Objectives: The aim of this review is to summarize, following a timeline, the current knowledge regarding the effects of the Sars-cov2 virus on male fertility, researching the pathological and clinical results of the studies published in the last year. Methods: A systematic research was performed on the major international online databases; Thirty-five articles were selected. Results: A statistically significant reduction in testosterone levels and sperm quality in subjects with COVID-19 has been highlighted in several papers; however, in many cases the tests have been conducted in patients with active disease and long-term consequences are still not known. Some studies have confirmed the presence of the virus in the testis in a low percentage of patients; viral presence in sperm has only been found in one study. Testicular discomfort, which could indicate viral orchitis, was highlighted in several works, with an incidence of up to 19% percent of patients. The presence of inflammatory lymphocytic infiltrates, IgG and inflammatory cytokines have been documented in several works; pathological signs of inflammation were found in 60.9% of testicular biopsies performed in one study. The entry of the virus into the testis cells, both stromal and seminal cells appeared to be Angiotensin Converting Enzyme-2 (ACE2) mediated, as it also occurs in other tissues. DNA fragmentation, reactive oxygen species (ROS) formation, autoantibody production and ACE2 mediated effect have all been hypothesized as cause of cellular damage. Conclusions: The results on effects of COVID-19 infection on the male reproductive system are currently insufficient as they are based on a small number of patients and therefore are often contradictory.Certain mechanisms of testicular damage are still to be assessed, as any risk categories like age, ethnicity, or others. As for the transmission of the virus through sperm, there is insufficient evidence to ensure that this cannot happen.
Our overall detection rate was 45.5% and 37.8% in Group A (patients with previous negative biopsy and persistent suspicion of PCA) and in Group B (biopsy naïve patients) respectively; clinical significant PCA detection rate was respectively 40% and 35.7%. These results are similar to current literature and promising for the future. We believe that using platforms of co-registered MRI/US fusion biopsy can potentially improve risk stratification and reduces understaging, undergrading and the need for repeat biopsies in biopsy naïve patients (using a stereotactic first mapping) and in patients with previous negative biopsy and persistent suspicion of PCA ( using a second MRI/US fusion biopsy).
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