8 research outputs found

    Utility of Google Trends in anticipating Coronavirus Disease 2019 (COVID-19) outbreaks in Poland

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    Google Trends for anosmia and dysgeusia have a high predictive power for anticipating new COVID-19 cases 1-2 weeks ahead of official reports in Poland, serving as a useful infodemiological tool for anticipating an impending outbreak, with the potential of providing valuable buffer time to allocate necessary supplies and personnel to hospitals expecting a surge in COVID-19 patients. Upon verification by prospective research comparing model performance in different regions of Poland, public health organizations are encouraged to take advantage of this free forecasting system to anticipate and effectively manage COVID-19 outbreaks throughout Poland

    Complement levels at admission as a reflection of Coronavirus Disease 19 (COVID-19) severity state

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    Background: Complement system hyperactivation has been proposed as a potential driver of adverse outcomes in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infected patients, given prior research of complement deposits found in tissue and blood samples, as well as evidence of clinical improvement with anticomplement therapy. Its role in augmenting thrombotic microangiopathy mediated organ damage has also been implicated in coronavirus disease 2019 (COVID-19). This study aimed to examine associations between complement parameters and progression to severe COVID-19 illness, as well as correlations with other systems. Materials and methods: Blood samples of COVID-19 patients presenting to the emergency department (ED) were analyzed for a wide panel of complement and inflammatory biomarkers. The primary outcome was COVID-19 severity at index ED visit, while the secondary outcome was peak disease severity over the course of illness. Results: Fifty-two COVID-19 patients were enrolled. C3a (p=0.018), C3a/C3 ratio (p=0.002), and sC5b-9/C3 ratio (p=0.021) were significantly elevated in with severe disease at ED presentation. Over the course of illness, C3a (p=0.028) and C3a/C3 ratio (p=0.003) were highest in the moderate severity group. In multivariate regression controlled for confounders, complement hyperactivation failed to predict progression to severe disease. C3a, C3a/C3 ratio, and sC5b-9/C3 ratio were correlated positively with numerous inflammatory biomarkers, fibrinogen, and VWF:Ag, and negatively with plasminogen and ADAMTS13 activity. Conclusion: We found evidence of complement hyperactivation in COVID-19, associated with hyperinflammation and thrombotic microangiopathy. Complement inhibition should be further investigated for potential benefit in patients displaying a hyperinflammatory and microangiopathic phenotype. This article is protected by copyright. All rights reserved

    The role of lipoprotein(a) in coronavirus disease 2019 (COVID-19) with relation to development of severe acute kidney injury

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    Lipoprotein(a) (Lp(a)) is a prothrombotic and anti-fibrinolytic lipoprotein, whose role has not been clearly defined in the pathogenesis of coronavirus disease 2019 (COVID-19). In this prospective observational study, serum Lp(a) as well as outcomes were measured in 50 COVID-19 patients and 30 matched sick controls. Lp(a) was also assessed for correlation with a wide panel of biomarkers. Serum Lp(a) did not significantly differ between COVID-19 patients and sick controls, though its concentration was found to be significantly associated with severity of COVID-19 illness, including acute kidney failure stage (r = 0.380, p = 0.007), admission disease severity (r = 0.355, p = 0.013), and peak severity (r = 0.314; p = 0.03). Lp(a) was also positively correlated with interleukin (IL)-8 (r = 0.308; p = 0.037), fibrinogen (r = 0.344; p = 0.032) and creatinine (r = 0.327; p = 0.027), and negatively correlated with ADAMTS13 activity/VWF:Ag (r = - 0.335; p = 0.021); but not with IL-6 (r = 0.241; p = 0.106). These results would hence suggest that adverse outcomes in patients with COVID-19 may be aggravated by a genetically determined hyper-Lp(a) state rather than any inflammation induced elevations

    Alterations in the lipid profile associate with a dysregulated inflammatory, prothrombotic, anti-fibrinolytic state and development of severe acute kidney injury in coronavirus disease 2019 (COVID-19): A study from Cincinnati, USA

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    Background and aims: Reduction of atherogenic lipoproteins is often the ultimate goal of nutritional interventions, however this is complicated given that hypolipidemia is frequently observed in coronavirus disease 2019 (COVID-19) patients. We aimed to explore the association of hypolipidemia with patient outcomes in terms of immunothrombosis and multiorgan injury, focusing on specialized apolipoproteins apo A1 and apo B. Methods: Lipid profiles of 50 COVID-19 patients and 30 sick controls presenting to the Emergency Department (ED) were measured in this prospective observational study. The primary outcome was development of severe acute kidney injury (AKI). Need for hospitalization and ICU admission were secondary outcomes. Lipoproteins were analyzed for independent association with serum creatinine (SCr) increase ratio and correlated with a wide panel of biomarkers. Results: COVID-19 cohort had significantly lower apo A1 (p = 0.006), and higher apo B/apo A1 ratio (p = 0.041). Patients developing severe AKI had significantly lower LDL-C (p = 0.021). Apo B/apo A1 was associated with 2.25-fold decrease in serum SCr increase ratio, while LDL-C with a 1.5% decrease. Hypolipidemia correlated with low plasminogen, ADAMTS13 activity/VWF:Ag, and high inflammatory biomarkers (CRP, IL-6, IL-8, IL-10), plasminogen activator inhibitor-1 (PAI-1), ED creatinine, and SCr increase ratio. Conclusion: Although favored in dietetics, findings of a low LDL-C in COVID-19 patients should be alarming in light of our observations. Low apo B/apo A1 ratio and LDL-C are predictive of renal deterioration in COVID-19 patients, and low LDL-C in particular may potentially serve to indicate COVID-19 related AKI driven by disrupted fibrinolysis and a secondary thrombotic microangiopathy-like process

    Liver fibrosis‑4 score predicts mortality in critically ill patients with coronavirus disease 2019

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    Background: Emerging evidence suggests that liver dysfunction in the course of coronavirus disease 2019 (COVID‑19) illness is a critical prognostic factor for mortality in COVID‑19 patients, and the Fibrosis‑4 (FIB‑4) score, developed to reflect level of hepatic fibrosis, has been associated with adverse outcomes in hospitalized COVID‑19 patients. This study aimed to investigate intensive care unit (ICU) admitted patients, a high‑risk subpopulation, research on which is lacking. Materials and Methods: This retrospective cohort study examined FIB‑4 scores and clinical endpoints including death, acute cardiac injury (ACI), acute kidney injury, and need for mechanical ventilation in critically ill COVID‑19 patients, without prior hepatic disease, throughout ICU stay. Results: Of 60 patients enrolled, 35% had ICU admission FIB‑4 >2.67. Among nonsurvivors FIB‑4 was significantly higher at admission (median 3.19 vs. 1.44; P < 0.001) and only a minority normalized <1.45 (36.0%). Each one‑unit increment in admission FIB‑4 was associated with 67.4% increased odds of death (95% confidence interval [CI], 9.8%–162.6%; P = 0.017). FIB‑4 >2.67 was associated with a median survival time of 18 days from ICU admission versus 40 days with FIB‑4 <2.67 (P = 0.016). Admission FIB‑4 was also higher in patients developing ACI (median 4.99 vs. 1.76; P < 0.001). FIB‑4 correlated with age (r = 0.449; P < 0.001), and aspartate transaminase with alanine transaminase (r = 0.674; P < 0.001) and lactate dehydrogenase (r = 0.618; P < 0.001). Conclusion: High ICU admission FIB‑4 is associated with mortality in critically ill COVID‑19 patients, with failure to normalize at time of death, however, the high score is likely a result of generalized cytotoxicity rather than advanced hepatic fibrosis

    Longitudinal analysis of electrolyte prolife in intensive care COVID-19 patients

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    ABSTRACTIntroduction According to a substantial body of research, electrolyte abnormalities are a common manifestation in coronavirus disease 2019 (COVID-19) patients and are associated with adverse outcomes. This study aimed to investigate electrolyte imbalances in COVID-19 patients and assess their relation to mortality.Methods Adult COVID-19 patients hospitalized in the Security Forces Hospital in Saudi Arabia from June 8th till August 18th, 2020 were enrolled in this retrospective observational study. We examined baseline characteristics, comorbidities, acute organ injuries, medications, and electrolyte levels including sodium, potassium, chloride, calcium, bicarbonate, phosphate, and magnesium on ICU admission, as well as every following day of ICU stay, until death or discharge. Patients were stratified according to survival, and differences in variables between groups were compared using Mann-Whitney’s U test or Fisher’s exact test. Longitudinal electrolyte profiles were modeled using random intercept linear regression models.Results A total of 60 COVID-19 patients were enrolled. Compared to survivors, non-survivors had significantly higher sodium and phosphate on admission and death, higher potassium and magnesium at death, and significantly lower calcium at death. Abnormalities in admission levels of chloride and bicarbonate were also more frequently observed in non-survivors. Furthermore, in the deceased group, we observed a daily increase in potassium and phosphate levels, and a daily decrease in sodium and chloride. Finally, calcium increased in non-survivors over time, however, not as significantly as in the survivor group.Conclusion Admission levels of electrolytes and changes over the course of ICU stay appear to be associated with mortality in COVID-19 patients

    Longitudinal analysis of electrolyte prolife in intensive care COVID-19 patients

    No full text
    According to a substantial body of research, electrolyte abnormalities are a common manifestation in coronavirus disease 2019 (COVID-19) patients and are associated with adverse outcomes. This study aimed to investigate electrolyte imbalances in COVID-19 patients and assess their relation to mortality. Adult COVID-19 patients hospitalized in the Security Forces Hospital in Saudi Arabia from June 8th till August 18th, 2020 were enrolled in this retrospective observational study. We examined baseline characteristics, comorbidities, acute organ injuries, medications, and electrolyte levels including sodium, potassium, chloride, calcium, bicarbonate, phosphate, and magnesium on ICU admission, as well as every following day of ICU stay, until death or discharge. Patients were stratified according to survival, and differences in variables between groups were compared using Mann-Whitney’s U test or Fisher’s exact test. Longitudinal electrolyte profiles were modeled using random intercept linear regression models. A total of 60 COVID-19 patients were enrolled. Compared to survivors, non-survivors had significantly higher sodium and phosphate on admission and death, higher potassium and magnesium at death, and significantly lower calcium at death. Abnormalities in admission levels of chloride and bicarbonate were also more frequently observed in non-survivors. Furthermore, in the deceased group, we observed a daily increase in potassium and phosphate levels, and a daily decrease in sodium and chloride. Finally, calcium increased in non-survivors over time, however, not as significantly as in the survivor group. Admission levels of electrolytes and changes over the course of ICU stay appear to be associated with mortality in COVID-19 patients.</p

    Complement Levels at Admission Reflecting Progression to Severe Acute Kidney Injury (AKI) in Coronavirus Disease 2019 (COVID-19): A Multicenter Prospective Cohort Study

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    Background: Dysregulation of complement system is thought to be a major player in development of multi-organ damage and adverse outcomes in patients with coronavirus disease 2019 (COVID-19). This study aimed to examine associations between complement system activity and development of severe acute kidney injury (AKI) among hospitalized COVID-19 patients. Materials and methods: In this multicenter, international study, complement as well as inflammatory and thrombotic parameters were analyzed in COVID-19 patients requiring hospitalization at one US and two Hungarian centers. The primary endpoint was development of severe AKI defined by KDIGO stage 2+3 criteria, while the secondary endpoint was need for renal replacement therapy (RRT). Complement markers with significant associations with endpoints were then correlated with a panel of inflammatory and thrombotic biomarkers and assessed for independent association with outcome measures using logistic regression. Results: A total of 131 hospitalized COVID-19 patients (median age 66 [IQR, 54-75] years; 54.2% males) were enrolled, 33 from the US, and 98 from Hungary. There was a greater prevalence of complement over-activation and consumption in those who developed severe AKI and need for RRT during hospitalization. C3a/C3 ratio was increased in groups developing severe AKI (3.29 vs. 1.71; p &lt; 0.001) and requiring RRT (3.42 vs. 1.79; p &lt; 0.001) in each cohort. Decrease in alternative and classical pathway activity, and consumption of C4 below reference range, as well as elevation of complement activation marker C3a above the normal was more common in patients progressing to severe AKI. In the Hungarian cohort, each standard deviation increase in C3a (SD = 210.1) was independently associated with 89.7% increased odds of developing severe AKI (95% CI, 7.6-234.5%). Complement was extensively correlated with an array of inflammatory biomarkers and a prothrombotic state. Conclusion: Consumption and dysregulation of complement system is associated with development of severe AKI in COVID-19 patients and could represent a promising therapeutic target for reducing thrombotic microangiopathy in SARS-CoV-2 infection
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