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What defines biochemical recurrence after prostatectomy?
Executive Summary
Biochemical recurrence (BCR) after radical prostatectomy is defined by a rising serum prostate‑specific antigen (PSA) after surgery, but no single universally agreed numeric threshold exists; most major analyses and guidelines use a confirmed PSA ≥0.2 ng/mL as the working definition, while other cutpoints (0.1–0.4 ng/mL) and clinical context affect management decisions [1] [2] [3]. Contemporary literature emphasizes combining PSA thresholds with kinetics, pathology, and imaging to guide salvage therapy rather than relying on a lone number [4] [5].
1. Why the PSA number matters — and why experts still argue about it
The simplest, most cited definition of BCR is two consecutive PSA values ≥0.2 ng/mL, a threshold commonly adopted in surgical series and guideline-adjacent literature because it balances early detection with avoidance of overtreatment [1] [2] [3]. Multiple cohort analyses and meta-analyses demonstrate that using slightly different cutpoints (0.1, 0.3, 0.4 ng/mL) changes the date of recurrence and the proportion of patients labeled as recurrent, but does not consistently overturn prognostic relationships between clinicopathologic factors and outcomes; thus, many authors argue the exact numeric cutoff is less important for research associations than for individual treatment timing [6] [7]. The debate persists because lower cutpoints increase sensitivity but risk unnecessary salvage interventions, while higher cutpoints delay therapy but reduce false positives.
2. Practical definitions clinicians use when patients ask “Has my cancer come back?”
In clinical practice, different institutions and publications operationalize BCR variably: some use a single PSA ≥0.4 ng/mL, others require three rising PSAs, and still others count any detectable PSA above 0.03 ng/mL in high‑risk contexts, with confirmation strategies meant to exclude lab variability or transient rises [8] [4] [6]. Guideline-oriented recommendations often emphasize the role of confirmatory testing and serial kinetics—PSA doubling time and velocity—to decide whether to recommend salvage radiotherapy or systemic therapy rather than treating a single isolated value [4] [5]. This pragmatic heterogeneity reflects the tension between population‑level reproducibility for research and patient‑level individualized decision making.
3. How other criteria and imaging are reshaping the meaning of recurrence
Recent analyses argue clinicians should “trust biology, not a number,” integrating PSA kinetics, pathological risk features (Gleason/Grade Group, stage), and next‑generation imaging to determine whether a rising PSA represents localized relapse amenable to salvage radiation or systemic/localized metastatic disease requiring different approaches [4] [5]. Studies show that earlier imaging with PSMA PET can detect oligometastatic disease at PSA levels previously considered too low for localization, which complicates reliance on any single PSA cutoff and supports personalized timing of salvage therapy [4]. Thus, the modern paradigm treats BCR as a clinical syndrome defined by PSA rise plus risk‑stratifying data, not only a numerical threshold.
4. What different authoritative bodies actually recommend and why they differ
Professional groups and high‑profile centers frequently converge on PSA ≥0.2 ng/mL confirmed as a commonly cited surgical BCR definition, while recommending that salvage treatment decisions consider PSA ≤0.5 ng/mL windows for optimal radiotherapy timing and emphasize PSA kinetics and life expectancy in counseling [2] [5]. Other investigators contend that waiting for higher thresholds risks missing curative windows, whereas immediate intervention at very low detectable PSA risks overtreatment; this yields divergent operational definitions used in trials and institutional protocols [7] [8]. The apparent disagreement reflects differences in prioritizing sensitivity versus specificity, available imaging, patient comorbidity, and evolving evidence on salvage therapy efficacy.
5. Bottom line for patients and researchers: definitions matter, but context matters more
For reporting and research, adopting two consecutive PSAs ≥0.2 ng/mL permits comparability across studies and aligns with many guideline‑adjacent references; for individual patients, clinicians should combine that numeric signal with PSA doubling time, pathological features, imaging results, and patient goals before recommending salvage therapy [1] [4] [5]. Emerging data supporting early, image‑guided interventions and the prognostic value of PSA kinetics mean clinicians increasingly treat PSA trends and biology as the action drivers rather than a single cutoff, highlighting the need for shared decision making and personalized risk stratification when BCR is suspected [7] [4].