Performance and inter-observer variability of prostate MRI (PI-RADS version 2) outside high-volume centres

Abstract

Objective: Despite the growing trend to embrace pre-biopsy MRI in the diagnostic pathway for prostate cancer (PC), its performance and inter-observer variability outside high-volume centres remains unknown. This study aims to evaluate sensitivity of and variability between readers of prostate MRI outside specialized units with radical prostatectomy (RP) specimen as the reference standard.

Materials and methods: Retrospective study comprising a consecutive cohort of all 97 men who underwent MRI and subsequent RP between January 2012 and December 2014 at a private hospital in Sweden. Three readers, blinded to clinical data, reviewed all images (including 11 extra prostate MRI to reduce bias). A tumour was considered detected if the overall PI-RADS v2 score was 3–5 and there was an approximate match (same or neighbouring sector) of tumour sector according to a 24 sector system used for both MRI and whole mount sections.

Results: Detection rate for the index tumour ranged from 67 to 76%, if PI-RADS 3–5 lesions were considered positive and 54–66% if only PI-RADS score 4–5 tumours were included. Detection rate for aggressive tumours (GS ≥ 4 + 3) was higher; 83.1% for PI-RADS 3–5 and 79.2% for PI-RADS 4–5. The agreement between readers showed average $\kappa$ values of 0.41 for PI-RADS score 3–5 and 0.51 for PI-RADS score 4–5.

Conclusions: Prostate MRI evidenced a moderate detection rate for clinically significant PC with a rather large variability between readers. Clinics outside specialized units must have knowledge of their performance of prostate MRI before considering omitting biopsies in men with negative MRI.

Keywords:

• Prostatic neoplasms
• magnetic resonance imaging
• radical prostatectomy
• interobserver agreement
• observer variation

Acknowledgements

None of the sponsors had any part in the study design or access to the data nor had they any influence on or access to the analysis, the results, or the manuscript. We sincerely thank Ewa Löfkvist for her kind assistance in retrieving the pathology reports and Helén Ahlgren for her excellent help with database management. We also thank Karin Stinesen Kollberg for English language editing and review.

Disclosure statement

Sigrid V. Carlsson has received a lecture honorarium and travel support from Astellas Pharma (unrelated to current study). No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by research grants from the Swedish Cancer Society (Contract number 2017/620), The Swedish Research Council [no. 2016-01973], and from the Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement [ALFGBG-724401 and ALFGBG-774531]. Part of Kimia Kohestanis work on this paper was supported by Anna-Lisa and Bror Björnsson’s Foundation, Märta and Gustaf Ågren’s Research Foundation, the Research Foundation at the Department of Urology at Sahlgrenska University Hospital, and the Royal and Hvitfeldtska Foundation. Sigrid V. Carlssons work on this paper was supported by research grants from the Sidney Kimmel Center for Prostate and Urologic Cancers, a Specialized Program of Research Excellence grant [P50-CA92629] from the National Cancer Institute to Dr. Howard Scher, a National Institutes of Health/National Cancer Institute Cancer Center Support Grant [P30-CA008748] to Memorial Sloan Kettering Cancer Center, a grant from the National Cancer Institute as part of the Cancer Intervention and Surveillance Modelling Network [U01CA199338-02], and the David H. Koch prostate cancer research fund.