ABSTRACT
In December 2019, a new Coronavirus called Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), appeared in China, spreading rapidly around the globe and becoming a pandemic. SARS-CoV-2 is the cause of a serious life-threatening disease known as COVID-19. The risk of SARS-CoV-2 infection in patients with preexisting systemic autoimmune diseases (AID) appears to be slightly higher than in the general population, but the clinical course does not appear to be different. However, we must bear in mind that the use of corticosteroids, immunomodulatory drugs, and biological therapy in patients with AID can modulate the risk of hospitalization and death. The alterations in the innate and adaptive immune response found in patients with cytokine storm due to COVID-19 are the reasons for the high morbidity and mortality. Thus, clinicians should early identify the symptoms and closely monitor patients with risk factors for developing these complications and the interactions with other systems such as the immune-neuro-endocrine system. © 2023 Elsevier Inc. All rights reserved.
ABSTRACT
The ability to eradicate deadly diseases and decrease the mortality of others makes vaccines one of the most important discoveries of the last century. Despite already having effective vaccines, scientific advances continue developing new antigens capable of producing more significant immune responses to achieve stronger immunity. © 2023 Elsevier Inc. All rights reserved.
ABSTRACT
The term "cytokine storm” was first proposed in 1993 by Ferrara et al. In 1991, Chatenaud described a systemic clinical picture called "Cytokine Release Syndrome” very similar to "Cytokine Storm Syndrome” so these terms can be used synonymously. During the COVID-19 pandemic, high-risk individuals (>65 years, with comorbidities) may develop cytokine storms as a consequence of multiorgan involvement seen during the acute and post-COVID-19 phases. On the other hand, the term immune neuroendocrine system was first proposed by Besedovsky H et al. Evidences obtained during COVID-19 infection demonstrated that SARS-CoV-2 infections can affect the immune neuroendocrine system, both in its invasion stage of different organs and tissues and in the recovery stage. This damage is caused by viral infection and/or cytokine storm. This chapter analyzes the devastating effect of SARS-CoV-2 infection and the cytokine storm on the immune neuroendocrine system. These evidences may lead to new therapeutic proposals. © 2023 Elsevier Inc. All rights reserved.
ABSTRACT
Objectives: To determine the risk factors, impact and outcomes of COVID-19 in autoimmune / inflammatory diseases (AID). Methods: Case (patients with AID) and controls (patients without AID) study. Both groups with SARS-CoV-2 by PCR. Clinical, biochemical, treatment and outcome characteristics were determined. Spearman correlation, X2 and multivariate analysis were performed. Results: AID, 90 (49.49 ± 14.2 years) vs controls, 90 (52.58 ± 13.5 years). AID: systemic lupus erythematosus (SLE) (n = 20, 22.2%), systemic sclerosis (n = 16, 17.8%), rheumatoid arthritis (n = 14, 15.6%), primary antiphospholipid syndrome (n = 12, 13.3%), autoimmune encephalitis (AIE) (n = 6, 6.7%), granulomatosis with polyangiitis (GPA) (n = 5, 5.6%) and multiple sclerosis (n = 3, 3.3%) were the most frequent. Treatment: anticoagulant 73.3%, glucocorticoid 53.3% and antimalarials 35.6%. The AID patients had less invasive mechanical ventilation (IMV) (p = 0.004), lower death (p = 0.006) and lower discharge with O2 (p = 0.001) (Table 1). AID: creatinine correlate positively with days with IMV (rho = 539, p 0.024). In AID, AIE and O2 saturation ≤ 88% provided risk for IMV (OR 88.42, CI 3.9-196.7, p = 0.005 and OR 10.05, CI 1.2-83.7, p = 0.033, respectively) while antimalarials were protective for IMV (OR 0.08, CI 0.0-0.9, p = 0.042). Regarding death in AID, oxygen saturation ≤ 88% and CO-RADS ≥4 were risk factors (OR 5.12, CI 1.5-16.4, p = 0.006 and OR 8.84, CI 1.2-64.0, p = 0.031, respectively) and anticoagulant use was protective (OR 0.26, CI 0.0-0.8, p = 0.019) (Table 2). Conclusion: Our study suggests that patients with AID have a better outcome than the control group. Multiple factors are involved in this outcome such as surveillance, chronic use of antimalarials, steroid and anticoagulation.We propose that at the molecular level high levels of IFN may be a protective factor for complications from SARS-CoV-2 infection. New longitudinal and molecular level studies in patients with mild/moderate, severe and critical COVID-19 will be necessary to know the impact of COVID-19 in AID.