EFFECT OF THE THIRD DOSE OF ASTRAZENECA VACCINE ON THE ABILITY TO GENERATE ANTI-RBD ANTIBODIES WITHIN TWO AT-RISK POPULATIONS, GERIATRICS AND HEALTH PERSONNEL IN THE PROVINCE OF TUCUMÁN (preprint)

This study aims to evaluate the effect on the ability to generate Anti-Anti RBD antibodies (Anti-SAR-CoV 2-Spike-RBD) to the third dose of the AstraZeneca vaccine in two at-risk populations in the Province of Tucumán. Humoral immune responses, assayed by anti-SARS-CoV-2-Spike-RBD IgG ELISA, were measured in 223 participants, including geriatric patients and healthcare workers, at 0, 14 and 28 days after receiving third dose of the AstraZeneca between October and December 2021 in Tucuman, Argentina. The antibodies title in geriatric patients with and without previous COVID-19 diseases and complete vaccine schedule increased significantly 14 days after receiving the third dose of the AstraZeneca vaccine (p<0.001). When compared Antibody Concentration in geriatric patients with and without a history of COVID-19 14 days post-vaccination, the increase in antibodies was higher in those who did not have a previous history of COVID-19 (p<0.05). The antibodies title in healthcare personnel with and without previous COVID-19 diseases and complete vaccination increased significantly 14 days post-vaccination with the third dose of AstraZeneca (p<0.01). There was a negative correlation between age and antibodies titer 14 days after the third dose of COVID vaccine in persons with no history of disease (rs= -0.36, p=0.0001). While persons with a history of COVID-19 did not have a significant correlation (rs= -0.03;p=0.8). The results obtained provide information on antibodies dynamics after the third dose with AstraZeneca in a context of vaccine heterogeneity, indicating the importance of baseline studies of antibodies and hybrid immunity when considering vaccination policies.

COVID-19 and diabetes: A bidirectional relationship. / COVID-19 y diabetes mellitus: una relación bidireccional.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19). Diabetes is one of the most frequent comorbidities in people with COVID-19 with a prevalence that varies between 7 and 30%. Diabetics infected with SARS-CoV-2 have a higher rate of hospital admission, severe pneumonia, and higher mortality compared to non-diabetic subjects. Chronic hyperglycemia can compromise innate and humoral immunity. Furthermore, diabetes is associated with a low-grade chronic inflammatory state that favors the development of an exaggerated inflammatory response and therefore the appearance of acute respiratory distress syndrome. Recent evidence has shown that SARS-CoV-2 is also capable of causing direct damage to the pancreas that could worsen hyperglycemia and even induce the onset of diabetes in previously non-diabetic subjects. Therapeutic strategies should be aimed at facilitating patient access to the healthcare system. Control of blood glucose and comorbidities must be individualized in order to reduce the incidence of complications and decrease the burden on health systems. In this article we will review the pathophysiological mechanisms that explain the bidirectional relationship between COVID-19 and diabetes mellitus, its implication in the prognosis and management of hyperglycemia in this group of patients.

Statins in COVID-19: Is there any foundation?

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19). Acute respiratory distress syndrome is the main cause of death from COVID-19 and occurs due to an exaggerated inflammatory response that causes the release of pro-inflammatory cytokines such as interleukins and tumor necrosis factor-alpha (TNF-α). Statins are lipid lowering drugs with pleiotropic effects. They have shown benefit in the management of inflammatory and autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis. Furthermore, due to their immunomodulatory properties, they have been used in the treatment of various infectious diseases such as community-acquired pneumonia and influenza. In this review we analyze the pathophysiological foundations that support the use of statins as an adjunctive treatment in patients with COVID-19. Resumen El coronavirus tipo 2 del síndrome respiratorio agudo grave (SARS-CoV-2) es el agente causal de la enfermedad por coronavirus 2019 (COVID-19). El síndrome de distress respiratorio agudo constituye la principal causa de muerte por COVID-19 y ocurre por una respuesta inflamatoria exagerada que provoca la liberación de citocinas proinflamatorias como interleucinas y factor de necrosis tumoral alfa (TNF-α). Las estatinas son fármacos hipolipemiantes con efectos pleiotrópicos. Han demostrado beneficio en el manejo de enfermedades inflamatorias y autoinmunes como el lupus eritematoso sistémico, la artritis reumatoide y la esclerosis múltiple. Además, debido a sus propiedades inmunomoduladoras se han utilizado en el tratamiento de diversas enfermedades infecciosas como neumonía adquirida en la comunidad e influenza. En esta revisión analizamos los fundamentos fisiopatológicos que apoyan el uso de estatinas como tratamiento coadyuvante en pacientes con COVID-19.

Statins in COVID-19: is there any foundation? / Estatinas en COVID-19: ¿existe algún fundamento?

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of coronavirus disease 2019 (COVID-19). Acute respiratory distress syndrome is the main cause of death from COVID-19 and occurs due to an exaggerated inflammatory response that causes the release of pro-inflammatory cytokines such as interleukins and tumor necrosis factor-alpha (TNF-α). Statins are lipid lowering drugs with pleiotropic effects. They have shown benefit in the management of inflammatory and autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis. Furthermore, due to their immunomodulatory properties, they have been used in the treatment of various infectious diseases such as community-acquired pneumonia and influenza. In this review we analyze the pathophysiological foundations that support the use of statins as an adjunctive treatment in patients with COVID-19.