Publications by authors named "Anna Leticia Soares"

Asymptomatic diabetic patients with different degrees of macrovascular complications can present different hemostatic changes. At this study, plasminogen activator inhibitor-1 (PAI-1) and D-dimer were evaluated in 12 women without diabetes and 64 type 2 diabetic women. All patients were classified into 3 different categories according to the carotid intima-media thickness (IMT) assessed by Doppler: 25 with <1 mm (normal), 15 with >1 mm and without plaque (intermediate), and 24 with stenosis lower than 50% of the vessel lumen (plaque).

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This study aimed to investigate whether endothelial cells are damaged and to evaluate fibrinolytic system function in patients with type 2 diabetes. For this proposal, plasma levels of von Willebrand factor (an endothelial marker of injury), homocysteine (an inductor of endothelial injury), D-dimer (a marker of coagulation cascade activation) and plasminogen activator inhibitor-1 (a fibrinolysis marker) were measured in individuals with both type 2 diabetes and high blood pressure, with type 2 diabetes, with high blood pressure and in healthy control individuals. No significant differences among groups were observed for von Willebrand factor and homocysteine plasma levels.

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Synopsis of recent research by authors named "Anna Leticia Soares"

  • - Anna Leticia Soares' research primarily focuses on the interaction between type 2 diabetes and macrovascular complications, with an emphasis on hemostatic markers and endothelial damage in affected patients
  • - Significant findings highlight the variations in plasminogen activator inhibitor-1 (PAI-1) and D-dimer levels among diabetic women with different degrees of carotid intima-media thickness, suggesting that these markers can reflect the presence of macrovascular disease
  • - The studies also explore the integrity of endothelial cells and fibrinolytic function in type 2 diabetes, revealing no significant differences in certain plasma markers like von Willebrand factor and homocysteine across diabetic and control populations, indicating complex mechanisms at play in diabetic vascular complications