The Inflammation Syndrome: Your Nutrition Plan for Great Health, Weight Loss, and Pain–Free Living

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Avoid touching your nose, eyes and mouth. Urge your child to follow your lead and avoid touching the face.

Earlier symptoms, including impaired sense of smell detected in a significant number of COVID patients strongly indicate the viral potential for olfactory transmucosal invasion into the CNS ( 75– 78). An animal study whereby intranasal administration of SARS-CoV-2 virus into K18-hACE2 mice demonstrated an infective progression with high viral RNA levels in nasal turbinates, followed by olfactory bulbs and eyes ( 79). The spread of infection into the brain may be explained by the high viral replicative rate in these tissues and subsequent direct infection of the adjacent neuron axons ( 79). Peak viral levels in the brain were about 1000 times higher, whereas the production of pro-inflammatory cytokine and chemokine mRNAs in the brain was about 10-50 times higher compared to the lungs ( 79). Brain sections of mice showed perivascular hemorrhage, increased leukocyte infiltration and neuronal cell degeneration ( 79). These results correlated with the clinical severity and mortality of the infected mice ( 79). Evidence from a post-mortem autopsy on 33 COVID19-infected individuals showed intact SARS-CoV-2 particles and its RNA in olfactory mucosa and other neuroanatomical regions receiving the axonal projections, supporting the notion of neuroinvasion via neural-mucosal barrier ( 80). It can sometimes be triggered by an infection, such as hepatitis B, but the exact cause is uncertain. or more organ systems affected (e.g., cardiac, renal, respiratory, hematologic, gastrointestinal, dermatologic, and neurological. The median duration of fever following initiation of therapy (usually IVIG with or without steroids) was 2 days in the anakinra group, and 3 days in the no anakinra group ( p = 0.43). 26% of patients in the anakinra group experienced rebound fever compared to 16% of those in the no anakinra group ( p = 0.35). On hospital day 2, 48% of individuals in the anakinra group continued to have fever, while 58% of patients in the no anakinra group had the same ( p = 0.44). The CRP reduction on hospital days 2 and 3 were not statistically significant between the two groups.Vasoactive support was applied to 21 patients (68%) in the anakinra group and 22 patients (71%) in the no anakinra group. There were no differences in the proportion of matched subjects receiving organ support between the two groups. The median duration of vasoactive support was 16.2 vs. 19.1 h in anakinra vs. no anakinra group, which was not different. The median VIS on day 1 was 7 vs. 6 in the anakinra vs. no anakinra groups, respectively, with no statistically significant difference. The VIS score was not different between the two groups on day 2 and on day 3. Riollano-Cruz M, Akkoyun E, Briceno-Brito E, et al. Multisystem inflammatory syndrome in children related to COVID-19: a New York City experience. J Med Virol Jan. 2021;93(1):424–33. https://doi.org/10.1002/jmv.26224. The underlying mechanism is complex. What is known is that the dysfunction of IL-6/Janus kinase/signal transducer and activator of transcription (IL-6/JAK/STAT) signaling pathway, interferon (IFN) cell signaling cascade, TNF-α-nuclear factor-kappa (TNFα-NF-κB) pathway, toll-like receptor (TLR) pathway, antibody-mediated pathway, Bruton tyrosine kinase (BTK) pathway, renin-angiotensin system (RAS) pathway and especially the Janus kinase signal transducer and activator transcription (JAK/STAT) pathway, are all integral to the progression of cytokine storm ( 45). In general, SARS-CoV-2 invades and activates a myriad of immune cells, such as endothelial cells, macrophages, monocytes, dendritic cells, natural killer cells and T-cells ( 45). In these cells, the viral particles stimulate multiple inflammatory pathways, producing low levels of antiviral interferons alongside high levels of cytokines (IL-1β, IL-2R, IL-6, IL-7, IL-8, IL-17 and TNF-α) and chemokines (CCL-2, CCL-3, CCL-5, CCL-7, CXCL-10), resulting in hyperinflammation and cytokine storm ( Figure1) ( 45). While the initial release of cytokines is therapeutic and aid in eliminating the virus, the uncontrolled cytokine secretion would be detrimental as they begin to target host cells ( 45, 46). Among the cytokines, IL-1β, IL-2R, IL-6, and TNF-α play a pivotal role in cytokine storm while IL-1β, IL-6, and TNF-α correlate well with the severity of disease ( 45, 47). On the other hand, the weakened T-cell immune effect further hamper viral elimination, allowing a vicious cycle of cytokine-induced hypercytokinaemia ( 48). A more detailed representation of the inflammatory signaling pathway involved in COVID-19 is shown in Figure1. Gender Difference in Severity and Mortality of COVID-19

The management of MIS-C was based on the severity of illness. Therapy typically incorporated IVIG and varying doses of methylprednisolone depending on disease severity. Those with mild disease received 2 mg/kg/day methylprednisolone for 3–5 days, those with moderate disease received 10 mg/kg/day for 1–3 days, while those with severe disease received 20–30 mg/kg/day for 1–3 days (Table 1). In the moderate and severe groups, this was followed by an oral steroid tapering regimen.

Causes

Godfred-Cato S, Bryant B, Leung J, et al. COVID-19-Associated Multisystem Inflammatory Syndrome in Children - United States, March-July 2020. MMWR Morb Mortal Wkly Rep Aug. 2020;14(32):1074–80. https://doi.org/10.15585/mmwr.mm6932e2. The symptoms of MIS-C are serious and are treated in the hospital. Not all kids have the same symptoms. But if no other diagnosis fits, health care professionals may diagnose MIS-C if a child: