Evidence map›Paper›PMID 42997172›Full record

ArticleTranslational andrology and urology2026

Development and internal validation of a clinical model to increase the diagnostic probability of prostate cancer in patients with prostate-specific antigen levels of 4.0-10.0 ng/mL.

Bao Xu, Jiahong Jiang, Litao Zhang, Qiuxia Ge, Jingping Liu, Jun Zhou

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Article in Translational andrology and urology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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6 authors.

Bao XuDepartment of Clinical Laboratory, Jiangsu Province (Suqian) Hospital, Suqian, China.
Jiahong JiangDepartment of Laboratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Litao ZhangDepartment of Laboratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Qiuxia GeDepartment of Laboratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jingping LiuDepartment of Laboratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jun ZhouDepartment of Laboratory Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Distinguishing prostate cancer (PCa) from benign prostatic hyperplasia (BPH) in the prostate-specific antigen (PSA) gray zone (4.0-10.0 ng/mL) remains a clinical challenge due to the limited specificity of PSA. While complex radiomics and AI models exist, their high resource requirements limit accessibility. We constructed a diagnostic model to distinguish PCa from BPH in patients with PSA ranging 4.0 to 10.0 ng/mL. Methods: This retrospective study recruited consecutive458 participants from January 2017 to September 2019. Eligible patients had PSA levels between 4.0-10.0 ng/mL and underwent prostate biopsy or surgery with histopathological confirmation of PCa or BPH by two independent pathologists. Candidate predictors included age, PSA, free PSA (FPSA), free/total PSA ratio (F/T ratio), prostate volume (PV), PSA density (PSAD), white blood cell count (WBC), neutrophil (NE), lymphocyte (LY), hemoglobin (HB), platelet (PLT), alanine aminotransferase (ALT), aspartate transaminase (AST), total protein (TP), albumin (ALB), globulin (GLB), creatinine (CREA), urea nitrogen (UREA), and phosphorus (PHOS). Multivariable logistic regression was applied to screen independent risk factors, with bootstrap resampling for internal validation. Model discrimination, calibration and clinical net benefit were assessed via receiver operating characteristic (ROC) curves, calibration plots and decision curve analysis (DCA). Results: Among 458 patients (192 with PCa, 266 with BPH), the PCa group had significantly higher PSA, PSAD, AST, TP, ALB, GLB and PHOS, but lower FPSA, F/T ratio and PV (all P<0.05). Age showed marginal significance (P=0.07) and was entered into the regression according to the P<0.1 screening standard. Age, PSA, FPSA, PV, AST, GLB and PHOS were independent PCa predictors. The model's area under the curve (AUC) was 0.834 [95% confidence interval (CI): 0.799-0.867], with optimism-corrected C-index 0.832 (95% CI: 0.796-0.869). Calibration (calibration: 0.92; Hosmer-Lemeshow test P=0.49) and DCA confirmed stable performance and clinical utility. At the Youden-index cutoff of 0.503, sensitivity reached 69.79% (95% CI: 62.7-76.2%), specificity 80.83% (95% CI: 75.5-85.4%). Conclusions: This clinical model shows promise for identifying PCa risk in patients with PSA 4.0-10.0 ng/mL; however, external validation in independent cohorts is needed before clinical implementation.

Indexed as

Benign prostatic hyperplasia (BPH)diagnostic modelprostate biopsyprostate cancer (PCa)

Identifiers

PMID42997172
PMCPMC13741067

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