Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Luteinizing hormone-releasing hormone agonist therapy for prostate cancer is a new method of management for metastatic disease. During the initial 1 to 2-week period of administration an increase in serum testosterone concentration can lead to an exacerbation of clinical symptoms (flare phenomenon). Two patients are summarized who received luteinizing hormone-releasing hormone agonist therapy without flare blockade and died suddenly during month 1 of therapy. A review of 765 patients in 9 series found 10.9% who suffered disease flare and 15 who died during disease flare. Of these 17 patients 12 were similar to our 2. These data suggest that any patient placed on luteinizing hormone-releasing hormone agonist therapy for prostate cancer merits some form of flare blockade during the initial 1 or 2 months of therapy.
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PMID:Sudden death due to disease flare with luteinizing hormone-releasing hormone agonist therapy for carcinoma of the prostate. 194 4

Several exciting new forms of therapy for metastatic prostatic cancer have been introduced recently. Luteinizing hormone-releasing hormone (LH-RH) agonists paradoxically inhibit pituitary release of luteinizing hormone, resulting in a fall of serum testosterone to castrate levels within two to four weeks. These drugs have no cardiovascular side effects. A nonsteroidal antiandrogen, flutamide, may be as effective as orchiectomy in men with untreated metastatic disease and has the advantage of preserving potency in most men. In recent reports, combining the LH-RH agonist with an antiandrogen resulted in "total medical castration," which may substantially improve objective response rates and patient survival. Ketoconazole, an antifungal drug, also rapidly inhibits testicular and adrenal androgen synthesis and decreases plasma testosterone to castrate levels within 72 hours. In men with hormone-resistant disease, combination chemotherapy may produce an objective response rate of 50%. In men with severely painful bony metastasis, an inexpensive drug used in Paget's disease, etidronate disodium, may be palliative.
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PMID:Advances in the treatment of metastatic prostatic cancer. 241 32

In most western countries, carcinoma of the prostate is the second most frequent cause of cancer death following carcinoma of the lung. In the pathogenesis of clinical carcinoma of the prostate, several mutational steps can be distinguished which correlate with subclinical and clinical situations. Focal carcinoma is identified in autopsy series at least 500-1,000 times more than is appreciated on clinical grounds alone. Still, focal carcinoma must be considered the precursor of all clinical disease. At least three mutational steps must be involved in the pathogenesis: the development of focal carcinoma from normal cells, the progression to hormone-dependent clinical carcinoma, and the progression to hormone-independent carcinoma. The geographic variation of these events suggests that exogenous factors play an important role in the pathogenesis of prostatic cancer. Focal, noninvasive carcinoma is found in the clinical situation incidentally upon treatment of obstruction in 8-12% of cases with benign prostatic hyperplasia. This lesion is usually not treated aggressively. The incidence of clinical prostatic carcinoma is strictly age-related. Because the tumor largely occurs after age 50, and competing causes of death play an important role, only about 50% of all patients with clinical prostatic carcinoma are likely to die of this disease. Prostatic carcinoma is most frequently diagnosed in the metastatic state (40-50%). The remainder are locally confined with an incidence of lymph node metastases of roughly 35%. Tumors diagnosed in the metastatic state have a distinctly poorer prognosis than tumors diagnosed as potentially curable lesions. Metastatic prostatic carcinoma is usually managed by means of androgen suppression. Hormone-dependent human tumor lines in nude mice suggest that endocrine-dependent cells are not killed by androgen withdrawal, but remain dormant and can be restimulated to grow. In the same sense, management of prostatic carcinoma appears to be palliative. Patients die of prostatic carcinoma because hormone-independent cell populations develop and cannot be influenced by hormonal management. Still-open questions concerning endocrine management are the timing of androgen withdrawal (early versus delayed) and the degree of androgen withdrawal (total versus subtotal). Luteinizing hormone-releasing hormone (LHRH) agonists and antiandrogens allow endocrine management with minimal side effects. Prolongation of life and cure can only be expected from simultaneous effective treatment of hormone-independent tumor cell populations.
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PMID:Current concepts in the management of prostatic cancer. 338 35

Androgens are thought to play a role in the pathogenesis of prostate cancer. We evaluated androgen levels in 3 age-matched groups of men who were part of the Baltimore Longitudinal Study of Aging: 1) 16 men with no prostatic disease by urologic history and exam (control group); 2) 20 men with a histologic diagnosis of benign prostatic hyperplasia (BPH) who had undergone simple prostatectomy; and 3) 20 men with a histologic diagnosis of prostate cancer (16 with local/regional cancer, and 4 with metastatic cancer). Luteinizing hormone (LH), total testosterone (T), and free T were measured on stored AM sera by radioimmunoassay (RIA). Free T was also calculated from the measured concentrations of total T and sex hormone binding globulin (SHBG). The median number of repeated sex steroid measurements ranged from 6-9 over a period from 7-25 years prior to the diagnosis of prostate disease. There were no significant differences in age-adjusted LH, total T, SHBG, or calculated free T levels among the groups at 0-5, 5-10, and 10-15 years before diagnosis. These data suggest that there are no measurable differences in serum testosterone levels among men who are destined to develop prostate cancer and those without the disease.
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PMID:Longitudinal evaluation of serum androgen levels in men with and without prostate cancer. 754 28

Adenocarcinoma of the prostate is the most common malignant neoplasm occurring in men. About half of patients present with metastatic disease. The mainstay of the treatment of stage D cancer of the prostate is hormonal therapy. Bilateral simple orchiectomy remains the gold standard with which other therapies must be compared. Luteinizing hormone-releasing hormone analogues and antiandrogens are now most commonly used but are costly. Initiating hormonal therapy immediately on diagnosing metastatic disease appears to have some advantage over delaying therapy until a patient is symptomatic. Total androgen blockade also appears to be beneficial in terms of survival but at high cost.
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PMID:Hormonal therapy for stage D cancer of the prostate. 802 85

The staging, screening and diagnosis, and treatment of prostate cancer are discussed. Prostate cancer kills about 40,000 men in the United States each year. Signs and symptoms range from dysuria to features of advanced metastatic disease. The American Urological System of staging prostate cancer designates four stages, A through D. The tumor is graded histologically with the Gleason scale. Methods used in the screening and diagnosis of prostate cancer include digital rectal examination, the prostate-specific antigen (PSA) assay, biopsy, transrectal ultrasonography, and determination of PSA density, velocity, and age specificity. The value of screening and treatment remains controversial because tumors are generally slow-growing and conclusive data showing an effect on survival time are lacking. Treatment methods consist of prostatectomy, radiation therapy, and hormonal drug therapy or bilateral orchiectomy. The choice is influenced primarily by the stage of the disease but also by the patient's age, physical condition, and response to prior therapy. Patients with stage A or B disease are considered for prostatectomy or radiation therapy. The primary treatment for stage C disease is radiation therapy. For stage D, the main approaches are watchful waiting and bilateral orchiectomy or hormonal drug therapy to reduce androgenic stimulation of prostate tissue. Long-term survival rates are high for stages A and B and considerably lower for stages C and D. Prostate cancer responds to estrogens, but adverse effects are frequent and potentially severe. Luteinizing hormone-releasing hormone agonists (leuprolide and goserelin) are as effective as estrogens but have less toxicity; a disadvantage of these agents is an initial flaring of the disease. Other hormonal agents used include antiandrogens-progestins, flutamide, and bicalutamide. Secondary hormonal treatments (aminoglutethimide and ketoconazole) are less effective than initial hormonal therapy. Antineoplastic agents have little or no effectiveness in prostate cancer. Although the value of screening for and treating prostate cancer continues to be debated, many experts recommend annual screening for all men over 50. Research to identify more effective drugs for treating advanced disease continues.
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PMID:Prostate cancer: current and evolving strategies. 867 58

The choice of endocrine agent for breast cancer depends on the menopausal status of the patient, the stage of disease, prognostic factors, and the toxicity profile of the agent. Endocrine therapies are typically given sequentially, with the least toxic therapy given first. Tamoxifen is considered first-line endocrine therapy for all stages of breast cancer. New antiestrogens in development include nonsteroidal agents related to tamoxifen and pure steroidal antiestrogens. Luteinizing hormone-releasing hormone agonists are an effective form of endocrine therapy for premenopausal women with advanced breast cancer, and aromatase inhibitors are effective in postmenopausal women. Newer and more selective aromatase inhibitors that are p.o. active and have improved side-effect profiles have been developed. Recent trials have found these agents to improve survival in comparison to the progestins; thus, aromatase inhibitors are replacing progestins as second-line therapy for metastatic disease. Current trials are examining the potential role of aromatase inhibitors as first-line therapy for metastatic disease or as adjuvant therapy for early disease. The antiprogestins and antiandrogens studied thus far have had only limited success in breast cancer clinical trials.
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PMID:Update on endocrine therapy for breast cancer. 953 18

Our aim was to assess testicular function in patients treated with high-dose radioiodine. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone levels were determined in 52 men with thyroid carcinoma before and 6, 12, and 18 months after radioiodine therapy (3.7-5.5 GBq (131)I; mean, 4.25 GBq (131)I) (group 1) and were also determined before and 18 months after the last radioiodine therapy in 22 patients who received high cumulative activities (13-27.7 GBq; mean, 20.3 GBq (131)I) (group 2). FSH levels were increased 6 months after therapy in all patients of group 1, while a decline was observed after 12 months, with 37 of 52 (71%) subjects presenting normal values. FSH values returned to normal after 18 months in all patients. In group 2, 12 of 22 (54.5%) patients presented elevated FSH and 8 (66%) of these individuals had oligospermia. Six months after radioiodine, increased LH levels were observed in only 5 of 52 (9.6%) patients of group 1, which returned to normal after 12 months, and in 5 of 22 (22%) of group 2. All patients showed normal testosterone levels. We conclude that 131I therapy may cause impairment of testicular function. A generally transient increase in FSH is highly common but is usually reversed within 18 months. Oligospermia was common (one third) after high cumulative (131)I activities. Becausee we did not perform a spermiogram before therapy, we cannot state that high cumulative (131)I activities cause permanent infertility. We recommend the routine use of sperm banks in the cases of men who still wish to have children and who will undergo therapy with (131)I activities of 14 GBq or more or in the case of patients with pelvic metastases.
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PMID:Testicular function after radioiodine therapy in patients with thyroid cancer. 1688 90

Luteinizing hormone-releasing hormone (LHRH) agonist therapy to induce medical castration has become the most common form of hormonal therapy for advanced and metastatic prostate cancer. When treatment is started, LHRH agonists initially stimulate the release of LH, causing a surge in serum testosterone that can precipitate a "flare" phenomenon or worsening of disease, particularly in patients with bone metastatic disease. Gonadotropin-releasing hormone (GnRH) receptor antagonism represents a newer approach to medical castration. Abarelix is a pure GnRH receptor antagonist that is devoid of any LHRH agonist activity. Results from 1 phase II and 3 phase III clinical trials demonstrate that abarelix produces medical castration more quickly and without causing testosterone surge, as compared with LHRH agonists with or without a nonsteroidal antagonist. The safety profile in terms of adverse events is comparable between the 2 types of treatment, but the lack of testosterone surge with abarelix might confer a safety advantage by abolishing the risk of a disease flare.
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PMID:Gonadotropin-releasing hormone antagonist in the management of prostate cancer. 1698 33

The use of androgen deprivation therapy (ADT) to treat prostate cancer has favorably impacted outcomes for men with prostate cancer. Androgen deprivation therapy is effective in reducing painful bony metastases and soft tissue visceral disease in advanced-stage prostate cancer. The use of ADT has expanded beyond the metastatic setting and can also be used as adjuvant therapy for patients with locally advanced prostate cancer who received surgery or localized radiation therapy. Luteinizing hormone-releasing hormone agonists are the most common medical therapy used to deprive men of androgen production. Despite the beneficial effects that ADT has on prostate cancer, ADT causes side effects that can impair quality of life. This article will review the impact and treatment of hot flashes in men treated for prostate cancer.
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PMID:Management of hot flashes in men with prostate cancer being treated with androgen deprivation therapy. 1863 64


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