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Preocupação a ser incluída no radar. Coronavirus pode causar doença de Parkinson? Vem aí uma terceira onda da covid-19?
Será o caso de buscar novos estudos e implementar busca ativa de achados iniciais?
Coronavirus may cause 'wave' of neurological disease
Covid-19 can cause worrying neurological symptoms like a loss of smell and taste, but Australian scientists are warning the damage the virus causes to the brain may also lead to more serious conditions such as Parkinson's disease. They say there is a worrying precedent. Five years after the Spanish flu pandemic in the early 1900s, there was up to a three-fold increase in the incidence of Parkinson's disease. Study co-author Kevin Barnham from the Florey Institute of Neuroscience and Mental Health said he believed a similar “silent wave” of neurological illness would follow this pandemic. Findings published in the Journal of Parkinson's Disease describe a “two-hit hypothesis”: The brain gets inflamed from something like a virus, then something else comes along later causing more damage and eventually Parkinson's disease develops. “Evidence is already suggesting the triggers for Parkinson's disease are there with this virus,” Professor Barnham said.
“We can't put a number on it, but with 30 million people worldwide affected by this virus, even a small shift in the risk of getting Parkinson's would lead to many more people being diagnosed.” Florey Institute scientist and co-author of the paper, Leah Beauchamp, said there was an opportunity to get ready. “We weren't prepared the last time - more than 100 years ago. We have the tools and we can get ahead of this now,” she said. “The real question is: Are we prepared to take action now to avoid history repeating itself?”
Leah C Beauchamp and others. Parkinsonism as a Third Wave of the COVID-19 Pandemic?, Journal of Parkinson's Disease, published online pre-press, 22 September 2020. ABC News.
How covid-19 may be linked to parkinson'a disease?
Vejam abaixo o Abstract do artigo
Abstract. Since the initial reports of COVID-19 in December 2019, the world has been gripped by the disastrous acute respiratory disease caused by the SARS-CoV-2 virus. There are an ever-increasing number of reports of neurological symptoms in patients, from severe (encephalitis), to mild (hyposmia), suggesting the potential for neurotropism of SARS-CoV-2. This Perspective investigates the hypothesis that the reliance on self-reporting of hyposmia has resulted in an underestimation of neurological symptoms in COVID-19 patients. While the acute effect of the virus on the nervous system function is vastly overshadowed by the respiratory effects, we propose that it will be important to monitor convalescent individuals for potential long-term implications that may include neurodegenerative sequelae such as viral-associated parkinsonism. As it is possible to identify premorbid harbingers of Parkinson’s disease, we propose long-term screening of SARS-CoV-2 cases post-recovery for these expressions of neurodegenerative disease. An accurate understanding of the incidence of neurological complications in COVID-19 requires long-term monitoring for sequelae after remission and a strategized health policy to ensure healthcare systems all over the world are prepared for a third wave of the virus in the form of parkinsonism
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2 em 1: Covid-19 e Parkinson - Covid-19 grave e fibrose pulmonar
2 em 1: Outro estudo sobre covid-19 e doença de Parkinson e estudo que aponta possível fibrose pulmonar em sobreviventes de Covid-19 grave
Outubro 2, 2020
Study shows patients with Parkinson’s disease, COVID-19 have a high mortality risk
By Denise Baez
A study of almost 80,000 adults with coronavirus disease 2019 (COVID-19) showed that people with Parkinson’s disease have a 30% higher risk of dying from the virus compared with people without Parkinson’s.
The results, published in Movement Disorders, come from an analysis of the TriNetX COVID-19 research network -- a health research database that includes more than 50 million patients, mostly from the United States.
As of July 15, 2020, the database listed 79,048 adults with COVID-19, of whom 694 had Parkinson’s disease. The mortality rate among patients without Parkinson’s disease was 5.5% compared with 21.3% among patients with Parkinson’s disease (P< .001).
Patients without Parkinson’s disease were older (median age, 79 years vs 50 years) and most were male (60.2% vs 44.7%).
In logistic regression, which accounted for age, sex, and race, the risk of dying from COVID-19 was significantly elevated among patients with Parkinson’s disease (odds ratio [OR] = 1.27; 95% confidence interval [CI], 1.04-1.53; P = .016).
To assess residual confounders, the researchers matched (for age, sex, and race) 5 patients with COVID-19 but without Parkinson’s disease to each patient with Parkinson’s disease. This analysis found an even higher risk of death among patients with Parkinson’s disease (OR = 1.30; 95% CI, 1.13-1.49; P< .001).
“We further replicated the analysis with 1,000 random matchings, and found similar results, with the effect being statistically significant in all but 2 replications,” wrote Qiang Zhang, MD, University of Iowa Health Care, Iowa City, Iowa, and colleagues.
The researchers acknowledged the limitations of their study, including confounding regional factors that could increase mortality and the fact that the TriNetX database does not include information on comorbidities or recovery.
“Despite these limitations, our results indicate that it will be critical to develop effective strategies whereby healthcare providers can prevent the transmission of COVID-19 while providing neurological care to patients with Parkinson’s disease,” the authors wrote.
Reference: https://onlinelibrary.wiley.com/doi/10.1002/mds.28325
SOURCE: Movement Disorders
Potential indicators for pulmonary fibrosis in survivors of severe COVID-19
A study published in the Journal of Infection detailed potential indicators for pulmonary fibrosis in survivors of severe coronavirus disease 2019 (COVID-19).
Wenhui Huang, The First Affiliated Hospital, Guangdong, China, and colleagues performed an observational cohort study of 81 survivors who recovered from severe COVID-19 pneumonia to investigate the potential indicators for post-fibrosis. The median hospitalization was 26 days and all patients had at least three follow-up CT scans after discharge. Pulmonary fibrosis was diagnosed based on the extensive and persistent fibrotic changes, including parenchymal bands, irregular interfaces, reticular opacities, and traction bronchiectasis with or without honeycombing on the follow-up CT scans. Patients were divided into two groups: fibrosis (N = 42) and non-fibrosis (N = 39).
The study found that patients in the fibrosis group were older (63 vs 51 years) and disproportionately male (73.8% vs 48.7%). In addition, patients in the fibrosis group also had more underlying diseases - any disease (78% vs 41%), diabetes (31% vs 23%), hypertension (40% vs 23%), chronic pulmonary disease (21% vs 7%), chronic liver disease (19% vs 13%), cardiovascular and cerebrovascular diseases (29% vs 15%) - than those in the non-fibrosis group. Additionally, patients in the fibrosis group were more likely to have had a fever (90.5% vs 69.2%, P = 0.034), had longer prehospital duration of fever (median 7 vs 3 days, P = 0.001), and were more likely to experience shortness of breath (respiratory rate of 22 vs 20, P = 0.024) on admission.
Further, researchers observed that patients in the fibrosis group had higher leucocyte count (6.78 x 109/L vs 4.75 x 109/L, P = 0.001), neutrophil count (5.14 x 109/L vs 3.03 x 109/L, P < 0.001) as well as elevated levels of C-reactive protein (CRP) (35.62 vs 10.90 mg/L, P = 0.001) and D-dimer (1.41 vs 0.26 mg/L, P = 0.001). In addition, longitudinal analysis demonstrated that the levels of neutrophils, CRP, lactate dehydrogenase (LDH) and neutrophil to lymphocyte ratio (NLR) were markedly above the normal range within 4 weeks in the fibrosis group, while CRP “dramatically elevated” in the next 4 weeks, in contrast to other parameters which declined. Conversely, in the non-fibrosis group, CRP and LDH levels were elevated within 2 weeks, then “decreased sharply” to normal. Researchers also reported that lymphopenia and eosinopenia occurred in most patients on admission.
The study also found that more patients in the fibrosis group suffered from severe complications such as respiratory failure (59.5% vs 17.9%), secondary infections (23.8% vs 0%) and acute respiratory distress syndrome (23.8% vs 0%), resulting in higher rates of ICU admission (81.0% vs 28.2%), compared to those in the non-fibrosis group.
“The [study] reported a series of early indicators after tracing backwards to the features of disease progression between fibrosis and non-fibrosis groups. Other than common factors of advancing age, male and underlying diseases, that had been well described, it should be noted that the dynamic evolution of inflammatory markers within two weeks of hospitalization might point to fibrosis,” the researchers said.
“More importantly, the long prehospital duration of fever, the rapid and shallow breathing, and the absence of eosinophil on admission might be a combination of early indicators. All these can be readily obtained in clinical practice; thus, it holds great promise for large-scale use in a catastrophic pandemic,” they added.
“In our study, all survivors had varying degrees of fibrotic damage, ranging from subtle linear opacities to diffuse distribution of crazy-paving pattern; 52% (42/81) of patients showed extensive and unimproved fibrosis in a longitudinal analysis of CT findings. The radiographical abnormalities strongly correlated with long-term impairment of lung function. It remains unclear why certain individuals are able to recover from lung injury, whereas others develop into fibrotic damage,” the researchers wrote.
The researchers said that a large cohort of prospective and long-term analysis should be performed for more evidence and that patients with mild or moderate infection would be included in their further study as the current study only enrolled survivors of severe or critical COVID-19 with a high likelihood of lung injury.
Reference: https://www.journalofinfection.com/article/S0163-4453(20)30632-0/fulltext
SOURCE: Journal of Infection