ABSTRACT
Despite the fact that the global COVID-19 pandemic has officially ended, we continue to feel its effects and discover new correlations between SARS-CoV-2 infection and changes in the organism that have occurred in patients. It has been shown that the disease can be associated with a variety of complications, including disorders of the nervous system such as a characteristic loss of smell and taste, as well as less commonly reported incidents such as cranial polyneuropathy or neuromuscular disorders. Nervous system diseases that are suspected to be related to COVID-19 include Guillain-Barré syndrome, which is frequently caused by viruses. During the course of the disease, autoimmunity destroys peripheral nerves, which despite its rare occurrence, can lead to serious consequences, such as symmetrical muscle weakness and deep reflexes, or even their complete abolition. Since the beginning of the pandemic, case reports suggesting a relationship between these two disease entities have been published, and in some countries, the increasing number of Guillain-Barré syndrome cases have also been reported. This suggests that previous contact with SARS-CoV-2 may have had an impact on their occurrence. This article is a review and summary of the literature that raises awareness of the neurological symptoms' prevalence, including Guillain-Barré syndrome, which may be impacted by the commonly occurring COVID-19 disease or vaccination against it. The aim of this review was to better understand the mechanisms of the virus's action on the nervous system, allowing for better detection and the prevention of its complications.
ABSTRACT
Background: The purpose of the study was to determine whether the use of ß-adrenoceptor antagonists (ß-blockers) can affect metalloproteinase 2 (MMP-2) and its tissue inhibitor (TIMP-2) in patients with chronic kidney disease (CKD) on conservative treatment. Methods: The circulating MMP-2/TIMP-2 system, proinflammatory cytokines (tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), and the marker of oxidative stress-Cu/Zn superoxide dismutase (Cu/Zn SOD)-were measured in 23 CKD patients treated with ß-blockers [ß-blockers (+)] and in 27 CKD patients not receiving the above medication [ß-blockers (-)]. Results: The levels of MMP-2, TIMP-2, and IL-6 were significantly lower in the ß-blockers (+) than in the ß-blockers (-) group, whereas Cu/Zn SOD concentrations were not affected by ß-blocker use. There was a strong, independent association between MMP-2 and TIMP-2 in both analyzed patient groups. In the ß-blockers (+) group, MMP-2 levels were indirectly related to the signs of inflammation, whereas in the ß-blockers (-) group, the alterations in the MMP-2/TIMP-2 system were associated with the oxidative stress marker and CKD etiology. Conclusions: This study is the first to suggest that the use of ß-blockers was associated with the reduction in IL-6 and the MMP-2/TIMP-2 system in CKD, providing a pharmacological rationale for the use of ß-blockers to reduce inflammation and abnormal vascular remodeling in CKD.
