Acute cardiac compromission in patients with MIS-C

Background and Aim: Multisystem inflammatory syndrome in chil-dren (MIS-C) is a late manifestation of SARS-CoV-2 infection. Cardiac involvement is common and presents as ventricular dys-function, shock, and coronary anomalies. The aim of the study is evaluate the influence of cardiac disfunction on clinical presen-tations and outcomes in a single center. Method(s): A retrospective study on patients diagnosed with MIS-C and referred to Buzzi Children's Hospital in Milan from November 2020 to February 2021. Patients were treated with intravenous immunoglobulins, corticosteroids and anti-throm-botic prophylaxis, in respect to our approved multidisciplinary protocol. According to the admission cardiac left ventricular ejec-tion fraction (LVEF), the patients were divided into group A (LVEF lt;45%) and group B (LVEF >=45%). Result(s): We collected 32 consecutive patients. Group A included 10 patients (9M/1F, aged 13 years [IQR 5-15]), and group B included 22 patients (15M/7M, aged 9 years [IQR 7-13]). At the presentation, significant differences were observed among shock (group A 6/10 vs group B 2/22, plt;0.01), gastrointestinal involvement (9/10 vs 11/22, p = 0.04) and duration of fever (5.3 vs 6.9 days, p = 0.02). All patients in group A required inten-sive care hospitalization (10/10 vs 12/22, p = 0.01). Interestingly, despite good cardiac function, two patients in group B presented with shock, probably due to vasoplegic/distributive cardiocircula-tory impairment secondary to the inflammatory state. Among biochemistry parameters, leukocytes, neutrophils, and CRP were significantly worse in group A (p = 0.001, p = 0.001 and p = 0.008, respectively). Pathological level of troponin T and NTproBNP were detected in all patients in group A and also in 33% and 77% of group B;with statistically significant higher median values in group A (Troponin T 72 [40-243] ng/L vs 22 [8-49] ng/L, p = 0.01;NTproBNP 14825 [11340-17810] ng/L vs 5921 [1114-11243] ng/L, p = 0.01). In group A, mitral regurgitation was more frequent (plt;0.01) and one patient had transient left main coronary dilation (Boston z-score +2.39). At the discharge, cardiac function normalized in all patients. Total length of hospital stay and cardiac recovery time were not statistically different between groups. Conclusion(s): If correctly diagnosed and early treated, all the MIS-C patients completely recovered, regardless of the initial cardiac involvement.

SARS-CoV-2 mRNA vaccine BNT162b2 triggers a consistent cross-variant humoral and cellular response.

As the SARS-CoV-2 pandemic continues to rage worldwide, the emergence of numerous variants of concern (VOC) represents a challenge for the vaccinal protective efficacy and the reliability of commercially available high-throughput immunoassays. Our study demonstrates the administration of two doses of the BNT162b2 vaccine that elicited a robust SARS-CoV-2-specific immune response which was assessed up to 3 months after full vaccination in a cohort of 37 health care workers (HCWs). SARS-CoV-2-specific antibody response, evaluated by four commercially available chemiluminescence immunoassays (CLIA), was qualitatively consistent with the results provided by the gold-standard in vitro neutralization assay (NTA). However, we could not observe a correlation between the quantity of the antibody detected by CLIA assays and their neutralizing activity tested by NTA. Almost all subjects developed a SARS-CoV-2-specific T-cell response. Moreover, vaccinated HCWs developed a similar protective neutralizing antibodies response against the EU (B.1), Alpha (B.1.1.7), Gamma (P.1), and Eta (B.1.525) SARS-CoV-2 variants, while Beta (B.1.351) and Delta (B.1.617.2) strains displayed a consistent partial immune evasion. These results underline the importance of a solid vaccine-elicited immune response and a robust antibody titre. We believe that these relevant results should be taken into consideration in the definition of future vaccinal strategies.

COVID-19 infection in severe Alpha 1-antitrypsin deficiency: Looking for a rationale.

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.