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... radioactive seeds into the prostate (brachytherapy). External beam radiation therapy is given over a course of 6 to 8 weeks through carefully defined portals. Refinements in technique have allowed greater doses of radiation to be administered with a lower risk of morbidity. Three-dimensional conformal radiotherapy is the preferred method of administration in a dose of 75 to 80 Gy. (Greenlee 32). Radiation therapy cannot cure nodal metastases.
Disease-specific, 7 -year survival with radiation therapy is approaching that of radical surgery, but 15 -year survival statistics are not as favorable. Androgen blockade in conjunction with radiation therapy has improved outcomes. This treatment choice is usually made for patients in their 70 s or for patients with large-volume local disease. (Greenlee 33). Brachytherapy involves the implantation of radioactive iodine or palladium seeds directly into prostatic tissue.
Interstitial seed placement was initially performed free-hand through a surgical incision, but long-term results were very disappointing and the procedure was abandoned in the early 1980 s. The advent of trans rectal ultrasonic monitoring during implantation markedly improved the distribution of seeds and has revived the use of brachytherapy. (Walsh & Partin 184). Locally extensive disease. Locally extensive prostate cancer, in which staging indicates extra capsular spread and / or seminal vesicle invasion, is usually considered incurable by surgical means.
External beam radiation is the treatment of choice. Studies comparing radiation alone with androgen blockade plus radiation have shown the combined approach to result in improved disease-specific survival. Some centers offer a surgical option to provide improved local control of disease, even if survival outcomes are not improved. (Walsh & Partin 186). Metastatic disease. Metastatic prostate cancer is incurable. Surgical and medical castration are equally effective for disease control, and economics and patient preferences are the determining factors in choosing between the two.
Medical castration is achieved by the IM administration of a long-acting luteinizing hormone-releasing hormone agonist such as leuprolide acetate (Lupron) or gosselin acetate (Zoladex). The addition of an anti androgen such as flutamide (Eulexin), bicalutamide (Casodex), or nilutamide (Nilandron) is controversial; recent reviews have failed to identify a survival benefit of combined androgen blockade. (Blumenstein 29). Top investigators disagree on when to start hormonal blockade and how to administer it. Recent studies suggest that intermittent androgen blockade may be as efficacious as continuous blockade, yet without the risk of bone density loss. No long-term studies have compared intermittent versus continuous androgen blockade in the treatment of metastatic prostate cancer. Until recently, palliative therapy was the only option for hormone-refractory metastatic disease.
Radiation therapy directed at painful bony metastases and radioactive isotopes with an affinity for osteoplastic bony lesions have been used to provide pain relief, but these measures do not prolong survival. A new generation of bisphosphonates (eg, pamidronate disodium) is showing promise in delaying the progression of osteoplastic metastases as well as providing palliative relief. This approach, however, does not extend disease-specific survival time. Bisphosphonates may be useful for patients with a rising PSA and associated bony metastases. (Blumenstein 30). Second-line hormonal therapy with ketoconazole, aminoglutethimide, and anti-androgenic steroids is commonly used when initial hormonal therapy fails. Withdrawal of an anti androgen that has been part of the therapeutic regimen may result in a short-term decline in the PSA level, which does not necessarily equate to prolonged disease-specific survival.
Chemotherapy. Chemotherapy is offering new hope in the treatment of hormone-refractory prostate cancer. The concept of treating hormonally independent prostate cancer cells concomitantly with hormonal blockade is under study. Protocols with paclitaxel (Taxol) and docetaxel (Taxotere) alone and in combination with other agents have shown promise in extending disease-specific survival. Protocols are now offered for the difficult situation in which PSA continues to rise after local and hormonal therapies. It is an agonizing decision for patients to trade symptom-free slow disease progression for participation in protocols that may use toxic therapies and are in their infancy as far as outcomes are concerned.
Patients should be counseled regarding the availability of such protocols in their area at the appropriate stages in their disease. As this discussion has shown, state-of-the-art therapy for prostate cancer remains controversial. The best we can accomplish is to make the individual prostate cancer patient aware of his options in light of his current disease state. Collaboration of the primary care physician with a urologist is essential to accomplishing this task. (Blumenstein 32).
Continuing discussing the effective medical treatment, we should mention other cases of its possible application. There are two typical cases of biopsy-proven pulmonary LAM in which a LHRH-A, buserelin, failed to stabilize the disease in spite of effective medical castration. In 1988, two main reasons prompted to try LHRH-As to treat LAM. First, menopause or surgical castration has sometimes been found to favorably influence LAM, and second, LHRH-As successfully have been used in the treatment of some estrogen-dependent diseases and in particular in the treatment of pulmonary "benign" metastasizing leiomyoma. They also produced favorable effects in a case of pulmonary leiomyomatosis. Buserelin was chosen from among other synthetic LHRH-As because of its potent and specific LHRH activity and its strong ability to cause a reversible medical castration. (Kitzsteiner & Mallen 248).
Luteinizing hormone releasing hormone is a hypothalamic deca peptide, which is carried through the pituitary portal system from the eminent ia media to the anterior pituitary gland. It binds specifically to high affinity receptors on the pituitary gonadotropic cells and stimulates the synthesis and release of gonadotrophin's (LH and FSH). Gonadotrophin secretion is characterized by its periodicity, largely dependent on the normal pulsatility (every 90 min) of the hypothalamic LHRH release. Continuous perfusion of natural LHRH leads, after a short period of increased gonadotropin release, to a turnoff of the gonadotropic cell function and inhibition of gonadotropin secretion (down regulation or desensitization by receptor loss).
Natural LHRH is quickly de gradated (half life to 3 to 4 min) by pituitary and hypothalamic peptidases. (Heinrich's & Raybin 916 - 19). During the last decade, many LHRH-As with activity 10 to 300 times higher than natural LHRH have been synthesized. The increased biologic activity of these agonists mainly resides in their prolonged half-life and in their high affinity for specific receptors on pituitary gonadotropic cells. Chronic administration of LHRH-As by intravenous, intramuscular or subcutaneous routes or nasal sprays (500 to 1, 200 [mu]g / day ) causes, after a 10 - to 15 -day period of increased gonadotropin release, a marked decrease in LH and FSH secretion. Simultaneously, blood levels of estradiol, estrone and androstenedione drop to values encountered after surgical castration. This LHRH-A-induced castration is quickly and perfectly reversible. (Heinrich's & Raybin 920 - 21).
In two patients who had normal utero-ovarian cyclic function before buserelin administration, we obtained a hypo gonadal hypogonadotrophic state, which was poorly tolerated by patient. Several possibilities could account for the failure of buserelin to control LAM in these patients. First, LHRH-A-induced hormonal castration is probably not as effective a castration as a surgical one. Second, surgical castration is not systematically effective in LAM. Finally, estrogen, glucocorticoid and progesterone receptors were not measured on the lung biopsy specimens of our patients. The lack of these receptors could have explained the poor response to hormonal therapy, even though rigorous correlation between hormonal therapy and steroid receptor level is lacking. (Eliasson 135 - 55).
Recently, the successful application of LHRH-As has been reported in two patients with advanced biopsy-proven LAM. Both patients were treated intramuscularly for, respectively, 19 and 21 months with two different LHRS-As (triptorelin, 4 mg / month ; gosselin, 3. 6 mg / month ). A marked improvement of their clinical status and blood gas values followed rapid chemical castration resulting from treatment with LHRH-As. However, no significant change was noticed in lung function and chest x-ray film findings. Differences in the type of LHRH-A or the way of administration (intramuscular vs nasal spray) are unlikely to explain the different therapeutic responses observed since a hypogonadotrophic hypogonadism was obtained in every patient. Furthermore, severity of the disease was comparable in the four patients when treatment with LHRH-As was started.
These apparently divergent results may again illustrate the variable responsiveness as reported after any treatment in LAM and probably underline our lack of knowledge concerning the pathogenesis of the disease. (Kitzsteiner & Mallen 249). It is not concluded from this negative report that LHRH-As have no place in the treatment of pulmonary LAM. They may be effective in some cases and prove to be predictive of the therapeutic benefit, which may follow surgical castration. Words: 2, 891.
Works Cited: Bergstrom P & Widwark A. High-precision conformal radiotherapy (HPCRT) of prostate cancer: A new technique for exact positioning of the prostate at the time of treatment. Int J Radiat Oncol Biol Phys 1998; 42 (2): 305 - 11. Blumenstein B.
Combined androgen blockade for the treatment of patients with metastatic prostate cancer: Summary of 15 years of clinical research. AUA Update Series l 999. Eliasson A. Treatment of lymphangioleiomyomatosis: a Meta-analysis. Chest 1989; 196: 135 - 55. Greenlee T.
Cancer statistics, 2000. CA Cancer J Clin 2000; 50 (1): 7 - 33. Heinrich's W & Raybin D. Successful treatment of pulmonary lymphangiomyomatosis with oophorectomy and progesterone. Am Rev Respir Dis 1985; 132: 916 - 21.
Kitzsteiner K & Mallen R. Pulmonary lymphangiomyomatosis treatment with castration. Cancer 1980; 46: 248 - 49. Richie J. Screening for prostate cancer. Why the controversy?
Contemporary Urology 1998; 10: 26 - 37. Walsh P. & Partin A. Cancer control and quality of life following anatomical radical retro pubic prostatectomy. Results after 10 years. J Urol 1994; 152: 183 - 6.
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