During December 2019 at Wuhan the SARS-CoV-2 epidemic emerged and rapidly occupies the entire world, present as pandemic responsible for pulmonary dysfunction like acute respiratory distress syndrome and pneumonia but with time clinicians and researchers have been found some extrapulmonary features of COVID-19 which may reflect either replication or dissemination of SARS-CoV-2 infection as widespread immunopathological sequelae1. The knowledge regarding extrapulmonary complexities in the hospitalized COVID-19 patients should be addressed to prevent and decrease the coincidental exposure2. The spike protein and ACE2 receptors through S protein and MPRSS2 play role in pathogenesis of SARS-CoV-2 infection3. ACE2 receptors are situated in heart, GI epithelium, alveolar II cells, vessels, renal and smooth muscles of entire body responsible for COVID-19 induced injury4,5. SARS-COV-2 actuates T lymphocytes via cytokines: interleukin (IL-1 and 6), GM-CSF, and interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) known as cytokine storm bringing about tissue injury6.