885-P: C-Reactive Protein Predicts COVID-19 Infection Severity and Length of Hospitalization

Abstract

Chronic stress can lead to many systemic complications and low-grade systemic inflammation including increased levels of inflammatory cytokines, such as C-reactive protein (CRP). CRP is a marker of systemic inflammation and is associated with depression and perceived stress. Elevations can result in weakened immune responses, thereby increasing the risk of complications and mortality from infections. Recent evidence suggests that uncontrolled inflammatory responses associated with COVID-19 are a major determinant of disease severity. Purpose: The purpose of the study was to determine the effects of chronic stress, measured by CRP, on the severity and the length of hospitalization in COVID-19 patients. Methods: This retrospective study used medical records from patients admitted to the University Medical Center, El Paso, TX with COVID-19 (n=436 (272M/164F); age 57.3 ± 0.8 years; BMI 29.42 ± 0.3 Kg/m2). Chronic stress was measured by blood CRP level. Severity of COVID-19 infection was determined by the peripheral oxygen saturation (SpO2) measured during the time of hospitalization. Length of hospitalization was determined by the number of days spent in the hospital. Patients were categorized into low CRP (< 3mg/L) vs. high CRP (> 3mg/L) groups and were compared using unpaired t-test. Results: Patients with high CRP level had greater COVID-19 severity, measured by SpO2 (Low CRP: 94.2% ± 0.4 vs. high CRP: 91.9% ± 0.4; p<0.01), and greater length of hospital stay (low CRP: 6.5 ± 1.3 days vs. high CRP 8.8 ±0.5 days; p<0.05). CRP level was also negatively associated with SpO2 (r= -0.16, p<0.001) and positively associated with the length of hospitalization (r= 0.23, p<0.0001). Conclusion: Higher levels of CRP are associated with worsened severity and increased length of hospitalization in COVID-19 patients. CRP levels should be considered in laboratory workup for COVID-19 patients and treatment should focus on reducing inflammatory damage. Disclosure H. Kreit: None. S. Bajpeyi: None. S. V. Cherukuri: None. R. A. Mandania: None. A. Deoker: None. A. A. Gupte: None. A. Mossayebi: None. J. B. Concha: None. H. Jung: None. A. E. Wagler: None.