: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection has been a global challenge. The complicated forms of the Coronavirus Disease 2019 (COVID-19) can evolve to multiple-organ failure, including several coagulopathies related to a sudden worsening of respiratory status. This article aimed to review studies about hematological and hemostatic laboratory disorders directly related to COVID-19 and to discuss how SARS-CoV-2 causes these abnormalities. The coagulation cascade model is associated with both COVID-19 and pulmonary involvement. Laboratory changes are relevant to evaluate the coagulation state - D-dimer, prothrombin time (PT), Activated Partial Thromboplastin Time (APTT), platelet count and fibrinogen. Pregnants and patients in Extracorporeal Membrane Oxygenation (ECMO) need special attention. Prophylactic interventions for COVID-19 coagulopathy should consider patients at risk for thrombotic events and potential contraindications. The mechanisms exerted by SARS-CoV-2 that impairs hemostatic balance include endothelial injury, inflammation, activation of the immune and complement systems. For diagnosis of coagulopathy, mainly Ddimer, but also PT, APTT and FDP, should be evaluated in COVID-19 patients. Intervention possibilities vary between lowmolecular-weight heparin (LMWH) and Unfractionated Heparin (UFH). Up to now, there is sufficient evidence that acutelyill patients with risk factors for coagulopathies will benefit from thrombophylaxis during hospitalization and post-discharge, but not all patients.

ObjectiveTo assess the diagnostic utility of biomarkers that could differentiate Chronic Traumatic Encephalopathy (CTE) from Alzheimer disease (AD).BackgroundCTE is a neurodegenerative disease associated with multiple head trauma. The diagnosis depends on neuropathologic findings postmortem, and patients can present cognitive and behavioral changes. These symptoms can usually be mistaken for other dementias, such as AD, leading to an underestimated frequency of CTE. Therefore, specific biomarkers can be useful for comprehending disease development, diagnosis and prognosis.Design/MethodsWe systematically searched the MEDLINE, Embase and Cochrane databases. We also searched the trial registries and reference lists of articles. We included studies that were relevant to the PICO question posed and analysed different biomarkers. We screened titles and abstracts and if they were pertinent, we assessed the full text and reported results narratively.ResultsTwenty-two studies were identified through database searching. One study was excluded due to duplicity among the databases. Twenty-one articles were assessed for eligibility and 6 were included in the qualitative synthesis. P-Tau and T-tau proteins were indicated as biomarkers of neurodegenerative diseases such as CTE and AD, but not from other tauopathies. Exosomal tau levels are higher in CTE patients than in AD patients, and it might be useful since it is very stable, crosses the blood–brain barrier and reflects their cellular origin. Pathophysiologic differences between CTE and AD are pointed out as a way to find specific biomarkers for CTE. The biomarkers associated with neuroaxonal damage (NFL), glial response with astroglial scarring (GFAP and sTREM2), and microvascular damage with disruption of the blood–brain barrier (cerebrospinal fluid/serum albumin ratio) are promising in that way.ConclusionsBiomarkers that arise from pathophysiologic processes distinct from the 2 diseases, appear to be promising. However, further well-designed studies are needed to assess the real utility of the biomarkers in differential diagnosis between CTE and AD.

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Background: The Renin-Angiotensin System (RAS) has been associated with several neuropathologies, including traumatic brain injury (TBI). Objectives: Assess the relationship between RAS and mild TBI within 24 hours after trauma. Design and setting: A case-control study developed by the Federal University of Minas Gerais and conducted at the Hospital João XXIII, Belo Horizonte, Minas Gerais, Brazil. Methods: Sociodemographic data and blood samples were collected from 52 individuals, of whom 28 suffered mild TBI in the 24 hours prior to collection and 24 healthy individuals made up the control group. The serum was used to measure the components of the RAS. Results: There were no significant sociodemographic differences between groups regarding to sex and age (p=0.782; p=0.077). Of the experimental group, 15 individuals reported loss of consciousness and 11 reported previous TBI. The experimental group showed significantly higher concentrations of angiotensin II (p=0.0234) and angiotensin-(1-7) (p=0.0225) and significantly lower concentrations of angiotensin converting enzyme (ACE) (p=0.0004) and ACE2 (p=0.0047). Conclusion: RAS seems to be involved in the pathophysiology of the hyperacute phase of mild TBI and the study of its components may contribute to identify prognostic biomarkers and new therapeutic targets for patients victims of TBI.

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