Racial Variation in the Outcome of Subsequent Prostate Biopsies in Men With an Initial Diagnosis of Atypical Small Acinar Proliferation

2017 ◽  
Vol 15 (6) ◽  
pp. e995-e999
Author(s):  
Robert Scott Libby ◽  
Jordan J. Kramer ◽  
Hoang Minh Tue Nguyen ◽  
Allison Feibus ◽  
Raju Thomas ◽  
...  
Keyword(s):  
Initial Diagnosis ◽  
Racial Variation ◽  
Atypical Small Acinar Proliferation ◽  
Prostate Biopsies

Rate of clinically significant prostate cancer on repeat saturation biopsy after a diagnosis of atypical small acinar proliferation

2021 ◽  
pp. 039156032199359
Author(s):  
Angelo Totaro ◽  
Luca Di Gianfrancesco ◽  
Francesco Pinto ◽  
Marco Racioppi ◽  
Giuseppe Palermo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Risk ◽  
Prostate Biopsy ◽  
Initial Diagnosis ◽  
Repeat Biopsy ◽  
Atypical Small Acinar Proliferation ◽  
Saturation Biopsy ◽  
Prostate Biopsies ◽  
History Of ◽  
Clinically Significant

Background: Atypical small acinar proliferation (ASAP) occurs in approximately 5% of prostate biopsies. Approximately 30%–40% of these patients may develop prostate cancer (PCa) within a 5-year period, often not clinically significant. Current guidelines recommend a repeat biopsy within 3–6 months after the initial diagnosis, but it seem not to be the best strategy. Methods: Objectives—evaluating the natural history of ASAP, stratifying the risk of csPCa after ASAP, identifying predictive factors of PCa after atypical diagnosis. Materials and methods—retrospective single-institutional study on patients undergoing prostate biopsy for suspicious PCa (2005–2016). We evaluated the incidence of overall PCa, intermediate-high risk of PCa and csPCa in case of ASAP, according to D’Amico classification and Epstein modified criteria. Results: Out of 4.567 patients undergoing prostate biopsy, ASAP was detected in 2.6% of cases. All patients with ASAP underwent repeat saturation biopsy within 6 months and PCa was diagnosed in 34.5%. According to D’Amico classification, 26%, 5.9%, and 2.5% had low, intermediate, and high-risk disease, respectively. According modified Epstein criteria, the incidence of csPCa was 12.6%. LRT showed that the overall probability to develop PCa doubled when PSA density (PSAD) moved from values lower than 0.13 ng/ml/cc to class 0.13–0.30 ng/ml/cc, and it tripled when PSAD was higher than 0.30 ng/ml/cc. Conclusions: The rate of csPCa in patients with an initial diagnosis of ASAP who had repeat biopsy was 12.6%. The overall PCa rate was 34.5%. Among patient undergoing RP, an upgrading from ncsPCa to csPCa was reported in 35% of cases. PSAD is the only predictive factor directly associated to the risk of developing PCa on repeat biopsy. These findings suggest that immediate repeat biopsy remains the correct strategy in absence of novel predictor factors and non-invasive diagnostic evaluations.

scholarly journals Clinical strategy of repeat biopsy in patients with atypical small acinar proliferation (ASAP)

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hwanik Kim ◽  
Jung Kwon Kim ◽  
Gheeyoung Choe ◽  
Sung Kyu Hong
Keyword(s):  
Initial Diagnosis ◽  
Repeat Biopsy ◽  
Atypical Small Acinar Proliferation ◽  
Prostate Biopsies ◽  
Gleason Pattern ◽  
Biopsy Core ◽  
Clinically Significant ◽  
Current Guidelines ◽  
Clinical Strategy

AbstractAtypical small acinar proliferation (ASAP) occurs in approximately 5% of prostate biopsies. Approximately 30–40% of patients with ASAP have biopsy detectable prostate cancer (PCa) within 5 years. Current guidelines recommend a repeat biopsy within 3–6 months after the initial diagnosis. The aim of the present study was to examine the association between ASAP and subsequent diagnosis of clinically significant PCa (csPCa). The need for immediate repeat biopsy was also evaluated. We identified 212 patients with an ASAP diagnosis on their first biopsy at our institution between February 2006 and March 2018. Of these patients, 102 (48.1%) had at least one follow-up biopsy. Clinicopathologic features including rates of subsequent PCa and csPCa were assessed. Thirty-five patients subsequently underwent radical prostatectomy (RP). Their pathologic results were reviewed. csPCa was defined as the presence of Gleason score (GS) ≥ 3 + 4 in ≥ 1 biopsy core. Adverse pathology (AP) was defined as high-grade (primary Gleason pattern ≥ 4) or non-organ-confined disease (pT3/N1) after RP. Of 102 patients, 87 (85.3%), 13 (12.7%), and 2 (2.0%) had one, two, and three follow-up biopsies, respectively. Median time from the initial ASAP diagnosis to the 2nd follow-up biopsy and the last follow-up biopsy were 21.9 months (range 1–129 months) and 27.7 months (range 1–129 months), respectively. Of these patients, 46 (45.1%) were subsequently diagnosed with PCa, including 20 (19.6%) with csPCa. Only 2 (2.0%) patients had GS ≥ 8 disease. Five (4.9%) patients had number of positive cores > 3. Of 35 patients who subsequently underwent RP, seven (20%) had AP after RP and 17 (48.6%) showed GS upgrading. Of these 17 patients, the vast majority (16/17, 94.1%) had GS upgrading from 3 + 3 to 3 + 4. 45.1% of patients with an initial diagnosis of ASAP who had repeat prostate biopsy were subsequently diagnosed with PCa and 19.6% were found to have csPCa. Our findings add further evidence that after a diagnosis of ASAP, a repeat biopsy is warranted and that the repeat biopsy should not be postponed.

Racial variation in the outcome of subsequent prostate biopsies in men with an initial diagnosis of atypical small acinar proliferation (ASAP).

2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 141-141
Author(s):  
Jordan J. Kramer ◽  
Robert Scott Libby ◽  
Allison H. Feibus ◽  
Nora M. Haney ◽  
Ian R. McCaslin ◽  
...  
Keyword(s):  
Prostate Biopsy ◽  
Medical Center ◽  
Specific Antigen ◽  
Low Grade ◽  
Veterans Health ◽  
Initial Finding ◽  
Racial Variation ◽  
Atypical Small Acinar Proliferation ◽  
Prostate Biopsies ◽  
Increased Risk

141 Background: African Americans (AA) are known to have more aggressive prostate cancer (PCa) and a greater probability of death from PCa. We sought to determine predictors of subsequent detection and risk stratification of PCa in a racially diverse group of men who presented with atypical small acinar proliferation (ASAP) on initial prostate biopsy. Methods: Upon receiving IRB approval, a retrospective analysis was performed on men from the Southeast Louisiana Veterans Health Care System and Tulane University Medical Center who presented with ASAP on initial prostate biopsy and subsequently received confirmatory prostate biopsies from September 2000 through July 2015. Confirmatory biopsy with a greater than 3-year interval from the initial were excluded. Self-identified race, age, body mass index (BMI), transrectal ultrasound (TRUS) volume, serum prostate-specific antigen (PSA), PSA velocity (PSAV), PSA density (PSAD), and elapsed time between biopsies were evaluated to determine if they were predictors of subsequent PCa diagnosis in patients with an initial finding of ASAP. Results: Of the 106 men in the analysis cohort, 75 (71%) were AA and 31 (29%) were not African American (non-AA). AA had higher PSA, PSAV, and PSAD (all p < 0.05). Age, BMI and TRUS volume were not statistically different between AA and non-AA. PCa was diagnosed in subsequent biopsy in 42 (40%) patients without significant racial variation; 30 (40%) AA vs 12 (39%) non-AA. Of the 42 men with PCa, 25 (24%) met Epstein pathological criteria for significant disease, although without racial variation; 18 (24%) AA vs 7 (23%) Non-AA. Only 10 (9%) men, again without racial variation, had any component of Gleason 4; 7 (9%) AA vs 3 (10%) non-AA. On multivariate analysis, increasing age, PSA and PSAD were significant predictors of cancer on repeat biopsy while race, BMI, TRUS volume and number of cores with ASAP were not. Conclusions: AA diagnosed with ASAP on initial prostate biopsy do not have increased risk of PCa on confirmatory biopsy compared to non-AA. Regardless of race, most cancers were low grade and lower volume, and AA with ASAP should be managed in a similar manner to non-AA with ASAP.

Using PSMA (prostate-specific membrane antigen) evaluation on prostate biopsies for risk stratification at time of initial diagnosis.

2019 ◽  
Vol 37 (7_suppl) ◽  
pp. 6-6 ◽  
Author(s):  
Marie C. Hupe ◽  
Christian Philippi ◽  
Doris Roth ◽  
Christiane Kuempers ◽  
Julika Ribbat-Idel ◽  
...  
Keyword(s):  
Risk Stratification ◽  
Treatment Decision ◽  
Disease Recurrence ◽  
Initial Diagnosis ◽  
Curative Surgery ◽  
Grade Group ◽  
Prostate Biopsies ◽  
Increased Risk ◽  
Risk Of Disease ◽  
Psma Expression

6 Background: Stratifying prostate cancer (PCa) patients into risk groups at time of initial diagnosis for individual treatment decision is still a major clinical challenge. PSMA expression has emerged as a promising prognostic biomarker since its overexpression in radical prostatectomy specimens (RP) has been linked to disease recurrence. Aim of our study was to assess the prognostic value of PSMA on prostate biopsies (Bx) thus improving risk stratification at time of initial diagnosis. Methods: Immunohistochemistry for PSMA expression was performed on 294 Bx with corresponding RP, 621 primary tumor foci from 242 RP, 43 locally advanced or recurrent tumors, 34 lymph node metastases, 78 distant metastases, and 52 benign prostatic samples. Grade group, PSA, TNM-, and R-status were assessed as clinico-pathologic features. Primary endpoint was recurrence-free survival (RFS). Chi-square, ANOVA-analyses, Cox regression and log rank tests were performed for statistical analyses. Results: PSMA expression significantly associates with grade group and initial PSA level. Elevated PSMA expression on both RP and Bx significantly correlates with an increased risk of disease recurrence after curative surgery. 5-year RFS rates are 88.2%, 74.2%, 67.7%, and 26.8% for patients with no, low, medium, or high PSMA expression on Bx, respectively. Elevated PSMA level on Bx predict a 4-fold increased risk of disease recurrence independently from initial PSA and grade group on Bx. PSMA expression significantly increases during PCa progression. Conclusions: PSMA qualifies as an independent prognostic biomarker on Bx at time of initial diagnosis in addition to the established markers PSA and grade group. PSMA predicts disease recurrence following curative surgery and potentially improves the discrimination indolent vs. aggressive disease. We propose the routine assessment of PSMA expression on Bx for outcome prediction and risk stratification at time of initial diagnosis prior to treatment decision.

Practice Patterns of Clinicians Following Isolated Diagnoses of Atypical Small Acinar Proliferation on Prostate Biopsy Specimens

2004 ◽  
Vol 128 (5) ◽  
pp. 557-560 ◽  
Author(s):  
Oluwole Fadare ◽  
Sa Wang ◽  
M. Rajan Mariappan
Keyword(s):  
Prostate Biopsy ◽  
Practice Patterns ◽  
Specific Antigen ◽  
Intraepithelial Neoplasia ◽  
High Rate ◽  
Pathology Report ◽  
Atypical Small Acinar Proliferation ◽  
Prostate Biopsies ◽  
Diagnostic Threshold ◽  
The Mean

Abstract Context.—The controversial diagnostic term atypical small acinar proliferation (ASAP) has gained some acceptance as a legitimate way for pathologists to describe minute foci of small prostatic acini that raise the suspicion of carcinoma but that fail to attain the requisite diagnostic threshold for carcinoma. Objective.—To investigate the practice patterns of clinicians following this diagnosis and to identify clinicopathologic parameters that may be of influence. Design.—All cases with a diagnosis of ASAP on a prostate biopsy specimen during a 7-year period were retrieved from our computerized database. Cases with concurrent diagnoses of adenocarcinoma and/or prostatic intraepithelial neoplasia were excluded. Medical and pathologic records for the remaining patients were reviewed and correlated with pathologic data. Results.—Fifty-five (2.8%) of 1964 prostate biopsies performed during this period provided the diagnosis of ASAP, of which 36 met our study criteria. The average age of the patients was 65 years, and the mean total prostate-specific antigen (PSA) level was 6.41 ng/mL. The rate of biopsy subsequent to an ASAP diagnosis was 67% (24/36), and the mean duration to subsequent biopsy was 246 days (median, 182 days; range, 71–728 days). Adenocarcinoma was diagnosed in 9 (38%) of 24 specimens taken during the subsequent biopsy. Neither age nor PSA level significantly predicted a greater likelihood for subsequent biopsy. Additionally, among patients who received a subsequent biopsy, the aforementioned parameters were not predictive of carcinoma in the second biopsy. The average number of cores following an ASAP diagnosis (6 cores) did not differ significantly from the average at initial biopsy (7.18 cores, P = .64). Pathology report characteristics, such as inclusion of a descriptive note or explicit recommendation of a second biopsy, did not significantly increase the likelihood of a subsequent biopsy. Reasons for a delay in or lack of a subsequent biopsy following an ASAP diagnosis were miscellaneous and attributable to the patients in most cases. Conclusion.—The diagnosis of ASAP generates a subsequent biopsy in two thirds of cases after an average duration of 246 days. Although closer follow-up may be recommended based on the high rate of association with carcinoma on subsequent biopsy, we found no evidence that any delays in or lack of a subsequent biopsy is attributable to a lack of understanding on the part of urologists of the significance of the diagnosis.

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