Concluding as to whether COVID-19 is accompanied by a cytokine “storm”, or just by a modest cytokine “breeze”, is indeed not so straightforward, whereby the clinical spectrum of this pathology is so broad than can span from a totally asymptomatic condition to a catastrophic systemic disease, characterized by multiple organ failure and leading to an almost inevitable death. It seems hence more reasonable to hypothesize that the outcome of SARS-CoV-2 infection may be strongly influenced by a variable individual response, and that progression of COVID-19 towards a “cytokine storm” phenotype, and thereby to more severe/critical illness, may be dependent on multiple factors, i.e., genetic (e.g., ABO blood group, polymorphisms in host cell receptors, immune response and inflammatory pathways), phenotypic (e.g., age, sex, ethnic origin, body weight, smoking status, presence of co-morbidities, frailty, nutritional deficiencies, viral strain and load, and so forth) and even environmental (e.g., social inequalities, timeliness and quality of care). However, what seems to clearly emerge from recent evidence on this matter, is that an accurate and early recognition of the “inflammatory phenotype” shall be regarded as an essential element for addressing the triage and managed care of patients with SARS-CoV-2 infection, either symptomatic or not. In fact, early treatment with specific cytokine antagonists, macrophage-targeted cell-signalling modifiers, corticosteroids and perhaps also anticoagulant drugs, may be much more effective in COVID-19 patients with hyperinflammatory response, while these agents may be almost worthless, or even detrimental, in those with no or low grade inflammation, thus strengthening the concept that patient selection and timing of therapy administration are essential elements in the managed care of SARS-CoV-2 infections.
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