Background: The prognostic nutritional index (PNI) has been described as a simple risk-stratified tool for several diseases. We explored the predictive role of the PNI on coronavirus disease 2019 (COVID-19) severity.Methods: A total of 101 patients with COVID-19 were included in this retrospective study from January 2020 to March 2020. They were divided into two groups according to COVID-19 severity: non-critical (n = 56) and critical (n = 45). The PNI was calculated upon hospital admission: 10 × serum albumin (g/dL) + 0.005 × total lymphocyte count (/mm3). Critical COVID-19 was defined as having one of the following features: respiratory failure necessitating mechanical ventilation; shock; organ dysfunction necessitating admission to the intensive care unit (ICU). The correlation between the PNI with COVID-19 severity was analyzed.Results: The PNI was significantly lower in critically ill than that in non-critically ill patients (P < 0.001). The receiver operating characteristic curve indicated that the PNI was a good discrimination factor for identifying COVID-19 severity (P < 0.001). Multivariate logistic regression analysis showed the PNI to be an independent risk factor for critical illness due to COVID-19 (P = 0.002).Conclusions: The PNI is a valuable biomarker that could be used to discriminate COVID-19 severity.

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Aims Calcific aortic valve disease (CAVD) is the most common heart valve disease in the Western world. It has been reported that zinc is accumulated in calcified human aortic valves. However, whether zinc directly regulates CAVD is yet to be elucidated. The present study sought to determine the potential role of zinc in the pathogenesis of CAVD. Methods and results Using a combination of a human valve interstitial cell (hVIC) calcification model, human aortic valve tissues, and blood samples, we report that 20 μM zinc supplementation attenuates hVIC in vitro calcification, and that this is mediated through inhibition of apoptosis and osteogenic differentiation via the zinc-sensing receptor GPR39-dependent ERK1/2 signalling pathway. Furthermore, we report that GPR39 protein expression is dramatically reduced in calcified human aortic valves, and there is a significant reduction in zinc serum levels in patients with CAVD. Moreover, we reveal that 20 μM zinc treatment prevents the reduction of GPR39 observed in calcified hVICs. We also show that the zinc transporter ZIP13 and ZIP14 are significantly increased in hVICs in response to zinc treatment. Knockdown of ZIP13 or ZIP14 significantly inhibited hVIC in vitro calcification and osteogenic differentiation. Conclusions Together, these findings suggest that zinc is a novel inhibitor of CAVD, and report that zinc transporter ZIP13 and ZIP14 are important regulators of hVIC in vitro calcification and osteogenic differentiation. Zinc supplementation may offer a potential therapeutic strategy for CAVD.