Colleagues and I just completed a manuscript on COVID-19 and it's already accepted for publication.
We are imploring healthcare delivery to change based on what we have learned from the novel coronavirus outbreak. And, more importantly, what healthcare and your doctor have NOT been able to do - like explain your risk.
Here are the highlights:
Health and disease is a continuum, not "all or none." This is true for any chronic condition and COVID-19.
Big data failed to offer solutions or information to impact policy because the data we are collecting is of very little value.
COVID-19 attacks many different organ systems in different people - just like any other virulent or stealth infection. This is the underpinning of most disease.
Here is a link to the paper in pre-publication, but final, form.
Abstract:
The emergent outbreak of disease from SARS-CoV-2 (COVID-19) has caused a global pandemic and highlights a need for a more proactive approach to medical diagnostics and care delivery since immunocompromised individuals and those with preexisting condition are subject to extraordinarily high morbidity and mortality. Acute Respiratory Distress Syndrome (ARDS) and multiorgan dysfunction are among the leading causes of death in critically ill patients with COVID-19. Elevated inflammatory cytokines, noted in COVID-19 cases, suggest that a cytokine storm, also known as cytokine storm syndrome (CSS), may play a major role in the pathology of COVID-19. This pathway suggests reaction by the innate immune system as the primary physiological defense mechanism against the virus. Our and emerging data indicate that those most vulnerable to mortality from COVID-19, including immunocompromised individuals and those with preexisting disease diagnoses, present with elevated cytokines at baseline and this burden likely contributes to adverse outcomes. Reactive treatments with immunosuppressant anti-inflammatories to reduce mortality from COVID-19-induced CSS is controversial but may offer a solution to reduce mortality from the latest stages of CSS. There is an urgent need for better risk characterization among populations, during a pandemic, to facilitate more targeted policy decisions based on vulnerability. Novel interventions, both proactive and reactive, to treat COVID-19-induced CSS, discussed here, may shorten the duration of any lockdown or requirement for social distancing. Here we discuss the pathogenesis of Severe Acute Respiratory Syndrome (SARS)-induced CSS, compare the CSS in COVID-19 with that in SARS and Middle East Respiratory Syndrome (MERS) and discuss physiological markers elevated in CSS. We illustrate interventions used to mitigate risk on the early CSS continuum that function as “vaccines” for innate, rather than adaptive, immunity. We propose a biphasic approach to moderate the severity of this and future viral-based pandemics. We also posit that the diagnostics and interventions used to mitigate pandemics may also be a model for a new healthcare approach when applied for the measurement and reduction of chronic disease burden and immunocompromised status. The approaches include measurement of preexisting risk by accurately determining pre-cytokine storm status on a population basis, similar to the measurement of pre-diabetes to forestall diabetes. Part 2 is the reversal of pre-cytokine storm status, proactively, using a broad array of interventions.
Conclusions:
The novel coronavirus has reinvigorated the discussion about vulnerable populations, immunocompromised status, risk stratification, management of chronic conditions, and control of pandemics in a highly connected world. Much effort has been applied to avoidance of this infection, curve flattening, and development of specific treatments with major emphasis on vaccines. However, the identification of cytokine storms in COVID-19 sufferers reminds us that human immunity is complex. Solutions may not lie in preparing adaptive immunity to fight this and future viral pandemics. Consideration of innate immunity and even that of non-specific immunity, may play an important role in protecting populations against acute infectious episodes and even extend to non-communicable diseases that drive up to 90% of morbidity and early mortality impacting the daily quality of life in approximately half of our global population. The concept and definition of “immunocompromised” must be re-evaluated and redefined in terms of its accurate, objective measurement and consequential interventions to improve health and not manage disease. The existing model of diagnostics has failed at efficiently and effectively risk stratifying populations. Consequently, policy necessary to balance economic shutdown versus population risk has been universal rather than targeted leading to dramatic and often tragic social and economic consequences. Information from “big data” has contributed little to actionable decisions largely because the preponderance of available objective health data provides little relevance to infectious pandemics. However, this regrettable circumstance also offers the long-term prospective of saving lives if we apply what we are learning about pandemic risk and outcomes to the general measurement of health and disease. The overlap of COVID-19 risk biomarkers and those associated with a myriad of chronic diseases is not coincidence and could be applied to population health, today, to both risk stratify populations under pandemics and for chronic disease. Measuring and acting upon pre-cytokine storm status should be considered for incorporation into the standard of care. The implications of this on policy, human well-being, healthcare resource allocation, interventions, costs, and productivity have the potential to far outweigh the harm created during the COVID-19 outbreak.
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Thomas J. Lewis, Ph.D.