Abstract
An altered immune response to pathogens has been suggested to explain increased susceptibility to infectious diseases in patients with diabetes. Recent evidence has documented several immunometabolic pathways in patients with diabetes directly related to the COVID-19 infection. This also seems to be the case for prediabetic subjects with proinflammatory insulin resistance syndrome accompanied with prothrombotic hyperinsulinemic and dysglycemic states. Patients with frank hyperglycemia, dysglycemia and/or hyperinsulinemia develop systemic immunometabolic inflammation with higher levels of circulating cytokines. This deleterious scenario has been proposed as the underlying mechanism enhancing a cytokine storm-like hyperinflammatory state in diabetics infected with severe COVID-19 triggering multi-organ failure. Compared with moderately affected COVID-19 patients, diabetes was found to be highly prevalent among severely affected patients suggesting that this non-communicable disease should be considered as a risk factor for adverse outcomes. The COVID-19 pandemic mirrors with the diabetes pandemic in many pathobiological aspects. Our interest is to emphasize the ties between the immunoinflammatory mechanisms that underlie the morbidity and lethality when COVID-19 meets diabetes. This review brings attention to two pathologies of highly complex, multifactorial, developmental and environmentally dependent manifestations of critical importance to human survival. Extreme caution should be taken with diabetics with suspected symptoms of COVID-19 infection.
Highlights
In the last few months, rapid publications reporting on the outbreak of the novel betacoronavirussevere acute respiratory syndrome (SARS)-Cov-2 have flooded the scientific literature [1]
Like other diseases associated with the coronavirus family such as SARS, COVID-19 is mainly a disease of the respiratory system that could interact with the metabolic and endocrine system [13]
The insulin curve showed striking elevation in the individuals with (L) adiponectin/leptin ratio (ALR). They concluded that in apparently symptom-free individuals a cluster of altered immunometabolic phenotypes related to impaired angiogenesis and hypoxia, inflammation, inappropriate extracellular matrix (ECM) remodeling and macrophage polarization could be place into a systemic and molecular construct coined as adipose tissue dysfunction, which would trigger the early events leading to the development of insulin resistance and systemic inflammation [49]
Summary
In the last few months, rapid publications reporting on the outbreak of the novel betacoronavirus. When have they highlighted that patients with overt diabetes and/or the metabolic syndrome might have up to contract COVID-19 [5]. On leading average,toeach infected person and the virus stays inof the oropharynx early in the COVID-19 course of disease a higher infectivity spreads the infection to additional persons and the virus stays in the oropharynx early in the course during presymptomatic stages (Figure 1). China, indicated affected were males and, as previously observed with influenza, a higher mortality was found among that the patient mean agecomorbidities was 59 yearsand old,the. Out as among those coexisting with influenza, conditions [8,9].a higher mortality was found among patients with preexisting comorbidities and the elderly [7].
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