDL apolipoprotein B levels, apolipoprotein B enrichment of LDL particles, and increase in HDL cholesterol. The higher apolipoprotein A-I to A-II ratio indicates an increase in HDL2 subfraction due to inhibition of endothelial hepatic lipase, increased secretion of apolipoprotein A-I, or both. These effects are attributed to estradiol, which decreased less than after orchiectomy, and to additional adrenal androgen inhibition by flutamide. We conclude that estradiol plays an important role in determining plasma lipoprotein concentrations in men, and androgens exert an antagonist effect. The lipoprotein profile resulting from the combination treatment is more beneficial than that resulting from orchiectomy or estrogen administration.
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PMID:Changes in plasma lipoproteins during various androgen suppression therapies in men with prostatic carcinoma: effects of orchiectomy, estrogen, and combination treatment with luteinizing hormone-releasing hormone agonist and flutamide. 327 21


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