Leah Shepherd1, Álvaro H Borges2, Lene Ravn3, Richard Harvey4, Mark Bower5, Andrew Grulich6, Michael Silverberg7, Gitte Kronborg8, Massimo Galli9, Ole Kirk2, Jens Lundgren2, Amanda Mocroft1. 1. Research Department of Infection and Population Health, University College London, London, UK. 2. Centre for Health & Infectious Disease Research (CHIP), Department of Infectious Diseases, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. 3. Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark. 4. Charing Cross Oncology Laboratory and Trophoblastic Disease Centre, Charing Cross Hospital Campus of Imperial College Healthcare National Health Service Trust, London, UK. 5. National Centre for HIV Malignancy, Chelsea and Westminster Hospital NHS Foundation Trust, London, UK. 6. Kirby Institute, The University of New South Wales, Sydney, NSW, Australia. 7. Kaiser Permanente Northern California, Oakland, CA, USA. 8. Institut for Klinisk Medicin, Hvidovre Hospital, Hvidovre, Denmark. 9. Clinic of Infectious Disease, Luigi Sacco Hospital, Milan, Italy.
Abstract
BACKGROUND: It is common practice to use prostate specific antigen (PSA) ≥4.0 ng/ml as a clinical indicator for men at risk of prostate cancer (PCa), however, this is unverified in HIV+ men. We aimed to describe kinetics and predictive value of PSA for PCa in HIV+ men. METHODS: A nested case control study of 21 men with PCa and 40 matched-controls within EuroSIDA was conducted. Prospectively stored plasma samples before PCa (or matched date in controls) were measured for the following markers: total PSA (tPSA), free PSA (fPSA), testosterone and sex hormone binding globulin (SHBG). Conditional logistic regression models investigated associations between markers and PCa. Mixed models were used to describe kinetics. Sensitivity and specificity of using tPSA >4 ng/ml to predict PCa was calculated. Receiver operating characteristic curves were used to identify optimal cutoffs in HIV+ men for total PSA. RESULTS: 61 HIV+ men were included with a median 6 (IQR 2-9) years follow-up. Levels of tPSA increased by 13.7% per year (95% CI 10.3, 17.3) in cases, but was stable in controls (-0.4%; 95% CI -2.5, 1.7). Elevated PSA was associated with higher odds of PCa at first (OR for twofold higher 4.7; 95% CI 1.7, 12.9; P<0.01) and last sample (8.1; 95% CI 1.1, 58.9; P=0.04). A similar relationship was seen between fPSA and PCa. Testosterone and SHBG level were not associated with PCa. tPSA level >4 ng/ml had 99% specificity and 38% sensitivity. The optimal PSA cutoff was 1.5 ng/ml overall (specificity =84%, sensitivity =81%). CONCLUSIONS: PSA was highly predictive of PCa in HIV+ men; however, the commonly used PSA>4 ng/ml to indicate high PCa risk was not sensitive in our population and use of the lower cutoff of PSA>1.5 ng/ml warrants consideration.
BACKGROUND: It is common practice to use prostate specific antigen (PSA) ≥4.0 ng/ml as a clinical indicator for men at risk of prostate cancer (PCa), however, this is unverified in HIV+ men. We aimed to describe kinetics and predictive value of PSA for PCa in HIV+ men. METHODS: A nested case control study of 21 men with PCa and 40 matched-controls within EuroSIDA was conducted. Prospectively stored plasma samples before PCa (or matched date in controls) were measured for the following markers: total PSA (tPSA), free PSA (fPSA), testosterone and sex hormone binding globulin (SHBG). Conditional logistic regression models investigated associations between markers and PCa. Mixed models were used to describe kinetics. Sensitivity and specificity of using tPSA >4 ng/ml to predict PCa was calculated. Receiver operating characteristic curves were used to identify optimal cutoffs in HIV+ men for total PSA. RESULTS: 61 HIV+ men were included with a median 6 (IQR 2-9) years follow-up. Levels of tPSA increased by 13.7% per year (95% CI 10.3, 17.3) in cases, but was stable in controls (-0.4%; 95% CI -2.5, 1.7). Elevated PSA was associated with higher odds of PCa at first (OR for twofold higher 4.7; 95% CI 1.7, 12.9; P<0.01) and last sample (8.1; 95% CI 1.1, 58.9; P=0.04). A similar relationship was seen between fPSA and PCa. Testosterone and SHBG level were not associated with PCa. tPSA level >4 ng/ml had 99% specificity and 38% sensitivity. The optimal PSA cutoff was 1.5 ng/ml overall (specificity =84%, sensitivity =81%). CONCLUSIONS: PSA was highly predictive of PCa in HIV+ men; however, the commonly used PSA>4 ng/ml to indicate high PCa risk was not sensitive in our population and use of the lower cutoff of PSA>1.5 ng/ml warrants consideration.
Authors: Michael S Leapman; Kimberly Stone; Roxanne Wadia; Lesley S Park; Cynthia L Gibert; Matthew B Goetz; Roger Bedimo; Maria Rodriguez-Barradas; Fatma Shebl; Amy C Justice; Sheldon T Brown; Kristina Crothers; Keith M Sigel Journal: J Urol Date: 2021-09-24 Impact factor: 7.600
Authors: Sudeh Izadmehr; Michael Leapman; Adele R Hobbs; Maria Katsigeorgis; Fatima Nabizada-Pace; Seyed Behzad Jazayeri; David B Samadi Journal: Int Urol Nephrol Date: 2016-06-18 Impact factor: 2.370