5 articles
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.
Elevated or imbalanced levels of markers of oxidative stress and inflammation are often observed in various somatic pathologies and mental disorders, including schizophrenia.
This study aims to investigate the mechanisms of pathogenesis and the evidence supporting the use of niacin skin and oral tests in patients with schizophrenia.
A literature review was conducted on the specific reactions to the niacin skin or oral test in patients with schizophrenia, first-episode psychosis, and those at clinical high risk for psychosis (CHR-P). Evidence-based data up to and including 2024 were reviewed, with 48 literary sources selected.
An attenuated niacin-induced flush, coupled with low vitamin B3 levels, an imbalance in the Redox-Ratio and omega-3/omega-6 fatty acids, and elevated phospholipase A2 levels, are the main evidence-based findings associated with schizophrenia.
The niacin skin and oral tests in patients with schizophrenia and those at high risk for psychosis are characterized by an abnormal response to niacin. Additional markers may further validate positive test results for niacin.
Oral lichen planus is a chronic inflammatory disease of unknown etiology, characterized by recurrent lesions, presenting as reticular lesions, sometimes accompanied by atrophic, erosive, and/or ulcerative areas. Despite being one of the most common conditions affecting the oral mucosa, oral lichen planus remains an ailment with undefined etiology and unclear pathogenesis, imprecise management, and uncertain premalignant potential.
A narrative literature review study was conducted. A bibliographic search was carried out in databases such as PubMed, Hinari, SpringerLink, the National Center of Biotechnology Information, and Medline. Articles published from 1990 to 2023 were selected using various combinations of keywords: “oral lichen planus,” and “epidemiology,” “etiology,” “pathogenesis,” “symptoms,” “management,” “histopathology,” and “malignant transformation.” After processing the data from these databases, 475 full articles were found. The final bibliography comprised 50 relevant sources, considered representative of the materials published on the topic of this synthesis article.
Oral lichen planus is an inflammatory condition associated with T-cell-mediated immune dysfunction. Triggers include autoimmune responses to local antigens, microorganisms, and stress. The disease results from a complex interplay of host factors, lifestyle, and environmental factors leading to T-cell-mediated immune dysregulation. Diagnosis of oral lichen planus is based on clinical features (multiple, bilateral, symmetrically distributed lesions, occurring most commonly on the buccal mucosa, dorsal tongue surface, and gingiva), histopathological findings (predominantly lymphocytic band-like infiltrate in the lamina propria, presence of apoptotic cells in the basal cell layer, absence of epithelial dysplasia), and immune-related changes (deposition of fibrinogen along the basement membrane zone, presence of granular fluorescent deposits containing IgA, IgG, and IgM in colloid bodies).
Oral lichen planus is a chronic inflammatory condition mediated by T-cells in response to various extrinsic antigens, modified autoantigens, or superantigens, with periods of remission and relapse and the potential for malignant transformation. The etiology and pathogenesis of this condition are complex, diagnosis relies on clinical features, histopathological findings, and immunological data, patient treatment is symptomatic, and the potential for malignant transformation varies. Nevertheless, prospective studies with large sample sizes, adequate treatment duration, and long-term follow-up are needed.
Chronic pancreatitis (CP) is a common disease with a complex pathogenesis, characterized by difficulties in its diagnosis and treatment.
To determine the main pathogenetic links of clinical and morphological forms of CP, markers of disease progression, to develop a diagnostic algorithm and principles of treatment of patients.
210 patients with CP were examined, who were divided into 4 groups: I - obstructive, II - calcifying, III - fibrous-parenchymal, IV – CP, complicated by pseudocyst. Instrumental, functional, morphological, biochemical, immunological, microbiological methods were used. To study the main morphological and biological changes in the pancreas during the development of CP and to study the effectiveness of the proposed treatment, we conducted experimental studies on 45 laboratory white Wistar male rats weighing 180-230 g.
Imbalance of the immune system, oxidative stress, toxic-metabolic disorders, and diseases of the biliary system are important in the development of various forms of CP. However, there are differences in the severity of these changes. The most pronounced activity of fibrotic processes in the pancreas is typical for patients with a long course of the disease and in the presence of complications (pseudocyst). The most unfavorable course and prognosis are seen in the calcifying form of CP. The markers of CP progression are the value of the calcification coefficient of 0.5-1.0, the translocation of DNase I from the cytoplasm to the nucleus of the acinar cell, the activation of collagen formation, the increase in the level of fibrosis activators (TGF-β1, TNF-a), and the intensification of lipid peroxidation processes. An early marker of apoptosis is the translocation of DNase I from the cytoplasm to the nucleus of an acinar cell.
The developed diagnostic algorithm allows assessing the pathophysiological features of functional and organic disorders of the pancreas, predicting the course of the disease and choosing the optimal treatment. The proposed treatment of patients with CP effectively reduces the severity of pain and oxidative stress, normalizes the cytokine profile, improves the general condition and quality of life of patients.
Vitamin D plays an important role in maintaining musculoskeletal health. As the glomerular filtration rate decreases, vitamin D deficiency also occurs. The aim of this paper is to highlight the level of vitamin D depending on the stage of chronic kidney disease.
A structured search was performed in the PubMed, Scopus and HINARI databases, where the relevant articles have been taken into account, published in the last 20 years. The search terms used (in English) were: „vitamin D deficiency”, „pathogenesis of vitamin D”, ”the impact of vitamin D in chronic kidney disease”, „chronic kidney disease”.
Several studies have shown that the change in vitamin D levels is dependent to the decrease of glomerular filtration rate. The lowest serum vitamin D concentration was observed in stage 5 of chronic kidney disease. Vitamin D deficiency occurs due to a decrease in the number of nephrons and a decrease in the number of proximal tubular cells that absorb vitamin D (25 (OH) D) to be subsequently hydroxylated to its active form by 1α-hydroxylase.
Patients with vitamin D-deficient due to chronic kidney disease have an increased risk of decreased bone mineral density and multiple fractures.