Delays in radical prostatectomy for prostate cancer and survival outcomes.
البيانات الوصفيةعرض كامل للتسجيلة
A recent publication in your journal, involving 619 Canadian patients undergoing radical prostatectomy (RP), suggests increased delays to time of surgery may be associated with higher rates of biochemical recurrence(BCR)1 in men with high risk disease. However BCR per se is not strongly correlated to the “hard” outcomes of developing metastases or increase cancer mortality which are more heavily influenced by Gleason score (GS) and pathological stage. The manuscript concludes “…further studies are warranted to … assess the impact of SWT (surgical wait time) on cancer-specific survival and overall survival (OS)” and additional retrospective studies with larger cohorts were requested. In the state of South Australia we have the longest running prostate cancer registry in the Southern Hemisphere, and have performed such an analysis in respect of prostate cancer outcomes and delays in care2. We identified 3,140 eligible patients between 1998 and 2013, included all treatment types (RP, radiotherapy [RT], androgen deprivation [ADT]), local and advanced disease and examined the effect of treatment delay (time from diagnosis to date of first treatment) on prostate cancer specific mortality (PCSM) and OS, using Cox Proportional Hazards modelling and competing risks regression, comparing quartiles of delay across the cohort. Adjustment was made for age, PSA levels, treatment modality and GS. Quartiles of delay were as follows (days)—Q1: 35, Q2: 86, Q3: 138.0, Q4: 264. Quartile two was used as the reference point and extensive subgroup analyses were conducted. Shorter delays were associated with hormonal treatment, high Gleason score and high PSA values. PCSM, in an age adjusted model, was highest in Q1 (HR-4.37) compared to Q3 (HR-1.29) and Q4 (HR-1.55). After additional adjustment for GS, PSA value and treatment type, Q1 still remained at highest risk (HR-2.46). The fact shorter delays were associated with poorer outcomes is possibly explained because patients with high PSA levels and high GS at biopsy are more likely to receive treatment sooner, because they represented more aggressive disease. When examining only patients treated with curative intent (RP or RT), delays in Q3 were associated with increased risk of PCSM (HR-2.07), though on sub analysis of RP alone and RT alone, no quartile showed increased risk. On examining the effect of NCCN risk profile, only those in “high risk” group appeared to be at increased risk of poor outcomes, particularly in the context of a short time to treatment. However this most likely reflects the underlying aggressive biology of the disease which led to these patients being treated more quickly in the first place. A similar trend was observed for OS, however after stratification by GS no association between delay and OS could be demonstrated, and within each GS stratum, delays in care were not associated with variation in overall survival. We draw readers’ attention to these findings, which in part, provide the additional evidence from a larger cohort which the authors request.
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