Prognostic role of Interleukin-6/lymphocytes ratio in SARS-CoV2 related pneumonia.

INTRODUCTION AND AIM: Interleukin-6 to lymphocyte (IL-6/Lym) ratio has been identified as a potential prognostic tool in patients with SARS-CoV2 related pneumonia. The aim of our study was to compare the prognostic power of IL-6/Lym ratio with other biomarkers in patients initially admitted in a non intensive unit and suffering for respiratory failure associated with SARS-CoV2 related pneumonia. MATERIALS AND METHODS: IL-6/Lym ratio, IL-6, D-Dimer, D-Dimer/fibrinogen ratio, fibrinogen, C-reactive protein (CRP), lymphocytes count and neutrophil/lymphocyte (N/L) ratio collected at hospital admission were tested as prognosticators of negative outcome, defined as combined endpoint in-hospital mortality and/or Intensive Care Unit (ICU) admission requiring oro-tracheal intubation (OTI). RESULTS: Study population encompassed two hundreds and twenty-three patients (46% females) with mean age ± DS 69.4 ± 13.3 years. Eighty-nine patients (39.9%) suffered for severe respiratory failure and required non invasive ventilation, helmets and/or high flow nasal cannula. Fourty-one patients (18.3%) died during hospital stay and/or required OTI. In these patients mean values of IL-6/Lym ratio, IL-6, CRP and N/L were significantly higher and lymphocytes count was significantly lower compared with patients discharged alive and/or not requiring OTI, while no difference was found in mean values of D-Dimer, D-Dimer/Fibrinogen ratio and fibrinogen. AUC (0.797, 95% CI: 0.738-0.848) of IL-6/Lym ratio was the highest compared with those of all the other analyzed biomarkers and the difference was significant with the exception of IL-6. At multivariate logistic regression IL-6/Lym ratio > 66.5 resulted the only independent biomarker associated with mortality and/or OTI (OR 5.65; 95% 1.63-19.54). CONCLUSION: IL-6/Lym ratio seems to be an optimal prognosticator in SARS-CoV2 related pneumonia. Its routinary use in COVID-19 patients could be warranted.

Stem-Cell-Derived Circulating Progenitors Dysfunction in Behçet's Syndrome Patients Correlates With Oxidative Stress.

Behçet's syndrome (BS) is a systemic vasculitis considered as the prototype of a systemic inflammation-induced thrombotic condition whose pathogenesis cannot be explained just by coagulation abnormalities. Circulating hematopoietic progenitor cells (CPC), a population of rare, pre-differentiated adult stem cells originating in the bone marrow and capable of both self-renewal and multi-lineage differentiation, are mobilized in response to vascular injury and play a key role in tissue repair. In cardiovascular and thrombotic diseases, low circulating CPC number and reduced CPC function have been observed. Oxidative stress may be one of the relevant culprits that account for the dysfunctional and numerically reduced CPC in these conditions. However, the detailed mechanisms underlying CPC number reduction are unknown. On this background, the present study was designed to evaluate for the first time the possible relationship between CPC dysfunction and oxidative stress in BS patients. In BS patients, we found signs of plasma oxidative stress and significantly lower CD34+/CD45-/dim and CD34+/CD45-/dim/CD133+ CPC levels. Importantly, in all the considered CPC subsets, significantly higher ROS levels with respect to controls were observed. Higher levels of caspase-3 activity in all the considered CPC population and a strong reduction in GSH content in CPC subpopulation from BS patients with respect to controls were also observed. Interestingly, in BS patients, ROS significantly correlated with CPC number and CPC caspase-3 activity and CPC GSH content significantly correlated with CPC number, in all CPC subsets. Collectively, these data demonstrate for the first time that CPC from BS patients show signs of oxidative stress and apoptosis and that a reduced CPC number is present in BS patients with respect to controls. Interestingly, we observed an inverse correlation between circulating CPC number and CPC ROS production, suggesting a possible toxic ROS effect on CPC in BS patients. The significant correlations between ROS production/GSH content and caspase-3 activity point out that oxidative stress can represent a determinant in the onset of apoptosis in CPC. These data support the hypothesis that oxidative-stress-mediated CPC dysfunctioning may counteract their vascular repair actions, thereby contributing to the pathogenesis and the progression of vascular disease in BS.