Introduction: Metabolic disorders are a public health issue because of the complications they cause, but they are also a major risk factor for the onset of gout. Aim: The current study set out to demonstrate clinically how the clinical-paraclinical evaluation methodology had advanced as well as to assess comorbidity in gout patients using diabetes mellitus (DM). We also wanted to examine the pancreatic dysfunction in gout patients of different ages (by assessing the glucose and glycolated Hb analyses). Materials and methods: Two hundred gout patients (mean age, men 60±8.0 years, women 63±9.0 years) were included in a descriptive, cross-sectional study. The diagnosis of gout was made according to the classification criteria for gout according to ACR and EULAR 2015. The raw data were analyzed using SPSS v. 26.0. Results: In the study, type 2 diabetes mellitus (DM2) was encountered with a comparable frequency among both middle-aged and elderly patients (33.8% and 41.8%, respectively, p=0.26). In only 15% of cases, DM2 preceded the development of gout (in 3% with the beginning and 12% with late onset), while the developmental age of the DM2 prior to gout was comparable (50.9±2.8 years in age group 1 and 55.1±6.9 years in age group 2). We found that elderly people experience gout much more frequently (up to 41%) when DM2 is present. However, DM2 is not considered a predictor of gout. Conclusions: In gout patients under the age of 59 inclusive, the mean age at diabetes onset is significantly lower than the age (37.49.6 years) at which diabetes develops in the general population. Early onset of diabetes is associated with early development of gout.

Introduction. 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. Material and methods. 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. Results. 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. Conclusions. 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.

Introduction: Psoriatic arthritis (PsA) is a chronic immune-mediated disease that extends beyond joint and skin involvement, being strongly associated with metabolic disturb ances and increased cardiovascular risk. Chronic inflammation, adipokine imbalance, and endothelial dysfunction contribute to accelerated atherosclerosis in this population. Aim: To assess the interrelationships between systemic inflammation, lipid metabolism, leptin levels, and subclinical atherosclerosis in PsA patients, with the goal of improving cardiovascular risk stratification and management. Materials and methods: A total of 256 PsA patients and 150 matched healthy controls were enrolled. Clinical evaluations included disease activity indices, BMI, and waist circumference. Biochemical assessments comprised lipid profile, leptin, and high-sensitivity C-reactive protein (hs-CRP). Carotid intima-media thickness (IMT) and plaque formation were evaluated via ultrasonography. Statistical comparisons were made using non-parametric and chi-square tests. Results: PsA patients exhibited significantly higher levels of total cholesterol (5.9 mmol/L vs. 5.0 mmol/L), triglycerides (1.2 mmol/L vs. 0.5 mmol/L), low-density lipoprotein cholesterol (4.0 mmol/L vs. 3.5 mmol/L), and atherogenic coefficient (3.5 vs. 2.6), with p-values 30 kg/m²), and leptin was elevated in 58% of PsA patients versus 8% of controls. Leptin levels correlated positively with hs-CRP (R=0.59) and BMI (R=0.75). Increased hs-CRP levels were associated with thicker IMT, more frequent plaque formation, and higher prevalence of coronary artery disease. Patients with hs-CRP >10 mg/L had the greatest cardiovascular burden. Conclusion: This study confirms that PsA is associated with significant pro-atherogenic lipid disturbances, obesity, elevated leptin levels, and subclinical atherosclerosis. The integration of lipid profile, leptin, and hs-CRP with vascular imaging offers a practical framework for early cardiovascular risk assessment. Multidisciplinary management, including metabolic and inflammatory targets, is essential for improving long-term outcomes in PsA patients.

Introduction. Axial spondylitis is a chronic inflammatory disease primarily affecting the axial skeleton but can also involve peripheral joints. Axial spondylitis is often associated with extra-articular manifestations, such as inflammatory bowel diseases, emphasizing the need for rigorous monitoring and personalized therapeutic approaches. The interactions between axial spondylitis and inflammatory bowel diseases fall under the concept of “immune-mediated inflammatory diseases”, sharing common pathogenetic mechanisms. This study analyzes the prevalence and characteristics of inflammatory bowel diseases in patients with axial spondylitis. Objective. The objective of this study was to describe the baseline characteristics of patients with axial spondylitis, evaluate the prevalence of inflammatory bowel diseases in this population, and identify correlations between the two conditions, contributing to a better understanding of their pathogenetic and clinical interactions. Material and methods. This prospective observational study included 257 axial spondylitis patients followed over two years. Patients were selected according to ASAS criteria for axial spondylitis and clinical guidelines for inflammatory bowel diseases. Analyses included clinical evaluations, laboratory tests, and imaging studies. Data were processed using SPSS v22.0. Continuous variables were expressed as mean ± standard deviation or median and interquartile range, and categorical variables as percentages. Correlations were assessed using Spearman’s coefficient, with results considered significant at p<0.05. Results. Among the 257 patients included (168 men and 89 women, mean age 48.2 ± 13.1 years), 13.2% were recently diagnosed with axial spondylitis. Of these, 5.1% had inflammatory bowel diseases, distributed as follows: Crohn’s disease (3.1%), ulcerative colitis (1.2%), and indeterminate colitis (0.8%). In 53.8% of cases, the diagnosis of inflammatory bowel diseases preceded axial spondylitis. Multivariate analysis identified the absence of a family history of axial spondylitis as a significant risk factor for inflammatory bowel diseases (OR = 3.4; p = 0.025). The prevalence of inflammatory bowel diseases increased with axial spondylitis duration, reaching 6.5% in patients with disease progression over eight years. Conclusions. The study highlights a high prevalence of inflammatory bowel diseases in axial spondylitis patients, indicating the need for rigorous clinical monitoring. The absence of a family history of axial spondylitis was identified as a major risk factor for inflammatory bowel diseases. These findings emphasize the importance of a multidisciplinary clinical approach, including active screening for inflammatory bowel diseases and collaboration between rheumatologists and gastroenterologists, to improve patient prognosis and quality of life.

Introduction. Despite numerous fundamental clinical studies on the frequency, pathogenesis, clinical features of spondyloarthritis (SpA) in intestinal infectious diseases (IID) and intestinal damage in SpA, there are currently a number of unresolved problems, one of which is the problem of early diagnosis of arthropathies, especially associated with IID, which makes it necessary to continue the research in the scientific problem. Purpose of the study. Appreciation of the features of early manifestations of axial arthropathies in intestinal infectious diseases in order to improve their early diagnosis. Objectives of the study. Identification of clinical variants of axial arthropathies in patients with infectious intestinal diseases and instrumental description of axial lesion by conducting comparative analysis of clinical and laboratory parameters in these patients depending on the presence of axial arthropathies. Development of an algorithm for the early detection of axial spondyloarthritis in intestinal infectious diseases. Material and methods. During 2015-2021, 141 patients were analyzed retrospectively, out of which 50 patients with SpA from the Republican Clinical Hospital „Timofei Moşneaga” and 91 patients with infectious intestinal diseases from the gastro-enterology and hepatology departments of the Republican Clinical Hospital „Timofei Moşneaga”. Depending on the etiology of IID, subjects were divided into 2 groups: the first group included patients with Yersinia enterocolitica or Campylobacter jejuni (Y±C), the second with Salmonella enteritidis or Shigella flexneri (S±Sh). Results. In patients with IID, the following clinical variants of arthropathies have been identified: axial lesion (spinal inflammatory pain according to ASAS criteria (2009) in 42.9%, axial spondyloarthritis (axSpA) in 28.6%, AS in 15.4%), arthralgia - 38.5%, arthritis - 13.2%. Conventional radiography imaging and magnetic resonance imaging (MRI) of the sacroiliac joints (SI) increased the incidence of SpA from 6.6% (n = 6) to 28.6% (n = 26). Conclusions. In patients with IID, the following clinical variants of arthropathies have been identified: axial lesion (spinal inflammatory pain according to ASAS criteria (2009) in 42.9%, axSpA in 28.6%, ankylosing spondylitis in 15.4%), arthralgia – 38.5%, arthritis – 13.2%. Imaging in the form of conventional radiography and MRI of SI joints increased the incidence of SpA from 6.6% (n = 6) to 28.6% (n = 26). Axial arthropathies, arthralgia, arthritis, and uveitis are encountered more frequently. At the same time, the possibility of detecting axSpA is greater if arthritis, arthralgia, inflammatory back pain, uveitis is present. Patients with S±Sh have a higher chance of developing axSpA compared to patients with Y±C.

Introduction : Infections such as Chlamydia trachomatis and Yersinia enterocolitica are recognized triggers of reactive arthritis, but their role in chronic spondyloarthritis (SpA)—including ankylosing spondylitis (AS) and psoriatic arthritis (PsA)—remains incompletely defined. Aim : To evaluate the potential role of selected urogenital and enterocolitic infections in the onset and clinical evolution of AS and PsA. Materials and methods : This prospective observational study included 1202 patients (709 PsA, 493 AS) followed between 2019 and 2025. Clinical subtypes, disease activity, and imaging features were assessed alongside multiplex PCR and serological screening for C. trachomatis , Mycoplasma spp., Ureaplasma spp., and Y. enterocolitica . Comparisons were made between infection-triggered and idiopathic cases. Results : Infection was found in 6.2% of PsA and 8.1% of AS patients, which was slightly higher than the control group. Infection-triggered cases presented more often with acute onset, oligoarthritis, and peripheral joint involvement (notably in AS, p =0.002). Over time, PsA showed a shift from oligoarticular to polyarticular and axial forms; axial PsA increased from 2.1% to 21.1% in 2 years. Radiographic and treatment outcomes were comparable between groups. A minority of infection-triggered cases showed remission following antibiotic therapy. Conclusions : Urogenital and enterocolitic infections may precipitate SpA in a small subset of genetically susceptible individuals, particularly with HLA-B27. While long-term disease trajectories resemble idiopathic forms, early identification of infectious triggers may aid in personalized management strategies. Further research is needed to clarify their role in chronic disease propagation and treatment responsiveness.