Prostate specific antigen in COVID‐19 patients

Dear Editor,

We read with interest the paper by Ruan et al. reporting that in patients with COVID‐19 there is no direct urogenital involvement, being SARS‐CoV‐2 RNA undetectable in the urogenital secretions. ¹

It is well known that subjects with SARS‐CoV‐2 infection may be asymptomatic or experience mild symptoms although patients may develop acute respiratory distress syndrome because of a SARS‐CoV‐2 related interstitial pneumonia requiring non‐invasive and invasive ventilation, intensive care unit (ICU) and leading also to death above all in aged subjects with multiple comorbidities. ² Other organs out of lungs have been identified as target of the SARS‐CoV‐2 and all tissues expressing the putative SARS‐CoV‐2 receptor ACE2, a fundamental protein allowing SARS‐CoV‐2 docking to the host cell, have been quoted as possible targets of the virus. ³ As recently demonstrated, in addition to the protein ACE2, SARS‐CoV‐2 utilizes the transmembrane protease serine 2 (TMPRSS2) to enter within the host cell and for viral spread. ³ These proteins have been shown to be expressed in many different tissues such as lungs, colon, liver, kidney, and also in the prostate. ⁴ Thus, prostate could be a putative target of SARS‐CoV‐2 although very scarce data have been reported on prostate involvement among male patients with SARS‐CoV‐2 infection.

To this regard, it has been recently demonstrated that only 0.32% of all prostate epithelial cells express ACE2 and 18.65% express TMPRSS2, but more importantly, only 0.61% of these cells co‐expressed ACE2 and TMPRSS2. ⁴ These observations seem to support the hypothesis that prostate might not be an organ suitable to SARS‐CoV‐2 infection.

During the recent outbreak of SARS‐CoV‐2 infection in Italy, our clinic at the University‐Hospital of Padova, located in the Veneto region, one of the red‐zones for COVID‐19 in Italy, was turned to a COVID‐19 ward, and we had the opportunity to evaluate PSA plasma levels in 23 consecutive patients (younger than 65 years old, mean age 57.1 years) hospitalized for confirmed COVID‐19 pneumonia. All patients showed elevated CRP plasma levels (mean 60.2 mg/L, n.v. 0–5 mg/L). No one patient complained symptoms compatible with prostate inflammation during the hospitalization period. Patients’ mean PSA plasma levels were 1.13 ng/ml, with no one patient with PSA plasma levels exceeding the upper limit of the normal range (4 ng/ml).

The present observations, although on a small number of patients, seem to exclude any prostate involvement leading to gland inflammation in COVID‐19 hospitalized patients, in agreement with the conclusions of Ruan et al. ¹ and with the results of Song et al. showing that prostate might not be a susceptible organ for SARS‐CoV‐2 infection. ⁴

Thus, the substantial absence of co‐expression of ACE2 and TMPRSS2 in prostate epithelial cells, ⁴ the absence of SARS‐CoV‐2 RNA in prostatic secretions of COVID‐19 patients ¹ and the absence of PSA plasma levels increase in patients hospitalized for COVID‐19 pneumonia (present report) seem to indicate that prostate might not be a target organ for SARS‐CoV‐2 in patients with COVID‐19. On the other hand, if prostate was a privileged organ for SARS‐CoV‐2 infection, cases of prostatitis would have emerged as the start of COVID‐19 pandemic last December 2019, with more than 100 million people infected (a number by defect), half of them being males. ⁵

CONFLICT OF INTEREST

The authors have nothing to disclose.