BACKGROUND:Psoriatic arthritis is a systemic, potentially severe condition associated with multiple comorbidities. It is characterized by peripheral and axial joint involvement, enthesitis, and association with various comorbidities. OBJECTIVE:This study aims to identify some of the determinants of the severity of psoriatic arthritis. We studied the prevalence and common pathogenic mechanisms of various comorbidities associated with PsA. METHODS:We studied 103 patients diagnosed with psoriatic arthritis. 69 met the inclusion criteria. We evaluated the disease activity index DAPSA, ESH, CRP, BMI, uric acid, cholesterol, triglycerides. Disease duration and type of joint involvement were also included. RESULTS:The patients in the studied group had an average age of 54.75 (sd±10.02) years and there were 36 (55.38%) women. Duration of the diseases 8.254 (sd±5.307) years and an average of DAPSA values of 20.58 (sd±8.522). CLINICAL MANIFESTATIONS:37 (56.92%) had peripheral damage; 6 (9.23%) had axial damage and 22 (33.85%) had mixed axial and peripheral damage. Inflammatory markers: ESR with an average serum value of 39.55 (sd±26.43) mm/h and average CRP values of 17.69mg/L (sd±28.71). The body mass index-an average value of 29.69Kg/m² (sd±5.979). Biological markers: uric acid with an average serum value of 9.832 mg/dl (sd±2.089), triglycerides 262.6 mg/dl (sd±41.58) and cholesterol 319.8mg/dl (sd±56.14). CONCLUSIONS:Serum levels of uric acid, cholesterol, triglycerides, ESR, and CRP influence psoriatic arthritis activity and response to treatment.

Background: Hyperuricemia is a prevalent comorbidity in psoriatic arthritis (PsA), yet its influence on the IL-1α/IL-17 cytokine balance remains unexplored. We aimed to characterize serum IL-1α and IL-17 profiles in PsA stratified by hyperuricemia status and to compare these with patients with hyperuricemia without psoriatic disease (HU). Methods: This cross-sectional study included 34 consecutively recruited PsA patients (19 hyperuricemic, 15 normouricemic) and 30 HU controls. Serum IL-1α and IL-17 were measured by ELISA. The PsA cohort was stratified by hyperuricemia status, cutaneous psoriasis, disease pattern, obesity grade, hypertension, sex, and enthesitis. Between-group comparisons used Mann-Whitney U and Kruskal-Wallis tests with Bonferroni-corrected post hoc analyses. Bivariate associations were assessed using Spearman's rank correlation. Results: Within the PsA cohort, hyperuricemic patients had significantly lower IL-17 than normouricemic patients (31.1 ± 15.7 vs. 49.5 ± 25.3 pg/mL; p = 0.01), while IL-1α did not differ significantly (37.3 ± 11.7 vs. 34.0 ± 8.19 pg/mL; p = 0.24). No correlation was observed between IL-1α and IL-17 (ρ = -0.05), indicating independent immunological axes. In the three-group comparison, IL-17 differed significantly across PsA-normouricemic, HU, and PsA-hyperuricemic subgroups (p = 0.022), whereas IL-1α was comparable across all three groups (p = 0.584). None of the traditional clinical classifications-disease pattern, cutaneous psoriasis, or sex-were significantly associated with either cytokine. Conclusions: Hyperuricemia was associated with significantly lower circulating IL-17 in PsA without a corresponding change in IL-1α levels, and this association appeared more pronounced within the inflammatory context of psoriatic disease than in hyperuricemia alone. These exploratory findings suggest that metabolic factors may play a role in defining the immunological profile of PsA and warrant prospective validation in larger cohorts. Owing to the cross-sectional design, this study does not allow inference of causal relationships between hyperuricemia and cytokine alterations.

Background/Objective: Psoriasis is a systemic inflammatory disease often associated with metabolic comorbidities, including hyperuricemia. While biological therapies effectively target inflammatory pathways, their specific impact on serum uric acid (SUA) levels remains debated. This study aimed to evaluate whether biological therapy, while reducing systemic inflammation, influences SUA levels in patients with moderate-to-severe plaque psoriasis. Methods: A prospective longitudinal cohort study was conducted involving 30 patients with moderate-to-severe plaque psoriasis. Patients received biological treatment (adalimumab, secukinumab or ustekinumab) and tsDMARDS (apremilast). Clinical severity was assessed using the Psoriasis Area and Severity Index (PASI). C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), SUA levels and other laboratory markers were measured at baseline and after 48 weeks of therapy. Results: Biological therapy led to a significant reduction in PASI scores (from 21.6 ± 10.7 at baseline to 0.4 ± 0.86 after 48 weeks of therapy, p < 0.001), and CRP decreased from a median of 5.75 mg/L at baseline to 3.55 mg/L, p < 0.001. ESR also declined from 26.2 ± 11.4 mm/h to 19.0 ± 8.06 mm/h, p < 0.001. However, no statistically significant change was observed in mean SUA levels 5.49 ± 1.55 vs. 5.55 ± 1.60 mg/dL; p = 0.758. Subgroup analysis revealed that SUA levels remained stable regardless of the specific biological agent used or the degree of clinical improvement. Conclusions: Our findings suggest that while biological therapy is highly effective in controlling skin and systemic inflammation in psoriasis, it does not modify SUA levels. These results imply that hyperuricemia in psoriasis may be driven by metabolic factors independent of the primary inflammatory pathways targeted by current biologics.

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease in which environmental factors modulate genetically determined immune dysregulation. Vitamin D has emerged as a plausible modifier of disease expression because its active metabolite signals through the vitamin D receptor on innate and adaptive immune cells and influences antigen presentation, cytokine balance, and lymphocyte differentiation. This narrative review synthesizes current evidence on vitamin D status and supplementation in SLE with attention to organ-specific domains. Observational studies consistently report high rates of hypovitaminosis D in SLE and associations with less favorable clinical profiles, including higher global and renal disease activity, adverse cardiometabolic features, greater infection vulnerability, and neuropsychiatric manifestations. Preclinical models demonstrate neuroprotective and barrier-stabilizing actions of vitamin D analogs, supporting biological plausibility. Interventional trials indicate that supplementation safely corrects deficiency and shows signals of benefit for selected outcomes (e.g., modest activity reductions or fatigue in specific contexts), although effects on interferon signatures, complement, and autoantibodies are heterogeneous and often limited. Overall, current evidence supports optimization of vitamin D status as a low-risk adjunct in comprehensive SLE care while highlighting the need for adequately powered, organ-focused randomized trials using standardized measurements and prespecified endpoints to define causality, therapeutic targets, and long-term safety.

BACKGROUND:Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by chronic inflammation and various clinical symptoms, with vitamin D deficiency suggested as a contributing factor. This study aimed to evaluate the effects of vitamin D supplementation on fatigue and disease activity in SLE patients. METHODS:Patients diagnosed based on EULAR/ACR 2019 criteria were divided into three groups: no supplementation, 4000 IU, and 8000 IU of vitamin D daily for six months. Clinical assessments included serum complement levels (C3 and C4), fatigue scores (Functional Assessment of Chronic Illness Therapy (FACIT)-Fatigue and Fatigue Severity Scale (FSS)), and disease activity (Safety of Estrogens in Lupus Erythematosus National Assessment-Systemic Lupus Erythematosus Disease Activity Index (SELENA-SLEDAI)). RESULTS:Results showed significant increases in vitamin D levels and serum complement levels in the supplementation groups. Serum complement levels and fatigue scores improved significantly in both the 4000 IU and 8000 IU groups. Additionally, there was a slight reduction in SELENA-SLEDAI scores in the treated groups, but without statistical significance. CONCLUSIONS:The findings suggest that vitamin D supplementation positively affects fatigue and some parameters of disease activity in SLE patients, though its overall impact on disease activity needs further investigation.

This review offers insight into the complex interplay between cytokines and vitamin D, with focus on its role in systemic lupus erythematosus (SLE) pathogenesis. It offers a helpful resource for researchers and clinicians seeking to better understand and treat SLE and related autoimmune conditions. The pathogenesis of SLE is complex and involves a wide range of cytokines, primarily of the Th2 type; these cytokines mediate hyperactivity in B lymphocytes and antibody production. Notably, vitamin D is found to suppress the activity of critical Th17-related cytokines like IL-23 and IL-6, which is pivotal for Th17 cell development and function. This ultimately leads to reduced IL-17 production, an increase in regulatory T lymphocytes, and subsequent secretion of IL-10. Supplementation with vitamin D is seen to have positive effects on SLE, leading to lower disease activity scores, decreased levels of autoantibodies, and a reduction of fatigue.

Background: Systemic sclerosis (SSc) is a complex connective tissue disease characterized by microangiopathy, immune dysregulation, and fibrosis. Early detection of microvascular abnormalities using nailfold videocapillaroscopy (NVC) is crucial in assessing disease progression and associated disease's involvement such as interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH).Objective: This study aims to explore the relationships correlation between NVC patterns, clinical manifestations, and systemic complications in SSc.Methods: We analyzed the data of 63 patients, predominantly female (95%), with a mean age of 49 years and an average disease duration of 42 months. Patients were categorized into early, active, and late patterns based on NVC findings. Clinical features, including digital ulcers (DU), ILD, and PAH, were assessed. Pearson correlation analyses were performed to evaluate the relationships between capillary loss, neoangiogenesis, ILD, and PAH.Results: The early pattern group (mean mRSS 2.36) exhibited minimal microvascular damage and systemic involvement, with no DUs. In the active pattern group (mean mRSS 10.40), 34.38% had diffuse cutaneous SSc (dcSSc), with 15.63% presenting DUs, 65.63% ILD, and 37.5% PAH. The late pattern group (mean mRSS 18.00) showed the most severe disease, with 80% having DUs, 70% dcSSc, 90% ILD, and 70% PAH. Pearson correlation analyses revealed strong correlations between capillary loss and ILD (r = 0.7255) and PAH (r = 0.6369). A moderate correlation was found between neoangiogenesis and PAH (r = 0.5592).Conclusion: The study demonstrates that progressive microvascular damage in SSc, as visualized by NVC, correlates strongly with the severity of systemic complications. Early detection of capillary loss and neoangiogenesis using NVC is critical for timely interventions, which could improve patient outcomes by mitigating the progression of ILD and PAH.

OBJECTIVES:The study has as main objective the evaluation of the potential roles of vitamin D, the neutrophil to lymphocyte ratio (NLR), and the systemic inflammation index (SII) as future biomarkers regarding the classification of flares in systemic lupus erythematosus (SLE). MATERIAL AND METHODS:Individuals diagnosed with SLE were encompassed in this observational study. The current applicable criteria, namely The European Alliance of Associations for Rheumatology (EULAR)/American College of Rheumatology (ACR) 2019 criteria had to be fulfilled. The participants underwent specific musculoskeletal examination, paraclinical investigations including complete blood count (CBC), determination of serum creatinine levels, as well as liver enzymes, and also the markers of inflammation. The fractions of the serum complement (C3 and C4) were also evaluated, together with serum vitamin D concentrations. Safety of Estrogens in Lupus National Assessment-Systemic Lupus Erythematosus Disease Activity Index (SELENA-SLEDAI) was required in order to analyze the research group's disease activity. RESULTS:NLR and SII demonstrated validity, having statistically significant correlations with SELENA-SLEDAI (p value less than 0.001). The ROC analysis proved a strong discriminative power for NLR (AUC=0.96) and SII (AUC=0.963) in predicting severe disease flares. Optimal cut-off values were 3.45 for NLR and 877,002.19 for SII. Serum vitamin D concentrations had a weak association with the SLEDAI score (p=0.048, r=0.213). CONCLUSIONS:NLR and SII can be considered reliable biomarkers for discriminating between the levels of disease activity in SLE individuals. Low serum levels of vitamin D may also influence disease severity, but require further validation.

This study aims to analyze the changes in dermal thickness in patients with systemic scleroderma (SSc) in comparison with normal skin and also compare clinical forms with diffuse and limited cutaneous involvement. The study group consisted of female patients diagnosed with SSc with a disease history not exceeding 5 years. The areas of interest for ultrasound examination included the proximal phalanx of the third finger, the second intermetacarpal space, and the extension surface of the lower third of the forearm. The study included 20 patients diagnosed with SSc and 14 controls. SSc patients were subdivided into two subgroups based on the clinical form. Compared to the control group, patients with SSc had higher mean measurements in all three skin areas, with statistically significant differences in the hand and forearm areas. Patients with diffuse SSc displayed, on average, higher skin thickness compared to limited SSc in all skin areas examined, with a statistically significant difference only in the forearm area. Based on disease manifestations, significant differences were observed only with regard to the presence of pulmonary hypertension in the diffuse SSc group. In conclusion, skin ultrasound is a useful and accessible imaging method for diagnosing and quantifying dermal fibrosis in systemic scleroderma.

OBJECTIVES:To quantify levels of two inflammation-related indexes, namely neutrophil-lymphocyte ratio (NLR) and systemic immune-inflammation index (SII) in systemic scleroderma patients and determine the association with clinical manifestations and features of heart ultrasound. METHODS:The study group consisted of 34 patients with diagnosis of systemic scleroderma which were admitted to the hospital during 2015-2019. Patient data included the presence and type of clinical manifestations of systemic scleroderma, chest imaging to screen for lung disease, heart ultrasound reports and the laboratory investigations needed to quantify inflammatory indexes. We analysed the levels of inflammatory indexes and compared results based on the prevalence of systemic manifestations. RESULTS:Higher serum levels of NLR and SII are associated with the presence of joint, lung and pericardial involvement. Statistical significance was observed only for NLR levels with regard to the presence of articular involvement and ILD. Low ejection fraction was also associated with higher levels of both inflammatory indexes, without statistical significance. CONCLUSION:Inflammatory indexes are cost-effective markers that reflect active disease manifestations of systemic scleroderma and can thus be a useful tool to include in the regular follow-up of patients in order to better inform organ-specific assessments.

In recent decades, researchers have investigated the bidirectional links between periodontal disease and systemic diseases, and the results have allowed the development of the concept of periodontal medicine. This concept incorporates and analyzes the mutually influential interactions that can occur between periodontitis and systemic diseases such as diabetes mellitus or cardiovascular diseases. Sjögren's syndrome (SS) is a chronic autoimmune disorder that targets the exocrine glands of the body, such as the lacrimal and salivary glands. The amount of saliva produced may gradually decrease with the progression of the disease, which can have an impact on the structures within the oral cavity. Although the reduction in saliva flow produces negative effects in the oral cavity, a direct association between Sjögren's syndrome and periodontal disease has not yet been demonstrated. Available studies on this topic have not identified significant differences in the periodontal status of patients with Sjögren's syndrome and control groups at the clinical and bacteriological levels. On the other hand, other studies on this topic consider that patients with periodontitis have a higher risk of developing Sjögren's syndrome than the general population. Therefore, the results remain inconclusive, highlighting the need for further complementary studies.

Psoriatic arthritis (PsA) is a heterogenous systemic inflammatory disorder that affects peripheral joints and skin, but also causes inflammation at entheseal sites, digits (dactylitis) and the axial skeleton. Despite considerable advances, our understanding of the pathogenesis and management of PsA is hampered by its complex clinical expression. We enrolled patients who met the ClASsification for Psoriatic Arthritis (CASPAR) criteria for PsA (n = 17), and healthy controls (n = 13). The lipid profile, C-reactive protein (CRP) and Dickkopf-related protein 1 (DKK-1) circulating levels were measured for all subjects. For the patients with PsA, (1) the erosive character of the articular disease was assessed by a musculoskeletal ultrasound and (2) the cardiovascular risk was evaluated using the Systematic Coronary Risk Evaluation (SCORE) chart and the ultrasound measurement of the carotid intima-media thickness. A higher titer of serum DKK-1 was associated with the presence of erosions (p < 0.005) and the cIMT correlated with DKK-1 levels in patients with PsA (r = 0.6356, p = 0.0061). Additionally, we observed a positive correlation between increased cIMT and CRP (r = 0.5186, p = 0.0329). Our results suggest that DKK-1 could be used as an early biomarker for the erosive character of the articular disease and for the assessment of the cardiovascular risk in PsA patients.

Background: Hyperuricemia is classically defined as serum uric acid (SUA) value higher than 6.8 mg/dL; between hyperuricemic patients, only 15-20% will develop gout. Our first goal was to find if there is a specificity of the "snowstorm" feature on ultrasound (US) for hyperuricemia. Moreover, we aimed to determine if there is a level of SUA from which the urates tend to appear in the synovial fluid, without generating a typical clinical gouty flare. Patients, Materials and Methods: We conducted a cross-sectional, transverse study, including 108 consecutive patients that displayed a set of clinical and imaging features, such as swollen knee and US proof for knee joint effusion. Results: Performing binary logistic regression, the relation between the explanatory variable (hyperechogenic spots) and the response variable (SUA) was demonstrated to be a significant one (p=0.005). The value of 0.397 for the statistical phi coefficient suggests a medium intensity association between the diagnosis of gout or asymptomatic hyperuricemia and whether the patients have hyperechogenic spots or not. We found the cut-off value for SUA equal to 4.815 mg/dL, regardless of gender, from which, the urate starts to precipitate. Values for men tend to be higher in comparison to the ones found for women (4.95 mg/dL vs. 3.9 mg/dL). Conclusions: The "snowstorm" aspect of the fluid might be the result of an increased level of SUA and more than this, the cut-off level for SUA to precipitate might be lower than the fore used values.

The objective of the cross-sectional study was to assess periodontal and implant health condition among individuals diagnosed with Sjogren's Syndrome (SS), taking into account the clinical circumstances associated with this patient population. The clinical parameters employed to evaluate the periodontal status of both natural teeth and implants included: periodontal probing depth (PPD) measured at six sites per tooth/implant, clinical attachment level (CAL), bleeding on probing index (BOP), plaque index (PLQ). Gingival crevicular fluid samples were collected for interleukin-16 level evaluation. After clinical and immunological assessment of the study and control groups, the data was centralized, compiled and submitted for statistical analysis. In all four types of assessed periodontal parameters, there were statistically significant differences between the SS patients with no dental implants and the other test (SSi) and control groups (Cni and Ci). Nevertheless, in SS patients with dental implants, plaque levels were similar to that of controls. In addition, other periodontal parameters (PPD, BOP and CAL) were similar in SS patients with dental implants and controls, with no statistically significant difference. The highest GCF IL-6 levels were found in SS patients with no dental implants, the differences to the other study and control groups being statistically significant. In patients with SS and dental implants, there were no statistically significant differences to the other groups. Individuals diagnosed with Sjogren's Syndrome (SS) exhibit a less favorable periodontal condition compared to controls without SS. Notably, SS patients who undergo dental implant procedures demonstrate an improvement in their periodontal status. This highlights the importance of proactive and ongoing dental and periodontal surveillance for SS patients, aiming to decrease the risk of developing periodontal diseases.

Complex regional pain syndrome (CRPS) is a complex condition characterized by chronic pain and various sensory, motor, and autonomic symptoms. It involves a complex interplay of mechanisms in the nervous system, including neuroinflammation, sensitization of pain pathways, and dysfunction of the sympathetic nervous system. Antioxidants may play a role in CRPS by helping to counteract oxidative stress, which is an imbalance between the production of reactive oxygen species (ROS) and the body's antioxidant defences. CRPS involves inflammation and tissue damage, which can lead to increased ROS production and oxidative stress. Our paper represents a preliminary study on various commercially available natural-based products regarding their antioxidant effect. Several natural products with antioxidant properties, such as vitamins C and E, polyphenols, flavonoids, and botanical extracts, have shown promise in preclinical studies for their potential to alleviate pain and reduce inflammation associated with CRPS. The potential use of natural-based products with antioxidant effects for mitigating CRPS symptoms is still an area of ongoing research and investigation, but nonetheless it holds promise.

The microbiota–gut–brain axis has garnered increasing attention in recent years for its role in various health conditions, including neuroinflammatory disorders like complex regional pain syndrome (CRPS). CRPS is a debilitating condition characterized by chronic neuropathic pain, and its etiology and pathophysiology remain elusive. Emerging research suggests that alterations in the gut microbiota composition and function could play a significant role in CRPS development and progression. Our paper explores the implications of microbiota in CRPS and the potential therapeutic role of boron (B). Studies have demonstrated that individuals with CRPS often exhibit dysbiosis, with imbalances in beneficial and pathogenic gut bacteria. Dysbiosis can lead to increased gut permeability and systemic inflammation, contributing to the chronic pain experienced in CRPS. B, an essential trace element, has shown promise in modulating the gut microbiome positively and exerting anti-inflammatory effects. Recent preclinical and clinical studies suggest that B supplementation may alleviate neuropathic pain and improve CRPS symptoms by restoring microbiota balance and reducing inflammation. Our review highlights the complex interplay between microbiota, inflammation, and neuropathic pain in CRPS and underscores the potential of B as a novel therapeutic approach to target the microbiota–gut–brain axis, offering hope for improved management of this challenging condition.