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Rassegna di Patologia dell'Apparato Respiratorio ; 37(2):81-85, 2022.
Article in Italian | EMBASE | ID: covidwho-1989036


Summary In June 2020, indications were developed for the resumption of pulmonary function testing in the course of a SARS-CoV-2 pandemic, in support of national, regional and company direc-tives, as well as for pulmonologists dedicated to pulmonary function laboratories. The present document represents an update of the previous one in the light of new knowledge and the current SARS-CoV-2 epidemiological situation.

Eur Rev Med Pharmacol Sci ; 26(2): 715-721, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1675570


OBJECTIVE: As N-acetylcysteine (NAC) is promising as a re-purposed drug for the adjunctive or supportive treatment of serious COVID-19, this article aimed to describe current evidence. MATERIALS AND METHODS: A search was performed in PubMed/Medline for "NAC", "viral Infection", COVID-19", oxidative stress", "inflammation", retrieving preclinical and clinical studies. RESULTS: NAC is a pleiotropic molecule with a dual antioxidant mechanism; it may neutralize free radicals and acts as a donor of cysteine, restoring the physiological pool of GSH. Serious COVID-19 patients have increased levels of reactive oxygen species (ROS) and free radicals and often present with glutathione depletion, which prompts a cytokine storm. NAC, which acts as a precursor of GSH inside cells, has been currently used in many conditions to restore or protect against GSH depletion and has a wide safety margin. In addition, NAC has anti-inflammatory activity independently of its antioxidant activity. CONCLUSIONS: Clinical and experimental data suggest that NAC may act on the mechanisms leading to the prothrombotic state observed in severe COVID-19.

Acetylcysteine/therapeutic use , Acetylcysteine/chemistry , Antioxidants/chemistry , COVID-19/metabolism , COVID-19/virology , Glutathione/chemistry , Glutathione/metabolism , Humans , Oxidative Stress , Randomized Controlled Trials as Topic , Reactive Oxygen Species/metabolism , SARS-CoV-2/isolation & purification , Virus Diseases/drug therapy , Virus Diseases/metabolism
Respir Med ; 183: 106440, 2021 07.
Article in English | MEDLINE | ID: covidwho-1219243


The clinical manifestations of COVID-19 are heterogeneous: 46.4% of patients admitted into hospital reported to have at least one comorbidity. Comorbidities such as COPD, diabetes, hypertension and malignancy predispose patients with Covid-19 to adverse clinical outcomes. Alpha 1-antitrypsin deficiency (AATD) is a genetic disorder caused by pathological mutation(s) in the SERPINA1 gene resulting in an imbalance in proteinase activity which may lead to premature emphysema and COPD. Our aim was to investigate whether people with severe AAT deficiency (AATD) have an increased risk of (severe) COVID-19 infection. We collected data on COVID-19 symptoms, laboratory-confirmed infection, hospitalization and treatment by means of a telephone survey, directly administered to Italian severe AATD subjects in May 2020. We then compared our findings with data collected by the Istituto Superiore di Sanità on the total population in Italy during the same period. We found an higher frequency of SARS-CoV-2 infection in our cohort (3.8%) compared to national data regarding infection, thus giving severe AATD a relative risk of 8. 8 (95%CI 5.1-20,0; p<0.0001) for symptomatic SARS-CoV-2 infection. Moreover, the relative risk (RR) was higher in AATD patients with pre-existing lung diseases (RR 13.9; 95%CI 8.0-33.6; p<0.001), but with a similar death rate (1 in 8, 12.5%) compared to the general population (13.9%; RR 0.9). These preliminary findings highlight the importance of close surveillance in the spread of COVID-19 in patients with severe AATD and underlines the need for further studies into the role of the antiprotease shield in preventing SARS-Cov-2 infection.

COVID-19/epidemiology , Pandemics , SARS-CoV-2 , alpha 1-Antitrypsin Deficiency/epidemiology , Biomarkers/blood , COVID-19/blood , Comorbidity , Global Health , Humans , Peptide Hydrolases/blood , Severity of Illness Index , alpha 1-Antitrypsin Deficiency/blood