Eric A Klein1, Jianbo Li2, Alex Milinovich2, Jesse D Schold2, Nima Sharifi3, Michael W Kattan2, Lara Jehi4. 1. Department of Urology, Glickman Urological and Kidney Institute, Cleveland, Ohio. 2. Department of Quantitative Health Sciences, Lerner Research Institute, Cleveland, Ohio. 3. Department of Cancer Biology and Genitourinary Malignancies Research Center,Lerner Research Institute, Cleveland, Ohio. 4. Department of Neurology, Neurological Institute Cleveland Clinic and Cleveland Clinic Lerner College of Medicine, Cleveland, Ohio.
Abstract
PURPOSE: TMPRSS2 is a host co-receptor for cell entry of SARS-CoV-2. A prior report suggested that use of androgen deprivation therapy, which downregulates TMPRSS2, may protect men with prostate cancer from infection. MATERIALS AND METHODS: This is a cohort study of a prospective registry of all patients tested for SARS-CoV-2 between March 12 and June 10, 2020 with complete followup until disease recovery or death. The main exposure examined was the use of androgen deprivation therapy, and the outcome measures were the rate of SARS-CoV-2 positivity and disease severity as a function of androgen deprivation therapy use. RESULTS: The study cohort consisted of 1,779 men with prostate cancer from a total tested population of 74,787, of whom 4,885 (6.5%) were positive for SARS-CoV-2. Of those with prostate cancer 102 (5.7%) were SARS-CoV-2 positive and 304 (17.1%) were on androgen deprivation therapy. Among those on androgen deprivation therapy 5.6% were positive as compared to 5.8% not on androgen deprivation therapy. Men on androgen deprivation therapy were slightly older (75.5 vs 73.8 years, p=0.009), more likely to have smoked (68.1% vs 59.3%, p=0.005) and more likely to report taking steroids (43.8% vs 23.3%, p <0.001). Other factors known to increase risk of infection and disease severity were equally distributed (asthma, diabetes mellitus, hypertension, coronary artery disease, heart failure and immune suppressive disease). Multivariable analysis did not indicate a difference in infection risk for those with prostate cancer on androgen deprivation therapy (OR 0.93, 95% CI 0.54-1.61, p=0.8). CONCLUSIONS: Androgen deprivation therapy does not appear to be protective against SARS-CoV-2 infection.
PURPOSE:TMPRSS2 is a host co-receptor for cell entry of SARS-CoV-2. A prior report suggested that use of androgen deprivation therapy, which downregulates TMPRSS2, may protect men with prostate cancer from infection. MATERIALS AND METHODS: This is a cohort study of a prospective registry of all patients tested for SARS-CoV-2 between March 12 and June 10, 2020 with complete followup until disease recovery or death. The main exposure examined was the use of androgen deprivation therapy, and the outcome measures were the rate of SARS-CoV-2 positivity and disease severity as a function of androgen deprivation therapy use. RESULTS: The study cohort consisted of 1,779 men with prostate cancer from a total tested population of 74,787, of whom 4,885 (6.5%) were positive for SARS-CoV-2. Of those with prostate cancer 102 (5.7%) were SARS-CoV-2 positive and 304 (17.1%) were on androgen deprivation therapy. Among those on androgen deprivation therapy 5.6% were positive as compared to 5.8% not on androgen deprivation therapy. Men on androgen deprivation therapy were slightly older (75.5 vs 73.8 years, p=0.009), more likely to have smoked (68.1% vs 59.3%, p=0.005) and more likely to report taking steroids (43.8% vs 23.3%, p <0.001). Other factors known to increase risk of infection and disease severity were equally distributed (asthma, diabetes mellitus, hypertension, coronary artery disease, heart failure and immune suppressive disease). Multivariable analysis did not indicate a difference in infection risk for those with prostate cancer on androgen deprivation therapy (OR 0.93, 95% CI 0.54-1.61, p=0.8). CONCLUSIONS: Androgen deprivation therapy does not appear to be protective against SARS-CoV-2 infection.
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