VITAMIN D TREATMENT OF PROSTATE CANCER

流行病学数据表明，维生素D可能在前列腺癌的发病机制中发挥作用。此外，体外和动物研究表明，维生素D抑制前列腺癌细胞的生长。这项研究旨在研究维生素D在治疗早期前列腺癌男性中的潜在临床效用。如果在前列腺癌的主要治疗（手术切除术或放射治疗）后，男性表现出前列腺肿瘤标志物前列腺特异性抗原（PSA）的血清水平升高，则男性被纳入本研究。他们必须患有A或B期疾病，并且没有转移的证据，因此具有最小的复发性疾病。该研究的主要终点是显示PSA水平的上升速率减缓，作为维生素D治疗（骨化三醇，Rocaltrol-Roche）时前列腺癌生长减缓的指标。到目前为止，本研究已招募了8名其他方面健康的男性。1例受试者在开始治疗前因发现潜在转移性疾病而被排除。7例受试者开始接受骨化三醇治疗。2例受试者因发生肾结石而退出治疗。1例受试者因其医生开始雄激素消融治疗而退出研究，但该受试者没有癌症进展的客观证据。所有7例受试者均显示出对治疗的有益应答，与治疗开始前的升高速率相比，PSA升高速率减慢。无论是在任何情况下，还是在整个群体中，这种放缓都是显著的。每例受试者的基线PSA倍增时间不同，对骨化三醇的反应至少是倍增时间的两倍。在一些患者中，倍增时间增加了五倍。尽管招募已结束，但由于PSA升高速率减缓表明对治疗的有益应答，2例男性患者的研究仍在进行中。

Epidemiologic data suggest that vitamin D may play a role in the pathogenesis of prostate cancer. Moreover, in vitro and animal studies have shown that vitamin D inhibits the growth of prostate cancer cells. This study was designed to examine the potential clinical utility of vitamin D in treating men with early stages of prostate cancer. Men were enrolled into this study if, after primary treatment of their prostate cancer (surgical prostatectomy or radiation therapy), they demonstrated a rising serum level of the prostate tumor marker, Prostatic Specific Antigen (PSA). They must have had stage A or B disease and not have evidence of metastasis, and therefore have minimal recurrent disease. The primary endpoint of the study is to show a slowing of the rate of rise of PSA levels as an index of slowed prostate cancer growth while on vitamin D therapy (calcitriol, Rocaltrol-Roche). Eight otherwise healthy men have thus far been enrolled in this study. One subject was excluded prior to the initiation of therapy due to the identification of potential metastatic disease. Seven subjects have been initiated on calcitriol therapy. Two subjects were withdrawn from therapy due to the development of kidney stones. One subject was withdrawn from the study because his physician initiated androgen ablation therapy, although there was no objective evidence of cancer progression in this individual. All 7 subjects have shown a beneficial response to the therapy, with a slowing of the PSA rate of rise compared to the rate of rise before therapy was initiated. The slowing was significant in every case as well as the group as a whole. The baseline PSA doubling time in each subject differed, the response to calcitriol was at least a doubling of the doubling time. In some patients the doubling time increased five-fold. Although recruitment has closed, study is ongoing in 2 men because of the beneficial response to therapy as indicated by slowed rate of PSA rise.