Dataset Information

Variation of Serum PSA Levels in COVID-19 Infected Male Patients with Benign Prostatic Hyperplasia (BPH): A Prospective Cohort Studys.

ABSTRACT:

Objective

To investigate the effect of SARS CoV-2 on serum total PSA levels in men with BPH diagnosed with COVID-19.

Methods

The PSA (Kit: Immunoassay Program- Cycle 18, Siemens Atellica IM Analyzer) levels in patients who had had a PSA check at least 3 months, but no more than 6 months, prior to diagnosis of acute COVID-19 infection, were examined retrospectively. PSA levels were measured and recorded from these patients on the first day of diagnosis of COVID-19. These patients were called back for urology outpatient follow-up at the third month after the end of the COVID-19 treatment. PSA levels measured in the pre-COVID-19 period, during the period of active infection with COVID-19, and in the post-COVID-19 period were compared.

Results

In total, 91 patients had a serum PSA level of 1.58 ± 1.09 ng/mL in the pre-COVID-19 period, a serum PSA level of 4.34 ± 3.78 ng/mL measured in the COVID-19 period and 2.09 ± 2.70 ng/mL in the post-COVID-19 period. It was determined that the serum PSA level measured during active COVID-19 infection was statistically significantly higher than the PSA levels measured according to the pre-COVID-19 period and the post-COVID-19 period (P < .001, P < .001; respectively).

Conclusion

SARS-CoV-2 infection in men diagnosed with BPH causes significant increases in PSA levels during the active period of the disease. Measurement of PSA values used in the diagnosis, differential diagnosis, and follow-up of prostate diseases in the acute period of infection and in the early period after infection treatment may cause false evaluations that may affect the diagnosis and treatment steps of prostate diseases in these patients.

SUBMITTER: Cinislioglu AE

PROVIDER: S-EPMC8493783 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Early studies suggested macrophages might play roles in inflammation-associated benign prostatic hyperplasia (BPH) development, yet the underlying mechanisms remain unclear. Here we first showed that CD68(+) macrophages were identified in both epithelium and the stromal area of human BPH tissues. We then established an in vitro co-culture model with prostate epithelial and macrophage cell lines to study the potential impacts of infiltrating macrophages in the BPH development and found that co-culturing prostate epithelial cells with macrophages promoted migration of macrophages. In a three-dimensional culture system, the sphere diameter of BPH-1 prostate cells was significantly increased during coculture with THP-1 macrophage cells. Mechanism dissection suggested that expression levels of epithelial-mesenchymal transition (EMT) markers, such as N-cadherin, Snail, and TGF-?2, were increased, and administration of anti-TGF-?2 neutralizing antibody during co-culture suppressed the EMT and THP-1-mediated growth of BPH-1 cells, suggesting THP-1 might go through EMT to influence the BPH development and progression. Importantly, we found that modulation of androgen receptor (AR) in BPH-1 and mPrE cells significantly increased THP-1 and RAW264.7 cell migration, respectively, and enhanced expression levels of EMT markers, suggesting that AR in prostate epithelial cells might play a role in promoting macrophage-mediated EMT in prostate epithelial cells. Silencing AR function via an AR degradation enhancer, ASC-J9, decreased the macrophage migration to BPH-1 cells and suppressed EMT marker expression. Together, these results provide the first evidence to demonstrate that prostate epithelial AR function is important for macrophage-mediated EMT and proliferation of prostate epithelial cells, which represents a previously unrecognized role of AR in the cross-talk between macrophages and prostate epithelial cells. These results may provide new insights for a new therapeutic approach to battle BPH via targeting AR and AR-mediated inflammatory signaling pathways.