Endocrine Abstracts

Introduction

The novel COVID-19 has been rapidly expanding and causing many deaths all over the world, since December 2019. The health condition and the coexistence of other diseases may affect the severity of SARS-CoV-2 infection.

The state of the art

PCOS is a common endocrine and metabolic disorder, afflicting females of reproductive age, with an incidence up to 10%. It is a heterogeneous clinical syndrome, characterized by hyperandrogenism, menstrual irregularity and hyperinsulinaemia, in which both genetic and environmental factors are thought to play a role. Women with PCOS are considered to belong to an age and sex group which is at lower risk for severe COVID-19. However, the possible pathophysiological mechanisms regarding PCOS and more severe COVID-19 have been hypothesized. Insulin resistance and hyperinsulinaemia result in enhanced hyperandrogenism. Androgens may drive clinical results in COVID-19. First, sexual hormones affect the immune system and testosterone suppresses it. Second, SARS-CoV-2 gains entry to target cells via the angiotensin-converting enzyme 2 (ACE-2) receptor and male hormones are effective in the ACE-2 passageway and simplify SARS-CoV-2 entry into cells. Finally, the lung expression of TMPRSS2 (transmembrane protease, serine 2), a cellular co-receptor necessary for SARS-CoV-2 infection, is associated with an androgen-regulated gene. What is more, Renin-Angiotensin-System (RAS) overactivity has been described in type 2 diabetes and obesity, the conditions markedly frequent in PCOS, which are known to be the factors increasing the risk of severe COVID-19. Moreover, the overactivity of the RAS system has been also proven in PCOS. Thus PCOS may predispose these women to more severe SARS-CoV-2 infection. Vitamin D deficiency, identified as a global public health matter, may be another important factor, potentially involved in the increased risk of developing severe forms of COVID-19 in PCOS women. It has been reported that poor vitamin D status can affect a variety of diseases, including SARS-CoV-2 infection, because of its crucial role in the functioning of the immune system. Vitamin D is also a negative endocrine RAS modulator and inhibits renin expression and generation. Hyper-cytokinemia, presented in obesity as well as in PCOS, may be another risk factor for severe SARS-CoV-2 infection in PCOS women.

Conclusions

The complexity of PCOS, including the coexistence of many metabolic disorders as well as hormonal and cytokine disturbances, may increase the susceptibility of severe COVID-19 in PCOS women. Further studies are needed to clarify the link between severe COVID-19 and PCOS, to provide the optimal management.