Abstract:The coronavirus disease 2019 (COVID-19) pandemic has caused millions of deaths worldwide. Acute ischemic stroke is a life-threatening risk factor for COVID-19 infection. Neutrophil-to-lymphocyte ratio (NLR) is one of the predictors of poor prognosis in acute ischemic stroke. The aim of this study was to assess the correlation between NLR values and the clinical outcome of acute thrombotic stroke patients with COVID-19 that was measured using the National Institutes of Health Stroke Scale (NIHSS). A cross-secti… Show more
“…Nevertheless, the rise in procalcitonin may be related to generic systemic inflammation seen in the later stages of illness that is not specific for secondary infections and so this phenomenon needs to be further examined [ 33 ]. Other promising prognostic markers in COVID-19 cases are under assessment, such as the neutrophil-to-lymphocyte ratio, although they are in need of further evaluation [ 34 ]. Fig.…”
Background
Coinfection at various sites can complicate the clinical course of coronavirus disease of 2019 (COVID-19) patients leading to worse prognosis and increased mortality. We aimed to investigate the occurrence of coinfection in critically ill COVID-19 cases, and the predictive role of routinely tested biomarkers on admission for mortality.
Methods
This is a retrospective study of all SARS-CoV-2-infected cases, who were admitted to King Fahad Hospital of the University between March 2020 and December 2020. We reviewed the data in the electronic charts in the healthcare information management system including initial presentation, clinical course, radiological and laboratory findings and reported all significant microbiological cultures that indicated antimicrobial therapy. The mortality data were reviewed for severely ill patients who were admitted to critical care units.
Results
Of 1091 admitted patients, there were 70 fatalities (6.4%). 182 COVID-19 persons were admitted to the critical care service, of whom 114 patients (62.6%) survived. The in-hospital mortality was 13.4%. Coinfection was noted in 67/68 non-survivors, and Gram-negative pathogens (Enterobacterales, Pseudomonas aeruginosa, and Acinetobacter baumanni) represented more than 50% of the etiological agents. We noted that the serum procalcitonin on admission was higher for non-survivors (Median = 1.6 ng/mL ± 4.7) than in survivors (Median = 0.2 ng/mL ± 4.2) (p ≤ 0.05).
Conclusion
Coinfection is a serious complication for COVID-19 especially in the presence of co-morbidities. High levels of procalcitonin on admission may predict non-survival in critically ill cases in whom bacterial or fungal co-infection is likely.
“…Nevertheless, the rise in procalcitonin may be related to generic systemic inflammation seen in the later stages of illness that is not specific for secondary infections and so this phenomenon needs to be further examined [ 33 ]. Other promising prognostic markers in COVID-19 cases are under assessment, such as the neutrophil-to-lymphocyte ratio, although they are in need of further evaluation [ 34 ]. Fig.…”
Background
Coinfection at various sites can complicate the clinical course of coronavirus disease of 2019 (COVID-19) patients leading to worse prognosis and increased mortality. We aimed to investigate the occurrence of coinfection in critically ill COVID-19 cases, and the predictive role of routinely tested biomarkers on admission for mortality.
Methods
This is a retrospective study of all SARS-CoV-2-infected cases, who were admitted to King Fahad Hospital of the University between March 2020 and December 2020. We reviewed the data in the electronic charts in the healthcare information management system including initial presentation, clinical course, radiological and laboratory findings and reported all significant microbiological cultures that indicated antimicrobial therapy. The mortality data were reviewed for severely ill patients who were admitted to critical care units.
Results
Of 1091 admitted patients, there were 70 fatalities (6.4%). 182 COVID-19 persons were admitted to the critical care service, of whom 114 patients (62.6%) survived. The in-hospital mortality was 13.4%. Coinfection was noted in 67/68 non-survivors, and Gram-negative pathogens (Enterobacterales, Pseudomonas aeruginosa, and Acinetobacter baumanni) represented more than 50% of the etiological agents. We noted that the serum procalcitonin on admission was higher for non-survivors (Median = 1.6 ng/mL ± 4.7) than in survivors (Median = 0.2 ng/mL ± 4.2) (p ≤ 0.05).
Conclusion
Coinfection is a serious complication for COVID-19 especially in the presence of co-morbidities. High levels of procalcitonin on admission may predict non-survival in critically ill cases in whom bacterial or fungal co-infection is likely.
“…SARS-CoV-2 infects cells using the angiotensin converting enzyme-2 (ACE-2) receptor; infection can produce an interstitial pneumonia that may progress to acute respiratory distress syndrome (ARDS) and death ( 7 , 8 ). COVID-19 severity has been shown to be modified by the presence of cardio-metabolic comorbidities as well as inflammatory markers which may reflect vascular or respiratory deterioration ( 9 – 12 ).…”
IntroductionCoronavirus disease (COVID-19) is a global pandemic. Vitamin D deficiency has been associated with susceptibility to infectious disease. In this study, the association between COVID-19 outcomes and vitamin D levels in patients attending a COVID-19 reference center in Mexico City are examined.MethodsConsecutive patients with confirmed COVID-19 were evaluated. All patients underwent clinical evaluation and follow-up, laboratory measurements and a thoracic computerized tomography, including the measurement of epicardial fat thickness. Low vitamin D was defined as levels <20 ng/ml (<50nmol/L) and deficient Vitamin D as a level ≤12 ng/ml (<30 nmol/L).ResultsOf the 551 patients included, low vitamin D levels were present in 45.6% and deficient levels in 10.9%. Deficient Vitamin D levels were associated with mortality (HR 2.11, 95%CI 1.24–3.58, p = 0.006) but not with critical COVID-19, adjusted for age, sex, body-mass index and epicardial fat. Using model-based causal mediation analyses the increased risk of COVID-19 mortality conferred by low vitamin D levels was partly mediated by its effect on D-dimer and cardiac ultrasensitive troponins. Notably, increased risk of COVID-19 mortality conferred by low vitamin D levels was independent of BMI and epicardial fat.ConclusionVitamin D deficiency (≤12 ng/ml or <30 nmol/L), is independently associated with COVID-19 mortality after adjustment for visceral fat (epicardial fat thickness). Low vitamin D may contribute to a pro-inflammatory and pro-thrombotic state, increasing the risk for adverse COVID-19 outcomes.
“…SARS-CoV-2 infects cells using the angiotensin converting enzyme-2 (ACE-2) receptor; infection can produce an interstitial pneumonia that may progress to acute respiratory distress syndrome (ARDS) and death (7,8). COVID-19 severity has been shown to be modified by the presence of cardio-metabolic comorbidities as well as inflammatory markers which may reflect vascular or respiratory deterioration (9)(10)(11)(12).…”
INTRODUCTION: Coronavirus disease (COVID-19) is a global pandemic. Vitamin D (25-OHD) deficiency has been associated with susceptibility to infectious disease. In this study, the association between COVID-19 outcomes and 25-OHD levels in patients attending a COVID-19 reference center in Mexico City are examined.
METHODS: Consecutive patients with confirmed COVID-19 were evaluated. All patients underwent clinical evaluation (including outcomes), laboratory measurements (including 25-OHD) and a thoracic computerized tomography (including the measurement of epicardial fat thickness). Low vitamin D was defined as levels <20ng/mL (<50nmol/L) and severely low (or deficient) 25-OHD as a level ≤12ng/mL (<30nmol/L)
RESULTS: Of the 551 patients included, low 25-OHD levels were present in 45.6% and severely low levels in 10.9%. Severely low 25-OHD levels were associated with mortality (HR 2.11, 95%CI 1.24-3.58, p=0.006) but not with critical COVID-19 (OR 0.97, 95%CI 0.94-0.99, p=0.042), adjusted for age, sex, body-mass index and epicardial fat. Using model-based causal mediation analyses the increased risk of COVID-19 mortality conferred by 25-OHD levels was partly mediated by its effect on D-dimer and cardiac ultrasensitive troponins. Notably, increased risk of COVID-19 mortality conferred by low vitamin D levels was independent of BMI and epicardial fat.
CONCLUSION: Vitamin D deficiency (≤12ng/mL or <30nmol/L), is independently associated with COVID-19 mortality after adjustment for visceral fat (epicardial fat thickness). Low 25-OHD may contribute to a pro-inflammatory and pro-thrombotic state, increasing the risk for adverse COVID-19 outcomes.
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