Prior administration of a non-steroidal anti-androgen failed to prevent the flare-up caused by a luteinizing hormone-releasing hormone agonist in a patient with metastatic prostate cancer.
Prior administration of a non-steroidal anti-androgen failed to prevent the flare-up caused by a luteinizing hormone-releasing hormone agonist in a patient with metastatic prostate cancer.
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DOI：
10.1186/s13104-015-1297-3
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发表时间：
2015-08-05
影响因子：
1.8
通讯作者：
Yonese J
中科院分区：
文献类型：
--
作者：
Uehara S;Yuasa T;Fujii Y;Yano A;Yamamoto S;Masuda H;Fukui I;Yonese J
‘Flare phenomenon’ after initial luteinizing hormone-releasing hormone agonist administration is a widely approved concept in the treatment of prostate cancer. In most guidelines, concomitant therapy with anti-androgens is recommended to prevent this flare phenomenon. However, there are few reports describing serum prostate-specific antigen transitions after hormonal therapy. Here, we present a case of a man who experienced the biochemical and clinical flare phenomenon despite prior anti-androgen use and who has detailed data. A 70-year-old Asian man with metastatic prostate cancer (multiple bone) was referred to our hospital. He was treated with prior anti-androgens and luteinizing hormone-releasing hormone agonist. Regardless of prior use of anti-androgens, his low back pain caused by bone metastases was deteriorated and serum prostate-specific antigen level was raised from 974.8 ng/mL to 2,555.5 ng/mL within 3 weeks. Then, his serum prostate specific antigen level started to decrease along with the pain. The nadir reached 1.0 ng/mL and remained for 6 months. Because the serum level of prostate-specific antigen then began to increase again, anti-androgen was discontinued for anti-androgen withdrawal syndrome. Then the serum level decreased again to less than 0.1 ng/mL. Until now, his serum prostate-specific antigen level has been maintained at less than 0.1 ng/mL for more than 30 months without any clinical progressions. We present the case of a patient in whom a clinical flare caused by an leuteinizing hormone-releasing hormone agonist was not prevented by prior anti-androgen administration. In addition, the nadir level of prostate-specific antigen when he received leuteinizing hormone-releasing hormone monotherapy was ten times lower than when he received concomitant therapy, and period of anti-androgen withdrawal syndrome was longer than usual. In this case, anti-androgen was probably not effective from the initial administration. Awareness of the possibility of ineffectiveness of anti-androgens is important in the treatment of symptomatic metastatic prostate cancer. Leuteinizing hormone-releasing hormone antagonist and surgical castration is a more reliable clinical approach for the prostate cancer patients with symptomatic metastatic disease.
