: 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.
Introduction: Acute leukemia (AL) is the most common cancer of childhood. Recently, an important advance in the survival rate of these patients. The objective of this study was to assess whether there is an association between the blood levels of Renin Angiotensin System (RAS) molecules in children with acute AL and disease presentation and evolution in pediatric patients. Materials and Methods: This is a cross-sectional study carried out in a group of pediatric patients with AL. We measured blood levels of Angiotensin II (Ang II) and Angiotensin-(1-7) [Ang-(1-7)] by enzyme immunoassay. The Ang-(1-7)/Ang II ratio was calculated as a parameter of the balance between the alternative and classical axes of the RAS. Results: Eleven patients with AL and 20 healthy controls matched by sex and age were included. Patients with AL had significantly higher levels of both peptides when compared with healthy controls (p < 0.05). However, no significant difference was found in the Ang-(1-7)/Ang II ratio between the two groups. A strong and positive correlation was detected between Ang II and Ang-(1-7) levels in patients with AL (r = 0.853; p < 0.0001). There was no significant difference between the levels of Ang II and Ang-(1-7), as well as the Ang-(1-7)/Ang II ratio, the type of AL and clinical outcomes. Conclusion: Both Ang-(1-7) and Ang II seem to be involved in the physiopathology of AL and other molecules of the RAS could be potentially explored for the development of new therapeutic options for AL.
Introduction: Acute leukemia (AL) is the most common cancer of childhood. In recent years, there has been an important advance in the survival rate of these patients. The objective of this study was to assess whether there is an association between the blood levels of Renin Angiotensin System (RAS) molecules in children with acute AL and disease presentation and evolution in pediatric patients. Materials and Methods: This is a cross-sectional study carried out in a group of pediatric patients with AL. We measured blood levels of Angiotensin II (Ang II) and Angiotensin-(1-7) [Ang-(1-7)] by enzyme immunoassay. The Ang-(1-7)/Ang II ratio was calculated as a parameter of the balance between the alternative and classical axes of the RAS. Results: Eleven patients with AL and 20 healthy controls matched by sex and age were included. Patients with AL had significantly higher levels of both peptides when compared with healthy controls (p < 0.05). However, no significant difference was found in the Ang-(1-7)/Ang II ratio between the two groups. A strong and positive correlation was detected between Ang II and Ang-(1-7) levels in patients with AL (r = 0.853; p < 0.0001). There was no significant difference between the levels of Ang II and Ang-(1-7), as well as the Ang-(1-7)/Ang II ratio, the type of AL and clinical outcomes. Conclusion: Both Ang-(1-7) and Ang II seem to be involved in the physiopathology of AL and other molecules of the RAS could be potentially explored for the development of new therapeutic options for AL.
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