INTRODUCTION
The novel coronavirus disease (COVID-19) emerged in late 2019 in China, spread globally, and was declared a pandemic by the World Health Organization (WHO) in March 2020. It is a zoonotic illness originating in bats and caused by a single-stranded RNA virus known as 2 severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 is primarily transmitted between people through respiratory droplets and contact routes, which is why social distancing and personal protective equipment is recommended to decrease the infectivity.1 The mean incubation period is 5.2 days and 95% of patients develop symptoms up to 12.5 days after exposure.2,3
Patients infected with COVID-19 can present fever, fatigue, dry cough, breathing difficulties, myalgias, sore throat, anosmia, neurologic and gastrointestinal disturbances, such as diarrhea, or be completely asymptomatic.4-7 The most severe cases develop dyspnea, with or without hypoxemia, a week after the onset of symptoms and deteriorate to acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation, septic shock, and metabolic acidosis. Patients most susceptible to negative outcomes are the elderly and those with comorbidities such as hypertension, obesity, diabetes, and renal failure.8 There have been some reports that increased COVID-19 viral load, viral dissemination, and severity of lung involvement is androgen-dependent rendering males more vulnerable to the disease but this has yet to be proven.9,10
Laboratory findings of COVID-19 infection include leukopenia, thrombocytopenia, elevated interleukin-6 (IL-6) levels, and increased D-dimer levels that increase the risk of venous thromboembolism.11 Aberrant release of proinflammatory cytokines resulting in cytokine storm syndrome is suggested
Patients infected with COVID-19 can present fever, fatigue, dry cough, breathing difficulties, myalgias, sore throat, anosmia, neurologic and gastrointestinal disturbances, such as diarrhea, or be completely asymptomatic.4-7 The most severe cases develop dyspnea, with or without hypoxemia, a week after the onset of symptoms and deteriorate to acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation, septic shock, and metabolic acidosis. Patients most susceptible to negative outcomes are the elderly and those with comorbidities such as hypertension, obesity, diabetes, and renal failure.8 There have been some reports that increased COVID-19 viral load, viral dissemination, and severity of lung involvement is androgen-dependent rendering males more vulnerable to the disease but this has yet to be proven.9,10
Laboratory findings of COVID-19 infection include leukopenia, thrombocytopenia, elevated interleukin-6 (IL-6) levels, and increased D-dimer levels that increase the risk of venous thromboembolism.11 Aberrant release of proinflammatory cytokines resulting in cytokine storm syndrome is suggested
