Long COVID – Reproductive, Genitourinary, Endocrine and Metabolism

The COVID-19-causing coronavirus, severe acute respiratory syndrome coronavirus 2, gains cellular entry via the angiotensin-converting enzyme 2 (ACE2) receptor, a process that requires the transmembrane serine protease 2 (TMPRSS2) protein. In numerous endocrine glands, ACE2 and TMPRSS2 are highly expressed. This, combined with many case reports of thyroid and pituitary dysfunction in COVID-19-infected patients, has sparked considerable interest in the virus’s effect on the endocrine system. Possible risk factors of coronavirus disease 2019 (COVID19) infection on fertility include the presence of angiotensin converting enzyme2 (ACE2), receptor entrance of the virus, on testes, a decrease in significant sex hormone ratios, and COVID19associated fever. Recent studies have demonstrated a gender disparity in COVID19 prevalence and comorbidity. Smaller, single-center investigations are actively clarifying the impact of COVID-19 on the genitourinary system and have begun to provide theories regarding the mechanism behind urine symptoms in COVID-19 patients. SARS-CoV-2 also induces a cytokine storm, an exaggerated immune response with a broad spectrum of cytokine production that establishes a systemic proinflammatory milieu, which may facilitate insulin resistance and beta cell hyperstimulation, ultimately leading to altered beta cell function and death. SARS-CoV-2 may also exacerbate the preexisting proinflammatory state exhibited in type 2 diabetes (T2D), hence decreasing patient survival and aggravating comorbidities. Post-COVID-19 persistence of these abnormalities in patients who have recovered from COVID-19. We mapped all reported reproductive, genitourinary, endocrine, and metabolic symptoms using Human Phenotype Ontology (HPO) and their respective pathways.

Reproductive, Genitourinary, Endocrine and Metabolism (RGEM)(18)