2 articles
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.
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.
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.
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.
Neuropsychiatric lupus erythematosus is still a disease with a very challenging diagnostic process, lacking high specificity and sensitivity assays. Autoantibodies can change this perspective, and because of their pathogenetic involvement, can become a very powerful tool for early detection and disease activity tracking. However, their biomarker potential still needs further evaluation. In this study, we focused on the pathogenetic mechanisms of neuropsychiatric lupus erythematosus and the involvement of brain-specific and systemic autoantibodies in the development of neuropsychiatric manifestations.
Medical articles addressing the correlation of autoantibodies concentrations in serum and cerebrospinal fluid and their potential pathogenetic mechanism, were reviewed. More than 100 articles were identified from databases such as PubMed, ScienceDirect, Frontiers, and Wiley, using keywords such as “neuropsychiatric lupus erythematosus”, “autoantibodies”, “pathogenesis”, “biomarker” and “neuropsychiatric manifestations”. From these, 47 articles were selected for the current review.
Autoantibodies truly are indeed a tool in the diagnostic process of neuropsychiatric lupus erythematosus, and many researchers have obtained statistically valid correlations between their presence and specific neuropsychiatric manifestations. Variations in their concentration not only reflect the disease activity but also the fact that they are involved in its development through interactions with neuronal and vascular targets. Besides autoimmunity, brain-blood barrier dysfunction is also another key part of the pathogenetic mechanism, with markers of this injury also being useful in the diagnostic methodology. With future research, specific combinations of these markers can be linked to distinct clinical manifestations by creating multi-biomarker panels, a robust framework for diagnosing neuropsychiatric lupus erythematosus.
Neuropsychiatric lupus erythematosus remains a condition that highly challenging to diagnose and manage due to the heterogeneity of symptoms and the lack of standardized diagnostic tools. Autoantibodies, along with other markers of vascular and inflammatory injury can aid specialists in dealing with this disease, but further research is needed to validate these biomarkers in diverse patient populations and to standardize assays for clinical application to improve the early detection and management of NPSLE, ultimately enhancing patient outcomes and quality of life.