Treatment of metastatic prostatic cancer with low-dose prednisone: evaluation of pain and quality of life as pragmatic indices of response.

Abstract

Thirty-seven men with symptomatic bone metastases from prostate cancer that had progressed following earlier treatment with estrogens and/or orchidectomy were treated with low-dose prednisone (7.5 to 10 mg daily). The rationale for this treatment was that some patients might still have hormone-sensitive disease that was stimulated by weak androgens of adrenal origin, and that these androgens could be suppressed by prednisone through its negative feedback on secretion of adrenocorticotrophic hormone (ACTH). Response to treatment was assessed by requirement for analgesics, by the McGill-Melzack pain questionnaire, and by a series of 17 linear analog self-assessment (LASA) scales relating to pain and to various aspects of quality of life. Fourteen patients (38%) had improvement in indices used to assess pain at 1 month after starting prednisone, and seven patients (19%) maintained this improvement for 3 to 30 months (median, 4 months). Reduction in pain was associated with improvement in other dimensions of quality of life, and in the scale for overall well-being. Prednisone treatment led to a decrease in the concentration of serum testosterone in seven of nine patients where it was not initially suppressed below 2 nmol/L, and caused a decrease in serum levels of androstenedione and dehydroepiandrosterone sulfate in more than 50% of patients. Symptomatic response was associated with a decrease in serum concentration of adrenal androgens. We conclude that (1) low-dose prednisone may cause useful relief of pain in some patients with advanced prostatic cancer; (2) relief of pain was associated with suppression of adrenal androgens; and (3) measures of pain and quality of life can be used to assess possible benefits of systemic therapy in patients with metastatic prostate cancer.

Enzalutamide in Japanese patients with chemotherapy‐naïve, metastatic castration‐resistant prostate cancer: A post‐hoc analysis of the placebo‐controlled PREVAIL trial

“…A greater number of Japanese patients received corticosteroids at baseline, which could be associated with the lower baseline pain, as corticosteroids have been shown to improve pain and overall well-being in mCRPC patients. 22,23 Although some differences in baseline characteristics might be as a result of differences in clinical practices, others might Overall safety population (n = 1715), n (%) Japanese subgroup (n = 61), n (%) [24][25][26][27] In one study, the difference in serum PSA concentrations between Japanese and Caucasian men remained statistically significant (P < 0.001), even after adjusting for age and prostatic size, which tends to be smaller in Asian men than in Caucasians. 25 It is unclear if the lower PSA in Japanese patients indicates less disease burden or simply reflects the differences between ethnicities.…”

A Phase II study of oral idarubicin as a treatment for metastatic hormone-refractory prostate carcinoma with special focus on prostate specific antigen doubling time

“…7 In considattrition. eration of the small sample size, a few items and scales were selected according to their relevance to the study RESULTS question 8,9 and based on expert judgment and psychoThe 30 eligible patients received a total of 122 cycles metric performance (sensitivity to course of disease (median per patient, 3 cycles; range, 1 -11 cycles). Four and treatment) in a previous small cell lung carcinoma patients were not evaluable for response; 3 of them trial.…”

“…We selected pain, fatigue, and general well-beserved in patients who relapsed after radical prostatectomy, radiation therapy, and hormonal treatment, reing as key endpoints in the evaluation of these patients. 8,9,20 These measures were not specifically develspectively. 19 The median PSA doubling time of 2.1 months observed in this study is very similar to that oped for patients with advanced prostate carcinoma.…”

Is there a role for chemotherapy in prostate cancer?

“…The mechanism of action of glucocorticoids is not clearly understood and is thought to involve suppression of adrenal androgens (Tannock et al, 1989). However, these studies are difficult to interpret and compare as patient populations are highly selected, and are heterogeneous in the intensity of previous and concomitant therapies (Sartor et al, 1998).…”