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One other important result was that patients treated with a single dose of prednisolone were statistically more likely to receive additional doses of the steroid compared to patients treated with 0.1 mg of prednisolone. Similarly, the odds of increasing the dose of prednisolone to a daily regimen of 2 mg were 1.5 times greater in patients treated with a dose greater than 0.3 mg than in patients treated with 0.2 mg. As with the data on the initial dose level of prednisolone, patients taking 2 mg of prednisolone were also more likely to continue to take it (OR = 1.5; 95% CI = 1.0-2.0). These patterns are similar to the findings on doses of prednisolone and of T1 testosterone in healthy young men, and suggest that prednisolone may be an effective alternative to T1 testosterone in patients with advanced prostate cancer who are receiving a combination hormone therapy.
An important limitation of these results is that they are based on a small number of patients. Because prednisolone is a steroid, which is typically given by intramuscular injection, only those patients who are taking these drugs at least once a week are included. The results based on only those patients who take prednisolone daily can potentially underestimate the effects of prednisolone on the progression of prostate cancer; however, patients who take prednisolone at least once a month will have an improved outcome compared to those who do not take the steroid. In addition, the data presented do not demonstrate that the efficacy of prednisolone or oral progestins is the same for advanced prostate cancer. Because of the differences in progestin side effects and the different potency of individual agents, no overall conclusion can be drawn about the efficacy of any given progestin treatment.
Given that progesterone is the most widely used hormone in cancer treatment, which is supported by all of the data presented, it seems reasonable to assume that a combination of oral corticosteroids and/or prednisolone would be equally efficacious, given that the progestin is the main mechanism of action and the steroids the secondary mechanism of action (Figure 1). The data presented thus far seem to support this assertion.
The authors are grateful to Dr. James C. White, an oncologist and professor of urology at the University of California, Berkeley, for his helpful discussions of the data presented. This study was supported by grants (5K23HG031924, 5K23HG099863, 5K23HG080802-12, and 15Y
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