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2.
J Hosp Infect ; 113: 145-154, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-33852950

RESUMO

BACKGROUND: SARS-CoV-2 predisposes patients to secondary infections; however, a better understanding of the impact of coinfections on the outcome of hospitalized COVID-19 patients is still necessary. AIM: To analyse death risk due to coinfections in COVID-19 patients. METHODS: The odds of death of 212 severely ill COVID-19 patients were evaluated, with detailed focus on the risks for each pathogen, site of infection, comorbidities and length of hospitalization. FINDINGS: The mortality rate was 50.47%. Fungal and/or bacterial isolation occurred in 89 patients, of whom 83.14% died. Coinfected patients stayed hospitalized longer and had an increased odds of dying (odds ratio (OR): 13.45; R2 = 0.31). The risk of death was increased by bacterial (OR: 11.28) and fungal (OR: 5.97) coinfections, with increased levels of creatinine, leucocytes, urea and C-reactive protein. Coinfections increased the risk of death if patients suffered from cardiovascular disease (OR: 11.53), diabetes (OR: 6.00) or obesity (OR: 5.60) in comparison with patients with these comorbidities but without pathogen isolation. The increased risk of death was detected for coagulase-negative Staphylococcus (OR: 25.39), Candida non-albicans (OR: 11.12), S. aureus (OR: 10.72), Acinetobacter spp. (OR: 6.88), Pseudomonas spp. (OR: 4.77), and C. albicans (OR: 3.97). The high-risk sites of infection were blood, tracheal aspirate, and urine. Patients with coinfection undergoing invasive mechanical ventilation were 3.8 times more likely to die than those without positive cultures. CONCLUSION: Severe COVID-19 patients with secondary coinfections required longer hospitalization and had higher risk of death. The early diagnosis of coinfections is essential to identify high-risk patients and to determine the right interventions to reduce mortality.


Assuntos
Infecções Bacterianas/mortalidade , COVID-19/mortalidade , Coinfecção/mortalidade , Micoses/mortalidade , Adulto , Idoso , Infecções Bacterianas/complicações , COVID-19/complicações , Feminino , Humanos , Tempo de Internação , Masculino , Pessoa de Meia-Idade , Micoses/complicações , Respiração Artificial
3.
Tissue Antigens ; 70(4): 349-50, 2007 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-17767566

RESUMO

The human leukocyte antigen-G (HLA-G) gene plays an important role in pregnancy and is related to negative signals for natural killer cells and T lymphocytes. Herein a new HLA-G allele (HLA-G*010111) is described in the Brazilian population--one of the most heterogeneous populations in the world. The new allele is associated with the 14-bp deletion at exon 8 and is similar to the HLA-G*01010105 allele, except for a C to G transversion at codon 117 in exon 3.


Assuntos
Alelos , Antígenos HLA/genética , Antígenos de Histocompatibilidade Classe I/genética , Sequência de Bases , Brasil , Antígenos HLA-G , Humanos , Dados de Sequência Molecular , Polimorfismo de Nucleotídeo Único , População
4.
Tissue Antigens ; 67(4): 318-20, 2006 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-16634868

RESUMO

Tumor necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine mainly secreted by macrophages and T-cells that play a key role in the pathogenesis of many infectious and inflammatory diseases. The TNF gene cluster is located within the class-III region of the highly polymorphic major histocompatibility complex on human chromosome 6p21. A cluster of six multiallelic microsatellites has been identified in the TNF region, named TNF a-e. TNFb, TNFc, TNFd, and TNFe are (GA)n repeats, whereas TNFa and TNFf are (GT)n and (CA)n repeats, respectively. The TNFd microsatellite locus maps 8-10 kb centromeric to the TNF-alpha gene, downstream to the TNF-beta gene.


Assuntos
Alelos , Repetições de Microssatélites/genética , Família Multigênica/genética , Fator de Necrose Tumoral alfa/genética , Sequência de Bases , Cromossomos Humanos Par 6/genética , Feminino , Marcadores Genéticos , Humanos , Pessoa de Meia-Idade , Dados de Sequência Molecular , Escleroderma Sistêmico/genética , Fator de Necrose Tumoral alfa/classificação
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