ADAlessia D'Alessandro

Alessia D'Alessandro

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Alessia D'Alessandro has a total of 8 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Open Access

    Local and Systemic Endothelial Damage in Patients with CEAP C2 Chronic Venous Insufficiency: Role of Mesoglycan

    by Angelo Santoliquido, Claudia Carnuccio, Luca Santoro, Angela Di Giorgio, Alessia D'Alessandro, Francesca Romana Ponziani, Flavia Angelini, Marcello Izzo, Antonio Nesci

    Chronic venous disease (CVD) involves complex pathophysiological mechanisms, particularly an imbalance between matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), contributing to venous remodeling and varicosities. Elevated MMP-2 and MMP-9 levels are commonly found in tissues affected by venous ulcers. Inflammation plays a central role in CVD, with higher levels of pro-inflammatory markers present in varicose veins compared to healthy ones. Syndecans, key components of the endothelial glycocalyx, are involved in inflammatory responses. Alterations in the glycocalyx structure are associated with vascular damage in both venous and arterial diseases. This study aimed to investigate inflammatory changes in CVD patients, focusing on glycocalyx damage and the therapeutic role of mesoglycan, a glycosaminoglycan-based drug. A prospective, monocentric study included 23 patients with C2 clinical–etiological–anatomical–pathological (CEAP) CVD. Serum samples were collected before and after mesoglycan treatment. Results showed significantly elevated levels of VCAM-1, MMP-2, MMP-9, SDC-1, IL-6, and IL-8 in blood from varicose veins versus the systemic circulation. Patients received 50 mg of mesoglycan orally every 12 h for 90 days. After treatment, a notable reduction in inflammatory markers was observed. These results support the hypothesis that mesoglycan may alleviate both local and systemic inflammation, providing insights into new therapeutic strategies for CVD management.


  • Open Access

    Local and Systemic Endothelial Damage in Patients with CEAP C2 Chronic Venous Insufficiency: Role of Mesoglycan

    by Angelo Santoliquido, Claudia Carnuccio, Luca Santoro, Angela Di Giorgio, Alessia D'Alessandro, Francesca Romana Ponziani, Flavia Angelini, Marcello Izzo, Antonio Nesci

    Chronic venous disease (CVD) involves complex pathophysiological processes where the imbalance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) contributes to venous remodelling and varicosities. Elevated levels of MMP-2 and MMP-9 are notably observed in tissues affected by venous ulcers. Local inflammation is a key feature in CVD, with increased concentrations of pro-inflammatory markers in varicose veins compared to healthy veins. Syndecans, components of the endothelial glycocalyx, play critical roles in inflammation. Recent studies have shown that alterations in glycocalyx structure are indicative of vascular damage in both venous and arterial diseases. This study aims to explore the inflammatory alterations in CVD patients, focusing on glycocalyx damage and the potential therapeutic effects of mesoglycan, a compound used in CVD treatment. A prospective, monocentric study was conducted with 23 patients diagnosed with CVD of CEAP class C2. Serum samples were analyzed at baseline and after mesoglycan treatment. Results showed significantly higher levels of VCAM-1, MMP-2, MMP-9, SDC-1, IL-6, and IL-8 in blood from varicose veins compared to systemic circulation. After treatment with mesoglycan, there was a notable reduction in these inflammatory markers, indicating a positive therapeutic effect. These findings support the hypothesis that mesoglycan may help reduce local and systemic inflammation in CVD. This study contributes to a better understanding of the inflammatory mechanisms in CVD and the role of mesoglycan in modulating these processes, offering insights into potential therapeutic strategies for managing CVD.