ArticleJournal of inflammation research2022
Clevidipine and COVID 19: From Hypertension to Inflammatory Response.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
2 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Globally, more than 4 million have died from COVID-19, World Health Organization (WHO) to declare COVID-19 a pandemic. The COVID 19 pathology, produced by SARS-COV2, a virus from the coronavirus family, emerged at the end of 2019. The majority of cases usually have a mild or moderate form, characterized by fever, cough, intense asthenia and multiple symptoms derived from the initial replicative effect and subsequent hyperimmune effect. Severe cases present with Acute Respiratory Distress Syndrome (ARDS), due to pneumonia with bilateral involvement, which lead to hospital admission of patients and the need for admission to intensive care units (ICU) of approximately 10‒20%. According to the different series; the mortality of the condition once the patient is admitted to the ICU is close to 35‒45%. Currently, more than 4 million people have died in the world due to this pathology. The volume of infections generated the declaration by the World Health Organization (WHO) of the pandemic situation. Factors associated with a higher risk of progression into severe disease include age and comorbidities, especially systemic arterial hypertension due to its high incidence in the general population. Clevidipine can be rapidly and effectively adjusted to the clinical status of the patient, since it can be withdrawn and its effects reversed in just a few minutes, and contains high concentrations of lipids, and it could reduce the inflammatory response induced by SARS-COV2, which is key to progression into severe disease. However, its application in pro-inflammatory settings has not yet been explored, although it must play a key role in inflammation as a scavenger molecule.
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