Minerva medica
-
Either central or peripheral baroreceptor reflex abnormalities, and/or alterations in neurohumoral mechanisms play a pivotal role in the genesis of neurally mediated syncope. Thus, improving our knowledge of the biochemical mechanisms underlying specific forms of neurally mediated syncope (more properly termed "neurohumoral syncope") might allow the development of new therapies that are effective in this specific subgroup. A low-adenosine phenotype of neurohumoral syncope has recently been identified. ⋯ The typical mechanism of syncope is an idiopathic paroxysmal atrioventricular block or sinus bradycardia, most often followed by sinus arrest. Since patients with low plasma adenosine levels are highly susceptible to endogenous adenosine, chronic treatment of these patients with theophylline, a non-selective adenosine receptor antagonist is expected to prevent syncopal recurrences. This hypothesis is supported by results from series of cases and from two controlled studies.
-
Angiotensin converting enzyme 2 (ACE2) receptor sites for severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2), responsible for the disease called COVID-19 are present in the liver, especially in correspondence with cholangiocytes. Liver damage during SARS-CoV-2 infection can be due to several mechanism including direct cytopathic effect, synergy of intestinal damage/liver damage (lipopolysaccharides/Kupfer and other cells interaction), uncontrolled immune reaction (lymphopenia and significant increase in C reactive protein, ferritin, lactate dehydrogenase, D-dimer, interleukin (IL)-6, IL- 10, IL-2, interferon-gamma, etc.), sepsis, drug-induced liver injury, hypoxia and thromboembolic events. An increase in aspartate aminotransferase (AST) from 14 to 58% and alanine transaminase (ALT) from 21 to 76% has been reported. ⋯ The consumption of alcohol reduces both innate and acquired immune activity and it has been hypothesized that this habit is correlated with liver increase of ACE2 receptors. Furthermore, nonalcoholic and alcoholic steatosis/steatohepatitis is a breeding ground for the development of oxidative stress. In this context, any encounter with SARS-CoV-2 infection can support and aggravate the systemic cytokine tsunami.