ABSTRACT
INTRODUCTION AND OBJECTIVE: In COVID-19, the rapid prediction of the severity of a patient's condition using modern biomarkers can accelerate the implementation of appropriate therapy, and thus improve the patient's prognosis. MATERIAL AND METHODS: A meta-analysis was conducted of data available in the literature on the differences in baseline suPAR blood concentration between patients (1) who tested positive and negative for COVID-19, (2) who had severe and non-severe COVID-19, and (3) COVID-19 survivors and non-survivors. RESULTS: SuPAR levels in SARS-CoV-2 negative and positive patients varied and amounted to 3.61±1.59 ng/ml vs. 6.45±3.13 ng/ml, respectively (MD = -3.18; 95%CI: -4.71 to -1.66; p<0.001). suPAR levels among non-severe and severe COVID-19 patients were 7.06±2.64 ng/ml and 5.06±3.16 ng/ml (MD = 0.18; 95%CI: -2.48 to 2.83; p=0.90), respectively. Pooled analysis showed that suPAR levels between severe versus critical COVID-19 patients to be 5.59±1.54 ng/ml and 6.49±1.43 ng/ml, respectively (MD = -1.00; 95%CI: -1.31 to -0.70; p<0.001). The suPAR levels between ICU survivors versus non-survivors amounted to 5.82±2.33 ng/ml and 8.43±4.66 ng/ml (MD = -3.59; 95%CI: -6.19 to -1.00; p=0.007). In the case of in-hospital mortality, the mean suPAR level among survivors to hospital discharge was 5.63±1.27 ng/ml, compared to 7.85±2.61 ng/ml for patients who did not survive (MD = -3.58; 95%CI: -5.42 to -1.74; p<0.001). CONCLUSIONS: SuPAR levels are significantly elevated in severe COVID-19 illness and maybe useful in predicting mortality. Further studies are needed to determine cut-off points and clarify the association of suPAR levels with disease progression. This is of utmost importance given the ongoing pandemic and overburdened health care systems.
Subject(s)
COVID-19 , Receptors, Urokinase Plasminogen Activator , Humans , SARS-CoV-2 , Disease Progression , BiomarkersABSTRACT
The SARS-CoV-2 (COVID-19) pandemic is a major issue that necessitates the use of cutting-edge disease prediction models. The aim of the study was to assess the existing evidence regarding association between Krebs von den Lungen-6 levels and COVID-19 severity. A literature search was performed on Web of Science, PubMed, Scopus and Cochrane Central Register of Controlled Trials databases from 1 January 2020 up to 2 August 2022. The electronic database search was supplemented by searching Google Scholar. In addition, reference lists of relative articles were also reviewed. KL-6 levels among COVID-19 positive vs. negative patients varied and amounted to 443.37 ± 249.33 vs. 205.73 ± 86.8 U/mL (MD = 275.33; 95%CI: 144.57 to 406.09; p < 0.001). The KL-6 level was 402.82 ± 261.16 U/mL in the severe group and was statistically significantly higher than in the non-severe group (297.38 ± 90.46 U/mL; MD = 192.45; 95%CI: 118.19 to 266.72; p < 0.001). The KL-6 level in the mild group was 272.28 ± 95.42 U/mL, compared to 268.04 ± 55.04 U/mL in the moderate COVID-19 group (MD = -12.58; 95%CI: -21.59 to -3.57; p = 0.006). Our meta-analysis indicates a significant association between increased KL-6 levels and SARS-CoV-2 infection. Moreover, KL-6 levels are significantly higher in patients with a more severe course of COVID-19, indicating that KL-6 may be a useful predictor to identify patients at risk for severe COVID-19.
ABSTRACT
Atherosclerotic cardiovascular diseases (ASCVD) are the major cause of mortality worldwide. Despite the continuous progress in ASCVD therapy, the residual risk persists beyond the management of traditional risk factors. Several infections including Helicobacter pylori infection, periodontal disease, and viral infections are associated with the increased risk of ASCVD, both directly by damage to the heart muscle and vasculature, and indirectly by triggering a systemic proinflammatory state. Hence, beyond the optimal management of the traditional ASCVD risk factors, infections should be considered as an important non-classical risk factor to enable early diagnosis and appropriate treatment. Here, we summarized the currently available evidence regarding the role of inflammation in ASCVD and the association between the particular infections and pathogens (Helicobacter pylori, periodontal disease, pneumonia, Cytomegalovirus, Human immunodeficiency virus, Herpes simplex virus, and severe acute respiratory syndrome coronavirus 2) on the development and progression of ASCVD. We also speculated about the potential therapeutic implications of the anti-inflammatory and anti-infective drugs on ASCVD outcomes, including drugs routinely administered in patients with ASCVD (statins, P2Y12 receptor inhibitors, and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers) and novel strategies aiming at residual risk reduction (colchicine, anti-cytokine drugs, and methotrexate). Considering the emerging association between infections and ASCVD, it is crucial to determine the possible advantages of infection prevention and treatment in patients with ASCVD.