Stroke risk in multiple sclerosis: a critical appraisal of the literature.

Observational studies suggest that the occurrence of stroke on multiple sclerosis (MS) patients is higher compared to the general population. MS is a heterogeneous disease that involves an interplay of genetic, environmental and immune factors. The occurrence of stroke is subject to a wide range of both modifiable and non-modifiable, short- and long-term risk factors. Both MS and stroke share common risk factors. The immune mechanisms that underlie stroke are similar to neurodegenerative diseases and are attributed to neuroinflammation. The inflammation in autoimmune diseases may, therefore, predispose to an increased risk for stroke or potentiate the effect of conventional stroke risk factors. There are, however, additional determinants that contribute to a higher risk and incidence of stroke in MS. Due to the challenges that are associated with their differential diagnosis, the objective is to present an overview of the factors that may contribute to increased susceptibility or occurrence of stroke in MSpatients by performing a review of the available to date literature. As both MS and stroke can individually detrimentally affect the quality of life of afflicted patients, the identification of factors that contribute to an increased risk for stroke in MS is crucial for the prompt implementation of preventative therapeutic measures to limit the additive burden that stroke imposes.

Impairment in selenocysteine synthesis as a candidate mechanism of inducible coagulopathy in COVID-19 patients.

Coagulopathy has recently been recognized as a recurring complication of COVID-19, most typically associated with critical illness. There are epidemiological, mechanistic and transcriptomic evidence that link Selenium with SARS-CoV-2's intracellular latency. Taking into consideration the vital role of selenoproteins in maintaining an adequate immune response, endothelial homeostasis and a non-prothrombotic platelet activation status, we propose that impairment in selenocysteine synthesis, via perturbations in the aforementioned physiological functions, potentially constitutes a mechanism of coagulopathy in COVID 19 patients other than those developed in critical illness.