There is some indication that coronavirus disease 2019 (COVID-19) causes hypothalamic-pituitary-adrenal axis insufficiency. However, being on glucocorticoids makes it difficult to fully investigate this axis, especially in patients with severe COVID-19. We aimed to discover if there was a connection between blood total cortisol and adrenocorticotropic hormone (ACTH) levels and mortality in patients with COVID-19. In Iran, 154 hospitalized patients with COVID-19 were studied in a prospective cohort study. ACTH and cortisol levels in the blood were measured on the first or second day of hospitalization. Most patients (52.6 vs. 47.4%) were men over 50 years old (55.8%), and 44.4% had an underlying illness. Serum cortisol and plasma ACTH medians were 15.6 (μg/dl) and 11.4 (pg/ml), respectively. 9.09% of the patients died. Cortisol levels were substantially lower in those who died (11.3 μg/dl) than in patients who were discharged (16.7 μg/dl, P < 0.01 ), while ACTH levels were unaffected. The most important factors determining mortality, according to the logistic model, were blood cortisol levels, the existence of an underlying disease, and the use of a mechanical ventilator. Cortisol levels that rose by one-unit correlated with a 26% lower risk of mortality. Comorbidities and mechanical ventilation increased the risk of death by 260 and 92 times, respectively. It can be concluded that in patients with COVID-19, a low cortisol level is linked to a high risk of mortality. Patients may sometimes have relative primary adrenal insufficiency. To judge and decide on therapeutic interventions, more reliable and long-term follow-up studies are required.
Background: The SARS-CoV-2 pandemic has prompted researchers around the world to identify risk factors associated with disease severity and mortality. The results suggest that the mortality of COVID-19 might be due to "cytokine storm" involving IL-6, and that obesity could be considered as a risk factor for the prevalence, severity, and mortality of COVID-19 patients. The current study aimed to evaluate the serum levels of IL-6 and adiponectin in patients and their relationship with disease progression. Methods: ELISA was used to assess the levels of IL-6 and adiponectin in serum samples of control group and patients with COVID-19 at the time of admission to the ICU or non-ICU wards. The results were analyzed using Mann-Whitney and Spearman tests. Results: ICU and non-ICU hospitalized patients had higher level of adiponectin compared to the control group (P0.001 and P=0.002, respectively). Moreover, the mean sera levels of adiponectin in patients admitted to ICU (10.18 15.4 ng /ml) was significantly higher than patients admitted to the non-ICU ward (3.14 3ng /ml, P = 0.001). Mean sera levels of IL-6 showed a similar, however the difference was not statistically significant (P= 0.18). In the ICU hospitalized patients with diabetes and hypertension, the IL-6 levels were significantly higher compared to patients without underlying disease (P = 0.01, P = 0.02, respectively). In addition, a significant direct correlation was observed between adiponectin expression and IL-6 (R = 0.2, P = 0.03). Conclusion: The results of the present study showed that the sera levels of adiponectin in COVID-19 patients with severe lung involvement were significantly higher than those with less lung involvement. This finding is of high importance mainly due to the critical role of the lung in adiponectin signaling, and as a result, adiponectin disorders may be associated with pulmonary complications in patients with COVID-19.
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