Systemic hypoferremia and severity of hypoxemic respiratory failure in COVID-19

Shah, Akshay; Frost, J. E. F.; Aaron, Louise; Donovan, Killian; Drakesmith, Hal; McKechnie, Stuart; Stanworth, Simon

doi:10.1186/s13054-020-03051-w

Cited by 84 publications

(106 citation statements)

References 6 publications

(5 reference statements)

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“…In fact, elevated serum ferritin was more of a feature of non-invasively ventilated patients. A study conducted to see the association between the iron profile and the hypoxemic respiratory failure in COVID-19 patients also did not find a significant link between serum ferritin and hypoxemia, thus the need for ventilation [15].…”

Section: Discussionmentioning

confidence: 91%

Role of Biochemical Markers in Invasive Ventilation of Coronavirus Disease 2019 Patients: Multinomial Regression and Survival Analysis

Asghar¹,

Kazmi²,

Khan³

et al. 2020

Cureus

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Background and objectives Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogen responsible for the coronavirus disease 2019 (COVID-19) pandemic. The disease mainly affects the respiratory system of the patient, in particular, the lungs, which leads to patients presenting with acute respiratory distress syndrome and acute respiratory failure, with 5-15% of patients requiring observation in the intensive care unit (ICU) with respiratory support in the form of ventilation. This study was aimed at identifying the role of biochemical markers in the risk stratification of invasive and non-invasive ventilation of hospitalized COVID-19 patients. Materials and methods The study was conducted as a prospective, observational study of all admitted COVID-19 patients. A comparative analysis was performed of the survivors who were on invasive versus (vs) non-invasive ventilation and the non-survivors similarly. After computing the descriptive statistics, a multinomial logistic regression model was applied to obtain an unadjusted odds ratio (OR) at 95% confidence interval (CI), with Hosmer-Lemeshow (HL) goodness-of-fit test used to predict the fitness of the data. Kaplan-Meier survival curves were obtained for each of the laboratory investigations predicting survival along with the intensive care stay and invasive ventilation. A log-rank test was carried out to compare the survival distributions. Results A total of 373 included patients in the study had a mean age of 52.78 ± 15.76 years with females younger than males, and indifference amongst invasive vs non-invasively ventilated (p=0.821). Females were slightly more prone to invasive ventilation (p=0.097). Overall, 39% of the subjects did not need respiratory support, while 13% were on a ventilator, 16% on bilevel positive airway pressure/continuous positive airway pressure (BiPAP/CPAP), and 31% on supplemental oxygen therapy. Among the laboratory markers, mean hemoglobin was evidently lower in the invasive group, leukocytosis and thrombocytopenia were present in both invasively ventilated and non-surviving patients, while neutrophilia and lymphocytopenia were statistically indifferent among the mode of ventilation. Elevated urea, creatinine, and sodium were also significantly deranged laboratory markers amongst the invasively ventilated group. C-reactive protein (CRP) and lactate dehydrogenase (LDH) were elevated significantly in the invasive group, while serum ferritin was more frequently raised in the non-invasively ventilated group. Procalcitonin (PCT) was significantly associated with invasive ventilation as opposed to the non-invasive group. D-dimer was equally raised in both the groups at admission but significantly elevated in the invasive group at discharge. A multinomial regression model signified D-dimer (

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Section: Discussionmentioning

confidence: 91%

Role of Biochemical Markers in Invasive Ventilation of Coronavirus Disease 2019 Patients: Multinomial Regression and Survival Analysis

Asghar¹,

Kazmi²,

Khan³

et al. 2020

Cureus

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“…A total of 777 records were collected by the databases and manual searching. After the exclusion of the duplicates, review articles, case reports, pre‐printed versions without peer‐review, and irrelevant studies by title or abstract screening, 187 studies remained for full‐text review; 52 studies 6,17‐67 were finally included into the meta‐analysis, and 18 studies were included in the qualitative synthesis (Figure 1). A total of 52 records involving 10 614 COVID‐19 patients confirmed between December 25, 2019, and June 1, 2020, were included.…”

Section: Resultsmentioning

confidence: 99%

Ferritin in the coronavirus disease 2019 (COVID‐19): A systematic review and meta‐analysis

Cheng

et al. 2020

Clinical Laboratory Analysis

313

281

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Objective The coronavirus disease 2019 (COVID‐19) has rapidly developed into a pandemic. Increased levels of ferritin due to cytokine storm and secondary hemophagocytic lymphohistiocytosis were found in severe COVID‐19 patients. Therefore, the aim of this study was to determine the role of ferritin in COVID‐19. Methods Studies investigating ferritin in COVID‐19 were collected from PubMed, EMBASE, CNKI, SinoMed, and WANFANG. A meta‐analysis was performed to compare the ferritin level between different patient groups: non‐survivors versus survivors; more severe versus less severe; with comorbidity versus without comorbidity; ICU versus non‐ICU; with mechanical ventilation versus without mechanical ventilation. Results A total of 52 records involving 10 614 COVID‐19‐confirmed patients between December 25, 2019, and June 1, 2020, were included in this meta‐analysis, and 18 studies were included in the qualitative synthesis. The ferritin level was significantly increased in severe patients compared with the level in non‐severe patients [WMD 397.77 (95% CI 306.51‐489.02), P < .001]. Non‐survivors had a significantly higher ferritin level compared with the one in survivors [WMD 677.17 (95% CI 391.01‐963.33), P < .001]. Patients with one or more comorbidities including diabetes, thrombotic complication, and cancer had significantly higher levels of ferritin than those without (P < .01). Severe acute liver injury was significantly associated with high levels of ferritin, and its level was associated with intensive supportive care, including ICU transfer and mechanical ventilation. Conclusions Ferritin was associated with poor prognosis and could predict the worsening of COVID‐19 patients.

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“…CQ and HCQ may inhibit the release of IL-6, IL-1B, and TNF-ɑ and so cause a decrease in hepcidin and inhibit viral replication [32]. Also, some drugs like tocilizumab suppress the synthesis of hepcidin [33]. Both host and pathogen need iron, and its deficiency impairs immunity in the host.…”

Section: Iron (Ferrous)mentioning

confidence: 99%

A Review on the Serum Electrolytes and Trace Elements Role in the Pathophysiology of COVID-19

Taheri

Bahrami

Habibi

et al. 2020

Biol Trace Elem Res

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All the world is involved in the COVID-19 disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Coronavirus is a positive-sense RNA and has an envelope. There is no specific drug for this disease and treatment methods are limited. Malnutrition and electrolyte imbalance can make dysfunction in the immune system and impairment of the immune system causes increasing the risk of infection. Understanding the aspects of biological features of the virus will help the development of diagnostic tests, pharmacological therapies, and vaccines. Here, we review and discuss increasing and decreasing some trace elements and imbalance of serum and plasma electrolytes involving in COVID-19.

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Systemic hypoferremia and severity of hypoxemic respiratory failure in COVID-19

Cited by 84 publications

References 6 publications

Role of Biochemical Markers in Invasive Ventilation of Coronavirus Disease 2019 Patients: Multinomial Regression and Survival Analysis

Role of Biochemical Markers in Invasive Ventilation of Coronavirus Disease 2019 Patients: Multinomial Regression and Survival Analysis

Ferritin in the coronavirus disease 2019 (COVID‐19): A systematic review and meta‐analysis

A Review on the Serum Electrolytes and Trace Elements Role in the Pathophysiology of COVID-19

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