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 Table of Contents  
Year : 2017  |  Volume : 3  |  Issue : 4  |  Page : 133-138

Real-world experience with abiraterone in metastatic castration-resistant prostate cancer

1 Mid-Western Cancer Centre, University Hospital Limerick, Limerick, County Limerick, Ireland
2 Department of Medical Oncology, Sligo University Hospital, Sligo, County Sligo, Ireland

Date of Submission09-Feb-2017
Date of Acceptance05-May-2017
Date of Web Publication14-Aug-2017

Correspondence Address:
Yasar Ahmed
Mid-Western Cancer Centre, University Hospital Limerick, St Nessan's Road, Dooradoyle, Limerick, County Limerick, V94 F858
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ctm.ctm_5_17

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Aim: To evaluate abiraterone in patients with metastatic castration-resistant prostate cancer (mCRPC).
Methods: This is a multicenter retrospective analysis, involving 44 consecutive abiraterone-treated mCRPC patients, in either chemotherapy-naive or postdocetaxel setting.
Results: The study cohort's median age was 68.7 (50–88) years, and the median duration of abiraterone treatment was 8 (1–36) months. Of the 44 patients, 23 (52%) and 21 (47%) patients were in chemotherapy- naive and postdocetaxel groups, respectively. Eastern Cooperative Oncology Group performance status score was 0–1 and 2–3 in 65% and 34% of chemotherapy-naive and 85% and 15% of postdocetaxel patients, respectively. Prostate-specific antigen (PSA) response was achieved in 13 (56.5%) chemotherapy-naive and 14 (66.6%) postdocetaxel patients. The median time to PSA progression was 12 (10.5–13.5) months. Objective radiological response was achieved in 11 (34.6%) patients, stable disease in 16 (55.1%) patients, and progressive disease in 3 (6.8%) patients. Median time to radiographic progression was 10.8 (10.3–11.4) months. Median overall survival was not reached (mean = 17 [14–20.5] months). The most common adverse events related to mineralocorticoid excess include hypokalemia (12%), fluid retention/edema (28%), and hypertension (8%).
Conclusion: This study supports the safety and efficacy of abiraterone for mCRPC patients in the real-world setting.

Keywords: Abiraterone, castrate resistant, metastatic prostate cancer

How to cite this article:
Ahmed Y, Osman N, Sheikh R, Picardo S, Watson G. Real-world experience with abiraterone in metastatic castration-resistant prostate cancer. Cancer Transl Med 2017;3:133-8

How to cite this URL:
Ahmed Y, Osman N, Sheikh R, Picardo S, Watson G. Real-world experience with abiraterone in metastatic castration-resistant prostate cancer. Cancer Transl Med [serial online] 2017 [cited 2018 Jun 20];3:133-8. Available from: http://www.cancertm.com/text.asp?2017/3/4/133/210636

  Introduction Top

Prostate cancer is the fifth leading cause of cancer-related deaths in men worldwide, accounting for approximately 307,000 deaths in 2014.[1] The cancer is increasing continuously in Ireland, reaching 11.9% of death rate.[1] Over 3400 men are diagnosed with prostate cancer every year, with more than 40% of cases localized at the time of diagnosis.[1] Surgical or medical androgen deprivation therapy forms the cornerstone in the management of patients with prostate cancer. The androgen receptor (AR) signaling pathway plays a critical role in the pathogenesis of prostate cancer, through the activation of AR, recognized in the early 1940s.[2] Castration, either surgical or biochemical, leads to significant testicular androgen suppression resulting in tumor regression. Although the initial response rate is high, nearly all men eventually develop castration-resistant disease.[3]

Metastatic castration-resistant prostate cancer (mCRPC) typically confers a poor prognosis with a median survival of approximately 2 years.[4] Docetaxel with prednisone was the first approved treatment for mCRPC, and until now, treatment options for patients progressing on or after docetaxel were limited. However, development of biomarkers for monitoring disease response and progression has recently helped to improve survival.[5]

In April 2011, the Food and Drug Administration approved abiraterone acetate for the treatment of patients with mCRPC following initial docetaxel treatment. This approval extended for chemotherapy-naive patients as well in December 2012.

Abiraterone, a potential androgen synthesis blocker, inhibits androgen biosynthesis from adrenal and intratumoral sources. This potent agent irreversibly inhibits Cytochrome P450 17alpha hydroxylase/17.20 lyase (CYP17), a dual function enzyme that is necessary for testosterone synthesis, thereby blocking androgen synthesis by the adrenal glands and testes as well as within the prostate tumor.[6],[7],[8],[9] It is currently recommended for chemotherapy-naive patients and after progression on chemotherapy.[10]

Despite the rapid introduction of abiraterone into daily practice, there exists a paucity of data with regard to the efficacy and safety of abiraterone in the real-world clinical practice setting. This forms the basis of the present study, which demonstrates the use of abiraterone in patients with mCRPC.

  Methods Top

Study population

mCRPC patients were the patients who experienced disease progression despite androgen deprivation therapy, with a continuous rise in prostate-specific antigen (PSA) or radiographic progression. Patients were assessed based on the Prostate Cancer Working Group 2 (PCWG2) criteria after achieving castration level of serum testosterone (< 50 ng/dL). A total of 44 consecutive abiraterone-treated mCRPC patients from two oncology centers were included in this retrospective study. All patients receiving a daily dose of abiraterone (1000 mg/day), combined with prednisolone (5 mg twice/day), from January 2015 to December 2016, were identified. All enrolled patients had a histological diagnosis of adenocarcinoma of the prostate and continued on androgen deprivation therapy. Abiraterone was continued until disease progression (biochemical/radiological), death, or intolerable adverse events (AEs). The study was approved by the Ethics Committees at both participating hospitals and was carried out as per the approved protocol.

Data collection and outcome measures

Patient demographics, clinicopathological features, and medical data such as age, Gleason score, Eastern Cooperative Oncology Group (ECOG) score, basal PSA, sites of metastasis, hemoglobin (Hb), and alkaline phosphatase (ALP) levels were collected retrospectively from medical records. Overall survival (OS) time, PSA, and radiological progression-free survival (PFS) were analyzed.

OS and PFS were defined as the time from the first dose of abiraterone to death and the time to the first event of radiographic or PSA progression or death, respectively. The biochemical and radiological progression of disease was assessed according to the PCWG-2 criteria. Patients achieving 50% PSA decline were considered as marker responders. PSA progression was defined as 25% increase over the nadir PSA. Data on all grade AEs related to mineralocorticoid excess (pedal edema, hypokalemia, and hypertension) were also collected. This was graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events 4.02 toxicity scale. PFS was calculated from the start of abiraterone therapy until progression or the time of the last follow-up visit, whichever occurred first.

Statistical analysis

Statistical analysis was performed using the Statistical Package for the Social Sciences (SPSS 21.0, SPSS Inc., Chicago, IL, USA). OS and PFS were analyzed using Kaplan–Meier method.

  Results Top

Patient-specific characteristics

During the study period, 44 patients, who fulfilled the study criteria, were included in the analysis. Patients' disease characteristics at baseline and at the time of initiation of abiraterone treatment are shown in [Table 1]. Of these 44 patients, 23 (52%) and 21 (47%) patients were in chemotherapy-naive and postdocetaxel groups, respectively.
Table1: Baseline characteristics

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The median age of the study cohort was 68.7 years (range: 50–88 years), when starting the abiraterone treatment. Overall, 75% of patients had an ECOG performance status of 0–1, while 34% of chemotherapy-naive and 15% of postdocetaxel patients had a score of 2–3.

Prior to commencing abiraterone, the majority of patients in both groups had bone metastases (87% and 85%, respectively). Nodal metastasis was observed in 26% of the prechemotherapy patients and 38% of the postdocetaxel patients. Median hemoglobin and ALP concentration was 11 g/dL and 305 U/L, respectively.


All patients had at least one postabiraterone PSA recorded. The median duration of abiraterone treatment was 8 months (range: 1–36 months). PSA response was achieved in 13 (56.5%) chemotherapy-naive patients and in 14 (66.6%) postdocetaxel patients. All biochemical responses occurred within the first 3 months of commencing treatment. The radiological evaluation of 29 patients was performed according to the PCWG2 criteria. Overall objective response was seen in 11 (37.9%) patients (complete objective response = 5 [17.2%], partial objective response = 6 [20.6%]), while stable disease was seen in 16 (55.1%) patients. Progressive disease was observed in 2 (6.8%) patients.


At the time of analysis, 23 patients experienced PSA and/or radiological progression. The median follow-up duration was 21 months, and the median duration of abiraterone treatment was 8 months (range: 1–36 months). Median time to PSA progression for all patients was 12 months (95% confidence interval [CI]: 10.5–13.5), while median time to radiographic progression was 10.8 months (95% CI: 10.3–11.4). Median OS from the start of abiraterone treatment was not reached (mean = 17 months, 95% CI: 14–20.5). However, the 1- and 2-year OS rate for chemotherapy-naive group and postdocetaxel group was 83% and 70%, respectively [Figure 1].
Figure 1: Kaplan–Meier estimate of overall survival for all patients (n = 44). The overall survival was not reached

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Adverse events

The most common AEs, related to mineralocorticoid excess, were recorded in 28 patients as follows: hypokalemia (12%), fluid retention/edema (28%), and hypertension (8%).

  Discussion Top

In patients with non-mCRPC, the American Urological Association recommends observation and androgen deprivation as the current standard of care.[5] Androgen deprivation therapy was developed in the 1940s following the discovery that androgens play a significant role in the pathogenesis of prostate cancer.[2] Androgen deprivation therapy results in biochemical response and objective tumor response in bone and soft tissue metastatic disease in about 80%–90% of cases with metastatic prostate cancer. Despite some observed response to androgen deprivation therapy, patients eventually experience disease progression.[11],[12],[13] In these cases, disease progression despite adequately depressed serum testosterone is considered castration-resistant disease. When prostate cancer progresses to more distant sites, prognosis is further affected, with a median survival of 9–30 months.

For mCRPC, docetaxel had long been considered as a first-line therapy based on the pivotal TAX327 and SWOG9916 trials.[14],[15] However, novel treatment options have emerged recently, resulting in prolonged OS. The American Society of Clinical Oncology recommends first-line treatment with abiraterone, enzalutamide, or radium-223 (for patients with bone metastases) or a limited course of docetaxel plus prednisone, for postdocetaxel-treated patients experiencing disease progression. The other drugs that are currently being used are sipuleucel-T, cabazitaxel, and prednisone.[5]

AR axis-targeted therapy such as abiraterone that interferes with androgenic stimulation of prostate cancer growth is considered as an essential standard of care for mCRPC. It was suggested that, even in the phase of resistance to medical castration, prostate cancer cells become castration dependent; the same cells seem sensitive to a further inhibition of testosterone synthesis.[2],[16]

The initial Phase III trial with abiraterone was conducted in patients with disease progression after docetaxel treatment.[17] Similar trials have been demonstrated in chemotherapy-naive patients as well.[9],[10],[11],[12],[18]

The pivotal COU-AA-301 trial assessed the effect of abiraterone with progressive mCRPC after docetaxel treatment. Treatment with abiraterone resulted in a 35.4% reduction in the risk of death (14.8 vs. 10.9 months [hazard ratio (HR) = 0.65; 95% CI: 0.54, 0.77; P < 0.001]). The median OS for the abiraterone group was longer by 4.6 months than in the placebo group (15.8 vs. 11.2 months; HR 0.74, 95% CI: 0.64–0.86; P < 0.0001).[11] Abiraterone significantly improved OS, tumor-specific end points,[11] and quality of life in patients with mCRPC progressing.[18] This occurs after convincing evidence for the continued importance of androgen axis signaling, even after chemotherapy, and represents an important advance in the therapy of mCRPC.

COU-A-A302 study assessed abiraterone in chemotherapy- naive mCRPC patients. They showed a similar OS and clinical benefit in terms of radiographic-free survival and PSA response.[12],[19] In clinical trial, abiraterone had improved OS compared with those who received placebo (34.7 months [32.7–36.8] for abiraterone vs. 30.3 months [28.7–33.3] for placebo; HR = 0.81, 95% CI: 0.70–0.93, P = 0.0033).[12],[19]

In the past 5 years, three Phase III trials with abiraterone have been shown to significantly extend survival in mCRPC patients.[11],[12],[17] A recent meta-analysis of randomized controlled trials of the novel generation of AR pathway-targeted agents confirmed their efficacy in improving outcome of mCRPC patients. It showed that agents such as abiraterone and enzalutamide achieved higher OS as compared to prednisolone or placebo.[20]

Dearden et al.[21] in their study on 553 patients from four European countries reported the outcomes that were similar to those found in the aforementioned COU-AA-302 study. Another retrospective Italian study recruited 189 patients, whose reported OS was 26 months and PFS was 10 months.[22] Thus, the clinical efficacy of abiraterone, with reference to its safety, OS, and PFS, in unselected patient population in a nontrial setting was comparable to that of the COU-AA-301 and COU-AA-302.

It is apparent that our results from real-world settings are comparable to those of pivotal clinical trials, as illustrated in [Table 2]. A closer analysis revealed that patient's cohort of our study has poorer performance status, but with nearly similar age group. In Phase III clinical trial, no patients with ECOG performance status of 3 were enrolled.[18],[19],[20]

The median duration of abiraterone treatment was 8 months (range: 1–36 months). In our cohort, abiraterone effectively achieved a PSA response (≥ 50% PSA decline) in 13 (56.5%) chemotherapy-naive patients and in 14 (66.6%) postdocetaxel patients. All biochemical responses were achieved within the first 3 months of treatment. This is comparable with COU-AA-302 trial as well with recently published data with a similar study design carried out in the UK,[26] the KSA,[27] and Hong Kong.[28]

We observed higher rate of PSA response (56%) in the postdocetaxel group as compared with the PSA response rate of 29.5% reported in the COU-AA-301 clinical trial. Our result is in line with those of other studies, done on patients treated in routine practice, in France and the Netherlands (53.2%), Italy (48.4%), Canada (45%), the KSA (56%), and Belgium (57.4%).[21],[22],[25],[27],[29]

Although OS was not reached in our study, median OS was established in COU-AA-301 and COU-AA-302 and other observational studies.[25],[26],[27],[30],[31] All the patients in our study demonstrated a good tolerance and compliance to abiraterone. However, a high proportion of included patients presented an advanced disease. No patient discontinued or interrupted treatment due to AEs.

In COU-AA-301 and COU-AA-302 trials, abiraterone was associated with elevated mineral corticoid levels' fluid retentions and edema. Our series showed similar rate of fluid retention and edema, but lower rate of hypertension and hypokalemia. Recently, van Praet et al.[25] retrospectively assessed 368 patients with mCRPC during the Belgian CU program. Concern was raised over a high incidence of hypokalemia. Similar assessments from French temporary authorization program and Italian named patient program and the Canadian program studies reported good clinical outcome and low AEs.[21],[22],[28] Zekri et al.[26] described a cohort of patients similar to that of our study, the results of which agree with our results, reporting no new AEs, thus confirming the safety of abiraterone usage.

There is no ideal design of prospective clinical trials to identify and document AEs. However, this is not necessarily the case in the real-life clinical practice. Hence, we focused on objective treatment-associated AEs, related to mineralocorticoid excess, such as hypokalemia and fluid retention/edema. The AEs' profile witnessed in our patients was similar to those observed in the landmark clinical trials.[16],[17],[18],[29]

This study had the typical shortcomings of retrospective studies. Diagnoses and outcome documentation was not protocol prescribed, and there are prevalence of selection bias as well as missing data. The clinical data were obtained primarily from only two oncology units, which may limit the generalization of our outcome to other clinical settings. Our data might not be descriptive for every patient with mCRPC treated in real-life practice. However, the objective outcomes were based on fixed data (laboratory data, radiological report, and time points). Thus, we presume that these limitations might not affect our study reliability to assess the clinical activity of abiraterone in patients with mCRPC.

This study supports the safety and efficacy of abiraterone in patients with mCRPC, in real-world setting. PFS and OS were comparable to Phase III clinical trial results. Abiraterone leads to significant biochemical and objective radiological responses as compared to those reported in clinical trials. Thus, from our study, we conclude that abiraterone is a safe and effective treatment for mCRPC patients.
Table2: Comparison of results of pivotal clinical trials with our study and similar real-world studies

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Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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  [Table 1], [Table 2]


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