In-hospital mortality and severe outcomes after hospital discharge due to COVID-19: A prospective multicenter study from Brazil.

Background: We evaluated in-hospital mortality and outcomes incidence after hospital discharge due to COVID-19 in a Brazilian multicenter cohort. Methods: This prospective multicenter study (RECOVER-SUS, NCT04807699) included COVID-19 patients hospitalized in public tertiary hospitals in Brazil from June 2020 to March 2021. Clinical assessment and blood samples were performed at hospital admission, with post-hospital discharge remote visits. Hospitalized participants were followed-up until March 31, 2021. The outcomes were in-hospital mortality and incidence of rehospitalization or death after hospital discharge. Kaplan-Meier curves and Cox proportional-hazard models were performed. Findings: 1589 participants [54.5% male, age=62 (IQR 50-70) years; BMI=28.4 (IQR,24.9-32.9) Kg/m² and 51.9% with diabetes] were included. A total of 429 individuals [27.0% (95%CI,24.8-29.2)] died during hospitalization (median time 14 (IQR,9-24) days). Older age [vs<40 years; age=60-69 years-aHR=1.89 (95%CI,1.08-3.32); age=70-79 years-aHR=2.52 (95%CI,1.42-4.45); age≥80-aHR=2.90 (95%CI 1.54-5.47)]; noninvasive or mechanical ventilation at admission [vs facial-mask or none; aHR=1.69 (95%CI 1.30-2.19)]; SAPS-III score≥57 [vs<57; aHR=1.47 (95%CI 1.13-1.92)] and SOFA score≥10 [vs <10; aHR=1.51 (95%CI 1.08-2.10)] were independently associated with in-hospital mortality. A total of 65 individuals [6.7% (95%CI 5.3-8.4)] had a rehospitalization or death [rate=323 (95%CI 250-417) per 1000 person-years] in a median time of 52 (range 1-280) days post-hospital discharge. Age ≥ 60 years [vs <60, aHR=2.13 (95%CI 1.15-3.94)] and SAPS-III ≥57 at admission [vs <57, aHR=2.37 (95%CI 1.22-4.59)] were independently associated with rehospitalization or death after hospital discharge. Interpretation: High in-hospital mortality rates due to COVID-19 were observed and elderly people remained at high risk of rehospitalization and death after hospital discharge. Funding: Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) and Programa INOVA-FIOCRUZ.

Association of IL-6, IL-10 and CXCL10 serum concentrations with visceral Kaposi's sarcoma in people living with HIV/AIDS

Human gammaherpesvirus 8 (HHV-8) is the etiologic agent of Kaposi's sarcoma (KS), one of the most common cancers in people living with HIV/AIDS. It is believe that the course of both HIV and HHV-8 infection is associated with the imbalance of anti- and/or pro-inflammatory cytokines. Here, we evaluated the IL-6, TNF-α, IL-10, CCL2 and CXCL10 serum concentrations in HIV- and HIV/HHV-8 (without KS) individuals, and in patients with cutaneous or visceral AIDS-KS. Serum concentrations of IL-6, IL-10 and CXCL10 were significantly higher in the AIDS-KS group compared to HIV and HIV/HHV-8 individuals. Similarly, the concentrations of theses cytokines were higher in patients with visceral than in those with cutaneous AIDS-KS. The TNF-α concentration was significantly higher in the HIV group compared to HIV/HHV-8 (with and without KS) individuals, and CCL2 levels did not present significant difference among the groups. The HIV viral load was undetectable in all patients from the HIV and HIV/HHV-8 groups. On the other hand, in the AIDS-KS group, most patients had detectable HIV viral load. In this context, we believe that the cytokine levels in AIDS-KS may be result of a complex interaction between HIV, HHV-8 and immunity

Association of IL-6, IL-10 and CXCL10 serum concentrations with visceral Kaposi's sarcoma in people living with HIV/AIDS.

Human gammaherpesvirus 8 (HHV-8) is the etiologic agent of Kaposi's sarcoma (KS), one of the most common cancers in people living with HIV/AIDS. It is believe that the course of both HIV and HHV-8 infection is associated with the imbalance of anti- and/or pro-inflammatory cytokines. Here, we evaluated the IL-6, TNF-α, IL-10, CCL2 and CXCL10 serum concentrations in HIV- and HIV/HHV-8 (without KS) individuals, and in patients with cutaneous or visceral AIDS-KS. Serum concentrations of IL-6, IL-10 and CXCL10 were significantly higher in the AIDS-KS group compared to HIV and HIV/HHV-8 individuals. Similarly, the concentrations of theses cytokines were higher in patients with visceral than in those with cutaneous AIDS-KS. The TNF-α concentration was significantly higher in the HIV group compared to HIV/HHV-8 (with and without KS) individuals, and CCL2 levels did not present significant difference among the groups. The HIV viral load was undetectable in all patients from the HIV and HIV/HHV-8 groups. On the other hand, in the AIDS-KS group, most patients had detectable HIV viral load. In this context, we believe that the cytokine levels in AIDS-KS may be result of a complex interaction between HIV, HHV-8 and immunity.