Est. 2014 · Chișinău, MoldovaPeer-Reviewed · Open Access · QuarterlyISSN 2345-1467 · e-ISSN 1857-4696
Peer-reviewed
Open access

Since MMXIV
MJHSMoldovan Journal of Health Sciences
Nicolae Testemițanu
State University of

Medicine & Pharmacy
MJHS
Keyword

hypercoagulability

1 article

Correlation between pathogenetic factors and vascular endothelial damage in patients with rheumatoid arthritis

Eugeniu Russu · Liliana Groppa · Lia Chișlari · Svetlana Agachi · Marius Semionov · Chiril Nartea · Iosif Leanca · Artemie Pastuhov
doi 10.52645/MJHS.2026.1.16pp. 112-119

Introduction

Systemic rheumatoid vasculitis accounts for 1 to 5% of complications seen in rheumatoid arthritis, while autopsy studies report an average of 23% incidence. This enormous difference in numbers emphasizes the rate of misdiagnosis or underdiagnosis of systemic rheumatoid vasculitis. It mainly affects people with a median age of 65 years. It is particularly noteworthy, as systemic rheumatoid vasculitis has a high mortality and relapse rate. Also, the multifactorial aetiology: cytokines/immune cells and other particles determines clinical complexity of this type of angiitis.

Materials and methods

A comprehensive literature search of articles published since 1996 was conducted using MEDLINE via PubMed and HINARI. The search included terms such as "rheumatoid vasculitis", "rheumatoid arthritis", and "endothelial dysfunction", focusing on mechanisms driving vascular damage. A total of 217 relevant sources were identified, including original studies, reviews, and book chapters. The study evaluated pathogenic factors like cytokines, immune complexes, and systemic inflammation, highlighting their roles in endothelial dysfunction and hypercoagulability.

Results

The main pathogenetic factors in systemic rheumatoid vasculitis were immune complexes, cytokines (IL-6/TNF-α and IL-17), immune and blood cells (CD20/TH17/Platelets) and others (microparticles, blood rheology modifications). Even though, taken separately, those factors appear to have little to no impact on vascular endothelium, their synergistic effect lead to significant endothelial damage.

Conclusions

To conclude, each disease has its own pathogenetic factors which determine the natural course of this pathology. Understanding these mechanisms plays an important role for clinicians helping them to diagnose and effective treatment. Taking into consideration the relationships between specific factors in rheumatoid angiitis, we can make more specific decisions for its diagnosis and treatment. We can also use the pathophysiology of systemic rheumatoid vasculitis as a foundation for developing prevention measures.