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1.
J Dent Res ; 101(12): 1450-1456, 2022 11.
Article in English | MEDLINE | ID: covidwho-1896164

ABSTRACT

The airborne transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) via respiratory fluids and droplets suggests that mouthwashes containing substances with virucidal activity can help reduce viral spread. We conducted a multicenter, double-blind, placebo-controlled, randomized trial to assess the virucidal activity of cetylpyridinium chloride (CPC) mouthwashes. Outpatients who tested positive for SARS-CoV-2 infection with or without symptoms were randomized to perform washes and gargles for 1 min with 15 mL of either colored distilled water or 0.07% CPC (Vitis CPC Protect) mouthwash. The study outcomes were the SARS-CoV-2 log10 viral RNA load and the nucleocapsid protein levels, both in saliva at 1 and 3 h after the intervention. In total, 118 patients were enrolled and randomized (mean [SD], age 46 [14] y). Thirteen of 118 participants (11%) did not complete follow-up or had insufficient sample volume for testing and were excluded from the analysis. The assessment of the viral load showed no significant differences between groups at any of the investigated points. However, the levels of SARS-CoV-2 nucleocapsid protein of lysed viruses were significantly higher in the CPC group compared with the control group at 1 h (adjusted difference 269.3 pg/mL; 95% confidence interval [CI], 97.1-441.5) and at 3 h postintervention (561.1 pg/mL; 95% CI, 380.0-742.2). In nonhospitalized patients with asymptomatic or mild symptomatic SARS-CoV-2 infection, a 0.07% CPC mouthwash, compared to placebo, was associated with a significant increase of nucleocapsid protein levels in saliva, indicating enhanced disruption of viral particles.


Subject(s)
COVID-19 , Cetylpyridinium , Mouthwashes , SARS-CoV-2 , Virus Shedding , Humans , Middle Aged , Cetylpyridinium/therapeutic use , Chlorides , Double-Blind Method , Mouthwashes/therapeutic use , Nucleocapsid Proteins , RNA, Viral , Virus Shedding/drug effects
2.
Revista de la Federacion Argentina de Cardiologia ; 50:20-23, 2021.
Article in Spanish | EMBASE | ID: covidwho-1857661

ABSTRACT

A cytokine storm, probably due to an imbalance in T-cell activation, could contribute to cardiovascular disease in COVID-19. Cohort studies estimated that 7-80% of hospitalized patients presented acute myocardial injury, with a greater expression in patients admitted to the intensive care unit vs. those who did not (22.2% vs. 2.0%), and in those who died vs. survivors (59% vs 1%). The first reports from China suggested an incidence of arrhythmias in hospitalized patients of 17%, rising in critical care to 44%. We present the case of a patient with a positive swab for SARS-CoV-2 infection with an interstitial-alveolar parenchymal infiltrate distributed in a genera-lized way in both lung fields, who required respiratory mechanical assistance. On the fourth day of hospitalization, he developed sinus bradycardia, requiring treatment with atropine and infu-sion of isoproterenol, resolving the clinical picture after 24 hours. The causal mechanism of sinus bradycardia is not exactly known, it is believed that it could be multifactorial, including severe hypoxia, hypotension, intrinsic imbalances of the autonomic nervous system, alteration in the regulation of the angiotensin-converting enzyme 2, drug interactions and immune-inflammatory direct damage on the sinus node.

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