Assessment of Hypokalemia and Clinical Characteristics in Patients With Coronavirus Disease 2019 in Wenzhou, China

Dong, Chen; Li, Xiaokun; Song, Qifan; Hu, Chenchan; Su, Feifei; Dai, Jianyi; Ye, Yinghai; Huang, Jianping; Zhang, Xiaoming

doi:10.1001/jamanetworkopen.2020.11122

Cited by 210 publications

(260 citation statements)

References 16 publications

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“…The univariate regression analysis illustrated the severity was associated with age, sex, comorbidities (hypertension and diabetes), dyspnea, respiratory rate, white blood cell, lymphocyte, CRP, hypokalemia, and LDH, which is consistent with the ndings in several previous studies ( Table 1, Table 2 and Figure 1) [12,13]. As mentioned already, most of the previous studies individually looked into the possible risk factors, which is disadvantageous in ranking the risk factors according to OR values, as compared with the current multiple logistic regression model that investigated the interactive effects by the possible risk factors.…”

Section: Discussionsupporting

confidence: 90%

Prediction Model of Severe Coronavirus Disease 2019(COVID-19) Cases Shows the Leading Risk Factor of Hypocalcemia

Dai

et al. 2020

Preprint

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Background A striking characteristic of Coronavirus Disease 2019(COVID-19) is the coexistence of clinically mild and severe cases. A comprehensive analysis of multiple risk factors predicting progression to severity is clinically meaningful. Methods The patients were classified into moderate and severe groups. The univariate regression analysis was used to identify their epidemiological and clinical features related to severity, which were used as possible risk factors and were entered into a forward-stepwise multiple logistic regression analysis to develop a multiple factor prediction model for the severe cases.Results 255 patients (mean age, 49.1±SD 14.6) were included, consisting of 184 (72.2%) moderate cases and 71 (27.8%) severe cases. The common symptoms were dry cough (78.0%), sputum (62.7%), and fever (59.2%). The less common symptoms were fatigue (29.4%), diarrhea (25.9%), and dyspnea (20.8%). The univariate regression analysis determined 23 possible risk factors. The multiple logistic regression identified seven risk factors closely related to the severity of COVID-19, including dyspnea, exposure history in Wuhan, CRP (C-reactive protein), aspartate aminotransferase (AST), calcium, lymphocytes, and age. The probability model for predicting the severe COVID-19 was P=1/1+exp (-1.78+1.02×age+1.62×high-transmission-setting-exposure +1.77×dyspnea+1.54×CRP+1.03×lymphocyte+1.03×AST+1.76×calcium). Dyspnea (OR=5.91) and hypocalcemia (OR=5.79) were the leading risk factors, followed by exposure to a high-transmission setting (OR=5.04), CRP (OR=4.67), AST (OR=2.81), decreased lymphocyte count (OR=2.80), and age (OR=2.78). Conclusions This quantitative prognosis prediction model can provide a theoretical basis for the early formulation of individualized diagnosis and treatment programs and prevention of severe diseases.

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Section: Discussionsupporting

confidence: 90%

Prediction Model of Severe Coronavirus Disease 2019(COVID-19) Cases Shows the Leading Risk Factor of Hypocalcemia

Dai

et al. 2020

Preprint

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“…Kinin inhibition may, therefore, promote endothelial repair through reducing vascular permeability, although whether this is an effective therapeutic approach is yet to be confirmed within the literature. In contrast to this, consistent reports of hypokalaemia in patients with severe COVID-19 (61,62) suggest an increase in aldosterone, via elevations in Ang II, resulting in an increase in ACE, which acts to metabolize bradykinin (63). Therefore, the role of bradykinin in the pathogenesis of microvascular dysfunction in COVID-19 is questionable and more likely a result of the effects of Ang II, stemming from a downregulation of ACE2 after viral entry into cells.…”

Section: Potential Mechanisms Of Endothelial Dysfunction In Covid-19mentioning

confidence: 93%

Vascular Manifestations of COVID-19 – Thromboembolism and Microvascular Dysfunction

Roberts

Colley

Agbaedeng

et al. 2020

Front. Cardiovasc. Med.

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The coronavirus pandemic has reportedly infected over 31.5 million individuals and caused over 970,000 deaths worldwide (as of 22nd Sept 2020). This novel coronavirus, officially named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), although primarily causes significant respiratory distress, can have significant deleterious effects on the cardiovascular system. Severe cases of the virus frequently result in respiratory distress requiring mechanical ventilation, often seen, but not confined to, individuals with pre-existing hypertension and cardiovascular disease, potentially due to the fact that the virus can enter the circulation via the lung alveoli. Here the virus can directly infect vascular tissues, via TMPRSS2 spike glycoprotein priming, thereby facilitating ACE-2-mediated viral entry. Clinical manifestations, such as vasculitis, have been detected in a number of vascular beds (e.g., lungs, heart, and kidneys), with thromboembolism being observed in patients suffering from severe coronavirus disease (COVID-19), suggesting the virus perturbs the vasculature, leading to vascular dysfunction. Activation of endothelial cells via the immune-mediated inflammatory response and viral infection of either endothelial cells or cells involved in endothelial homeostasis, are some of the multifaceted mechanisms potentially involved in the pathogenesis of vascular dysfunction within COVID-19 patients. In this review, we examine the evidence of vascular manifestations of SARS-CoV-2, the potential mechanism(s) of entry into vascular tissue and the contribution of endothelial cell dysfunction and cellular crosstalk in this vascular tropism of SARS-CoV-2. Moreover, we discuss the current evidence on hypercoagulability and how it relates to increased microvascular thromboembolic complications in COVID-19.

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“…We were prompted to present this case by the results of a pre-printed retrospective study including 175 COVID-19 patients showing that 55% were diagnosed with hypokalaemia during their hospitalisation. 1 However, these findings were not confirmed by another study reporting mean potassium levels of 3.8 mmol/L (interquartile range: 3.5-4.2). 2 Considering the life-threatening risk of electrolyte abnormalities and especially hypokalaemia, it is useful to consider potential factors contributing to hypokalaemia in COVID-19 patients (Fig.…”

mentioning

confidence: 76%

Multifaceted persistent hypokalaemia in a patient with coronavirus disease 2019

Barkas

Filippas-Ntekouan

Liontos

et al. 2020

Internal Medicine Journal

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Multifaceted persistent hypokalaemia in a patient with coronavirus disease 2019 A 69-year-old woman with a 2-day history of fever, dry cough, sore throat, fatigue and diarrhoea was admitted in the Infectious Disease Unit in University Hospital of Ioannina in Greece after being confirmed positive for SARS-CoV-2. Previous medical history was unremarkable. On physical examination, temperature was 38.5 C, blood pressure 135/80 mmHg, pulse rate 99 b.p.m., respiratory rate 20/min and oxygen saturation 85% while the patient

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Assessment of Hypokalemia and Clinical Characteristics in Patients With Coronavirus Disease 2019 in Wenzhou, China

Cited by 210 publications

References 16 publications

Prediction Model of Severe Coronavirus Disease 2019(COVID-19) Cases Shows the Leading Risk Factor of Hypocalcemia

Prediction Model of Severe Coronavirus Disease 2019(COVID-19) Cases Shows the Leading Risk Factor of Hypocalcemia

Vascular Manifestations of COVID-19 – Thromboembolism and Microvascular Dysfunction

Multifaceted persistent hypokalaemia in a patient with coronavirus disease 2019

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