scholarly journals POST-COVID-19 SYNDROME: CHARACTERIZATION OF A COHORT AND ASSOCIATION WITH ACUTE DISEASE SEVERITY

CHEST Journal ◽  
2021 ◽  
Vol 160 (4) ◽  
pp. A561
Author(s):  
Fernanda Oliveira Baptista da Silva ◽  
Bianca Peixoto ◽  
Marcos Bethlem ◽  
Nina VISCONTI ◽  
Michelle Cailleaux-Cezar ◽  
...  
2020 ◽  
Author(s):  
Mansoor Kodori ◽  
Zohreh Ghalavand ◽  
Abbas Yadegar ◽  
Gita Eslami ◽  
Masoumeh Azimirad ◽  
...  

Abstract Background: Clostridioides difficile is the main cause of healthcare-associated diarrhea worldwide. It is proposed that certain C. difficile toxinotypes with distinct pathogenicity locus (PaLoc) variants are associated with disease severity and outcomes. Additionally, few studies have described the common C. difficile toxinotypes, and also little is known about the tcdC variants in Iranian isolates. We characterized the toxinotypes and the tcdC genotypes from a collection of Iranian clinical C. difficile tcdA+B+ isolates with known ribotypes (RTs).Methods: Fifty C. difficile isolates with known RTs and carrying the tcdA and tcdB toxin genes were analyzed. Toxinotyping was carried out based on a PCR-RFLP analysis of a 19.6 kb region encompassing the PaLoc. Genetic diversity of the tcdC gene was determined by the sequencing of the gene.Results: Of the 50 C. difficile isolates investigated, five distinct toxinotypes were recognized. Toxinotypes 0 (33/50, 66%) and V (11/50, 22%) were the most frequently found. C. difficile isolates of the toxinotype 0 mostly belonged to RT 001 (12/33, 36.4%), whereas toxinotype V consisted of RT 126 (9/11, 81.8%). The tcdC sequencing showed six variants (35/50, 70%); tcdC-sc3 (24%), tcdC-A (22%), tcdC-sc9 (18%), tcdC-B (2%), tcdC-sc14 (2%), and tcdC-sc15 (2%). The remaining isolates were wild-types (15/50, 30%) in the tcdC gene.Conclusions: The present study demonstrates that the majority of clinical tcdA+B+ isolates of C. difficile frequently harbor tcdC genetic variants. We also found that the RT 001/ toxinotype 0 and the RT 126/ toxinotype V are the most common types among Iranian isolates. Further studies are needed to investigate the putative association of various tcdC genotypes with CDI severity and its recurrence.


2017 ◽  
Vol 152 (5) ◽  
pp. S990
Author(s):  
Christine Olbjørn ◽  
Milada C. Smastuen ◽  
Christina Casen ◽  
Torbjørn Lindahl ◽  
Britt Nakstad ◽  
...  

2021 ◽  
Author(s):  
Márlon Juliano Romero Aliberti ◽  
Claudia Szlejf ◽  
Claudia Kimie Suemoto ◽  
Murilo Bacchini Dias ◽  
Wilson Jacob-Filho ◽  
...  

OBJECTIVE: To investigate the association between frailty and death in hospitalized patients with COVID-19. METHODOLOGY: Prospective cohort study with patients ≥ 50 years hospitalized with COVID-19. Frailty was assessed using the Clinical Frailty Scale and the frailty index. Patients with a Clinical Frailty Scale score ≥ 5 were considered frail. The primary endpoints were mortality at 30 and 100 days after hospital admission. We used Cox proportional hazard models to investigate the association between frailty and mortality. We also explored whether frailty predicted different mortality levels among patients within strata of similar age and acute disease severity (Sequential Organ Failure Assessment score). RESULTS: A total of 1,830 patients were included (mean age 66 years; 58% men; 27% frail according to Clinical Frailty Scale score). The mortality risk at 30 days (adjusted hazard ratio = 1.7; 95% CI 1.4 - 2.1; p <0.001) and 100 days (adjusted hazard ratio = 1.7; 95% CI 1.4 - 2.1; p <0.001) was almost double for frail patients. The Clinical Frailty Scale also predicted different mortality levels among patients within strata of similar age and acute disease severity. Frailty intensified the effect of acute disease severity on the risk of death (p for interaction = 0.01). Of note, the Clinical Frailty Scale achieved outstanding accuracy to identify frailty according to the frailty index (area under the ROC curve = 0.94; 95% CI 0.93 - 0.95). CONCLUSIONS: Our results encourage the use of the Clinical Frailty Scale in association with measures of acute disease severity to determine prognosis and promote adequate resource allocation in hospitalized patients with COVID-19.


2021 ◽  
Author(s):  
Flávio Moura Rezende Filho ◽  
Neringa Jurkute ◽  
João Brainer Clares Andrade ◽  
Bruna Ferraço Marianelli ◽  
Juliana M. Ferraz Sallum ◽  
...  

2020 ◽  
Vol 6 (1) ◽  
pp. e389 ◽  
Author(s):  
Anisha Lynch-Godrei ◽  
Rashmi Kothary

Hereditary sensory and autonomic neuropathy (HSAN-VI) is a recessive genetic disorder that arises because of mutations in the human dystonin gene (DST, previously known as bullous pemphigoid antigen 1). Although initial characterization of HSAN-VI reported it as a sensory neuropathy that was lethal in infancy, we now know of a number of heterozygous mutations in DST that result in milder forms of the disease. Akin to what we observe in the mouse model dystonia musculorum (Dstdt), we believe that the heterogeneity of HSAN-VI can be attributed to a number of dystonin isoforms that the mutation affects. Lack of neuronal isoform dystonin-a2 is likely the universal determinant of HSAN-VI because all reported human cases are null for this isoform, as are all Dstdt mouse alleles. Compensatory mechanisms by intact dystonin-a isoforms also likely play a role in regulating disease severity, although we have yet to determine what specific effect dystonin-a1 and dystonin-a3 have on the pathogenesis of HSAN-VI.


PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e48939 ◽  
Author(s):  
Thomas Cloke ◽  
Markus Munder ◽  
Graham Taylor ◽  
Ingrid Müller ◽  
Pascale Kropf
Keyword(s):  

2011 ◽  
Vol 32 (3) ◽  
pp. 587-594 ◽  
Author(s):  
Yu-Shi Bao ◽  
Shi-Ping Na ◽  
Ping Zhang ◽  
Xi-Bei Jia ◽  
Rui-Chan Liu ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Michael Levraut ◽  
Véronique Bourg ◽  
Nicolas Capet ◽  
Adrien Delourme ◽  
Jérôme Honnorat ◽  
...  

IntroductionMost of our knowledge into autoimmune encephalitis (AE) comes from N-Methyl-D-Aspartate Receptor (NMDAR) encephalitis. The concentrations of cytokines in cerebrospinal fluid (CSF) including IL-17A have been found to be increased and associated with poor outcome. However, data on the cytokine concentration in CSF and its correlation with outcome is lacking for other types of AE.ObjectiveTo report the concentrations of CSF sIL-2R, IL-6, IL-8, IL-10 and IL-17A and to correlate it with acute disease severity and the 1-year outcome in non-NMDAR AE.MethodsWe measured the CSF concentration of each cytokine in 20 AE patients, and compared IL-6 and IL-17A concentrations with 13 patients with CNS demyelinating diseases and 20 non-inflammatory controls. Patients were &gt; 18yr and had at least 1-year clinical follow-up. Intracellular and NMDAR antibody (Ab) -mediated encephalitis were excluded. A mRS ≤ 2 was retained as a 1-year good outcome.ResultsThe IL-17A concentration in CSF was higher in AE patients than in both control groups (p&lt;0.01). No difference was observed in CSF concentration of IL-6 between groups. At disease onset, a high CSF IL-17A concentration correlated with a high modified Rankin Scale (p&lt;0.05), a high Clinical Assessment Scale for Autoimmune Encephalitis score (p&lt;0.001) and ICU admission (p&lt;0.01). There was no correlation between the concentration of all CSF cytokines and the 1-year clinical outcome.ConclusionOur results show that CSF IL-17A could be interesting to assess initial severity in non-NMDAR AE. Thus, CSF IL-17A could be an interesting therapeutic target and be useful to assess early selective immunosuppressive therapy.


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