BACKGROUND:This report highlights a rare, catastrophic presentation of Systemic Lupus Erythematosus (SLE) manifesting as sudden cardiovascular collapse in a patient with no prior autoimmune history. The case is particularly novel due to the concurrent development of the Acute Motor Axonal Neuropathy (AMAN) variant of Guillain-Barré Syndrome (GBS) alongside multiorgan failure, mimicking septic and cardiogenic shock. CASE PRESENTATION:A 49-year-old woman suffered an out-of-hospital cardiac arrest following acute gastroenteritis, characterized by recurrent ventricular fibrillation and tachycardia. She rapidly developed multiorgan failure, including severe myocardial dysfunction (EF 29%), acute kidney injury, metabolic acidosis, and altered consciousness. While the initial presentation suggested sepsis, subsequent testing revealed positive antinuclear antibodies, lupus anticoagulant, and hypocomplementemia, meeting ACR/EULAR criteria for SLE. Electrophysiological studies for persistent weakness confirmed AMAN-type GBS. Following an aggressive multimodal immunotherapy regimen of corticosteroid pulses, Intravenous Immunoglobulin (IVIG), and rituximab, the patient achieved significant recovery of cardiac, renal, and neurological functions. CONCLUSIONS:This case demonstrates that SLE can present as a life-threatening "autoimmune storm" mimicking sepsis or primary heart failure. Early identification is vital in atypical critical illness, as aggressive immunotherapy can reverse even severe multiorgan dysfunction. Clinicians should consider autoimmune screening in cases of unexplained cardiac arrest and multiorgan failure to prevent diagnostic delays and improve outcomes.
INTRODUCTION:Malignancy is a significant comorbidity for patients with systemic scle-rosis (SSc). Data regarding the prevalence and risks of developing malignancy in SSc, particular-ly in the United Arab Emirates (UAE) population, are scarce. This study aims to investigate the proportion of benign and malignant tumors in the UAE's SSc patients. MATERIALS AND METHODS:SSc patients from the UAE Scleroderma Registry from April 2015 to April 2023 were characterized according to the presence of a tumor, whether benign or malig-nant. Descriptive statistics were utilized to examine the study's variables. RESULTS:Out of 133 patients, 33 (25%) had a history of a tumor. Benign and malignant tumors were reported in 54.5% and 42.4% of the cohort, respectively. The remaining 3.1% were tumors of unknown nature. Among the 133 patients, seven (21%) had genitourinary tumors, followed by 5 (15%) head and neck tumors, and 4 (12%) gastrointestinal tumors. The mean age of SSc diag-nosis was 38.9 ± 13.7 years. Among patients with tumors, there was SSc autoantibody positivity with topoisomerase I (Scl-70) (36%), anticentromere (ACA) (27%), and anti-polymerase III (ARA) (6%, p < 0.00001). IF-ANA was positive in 88% of patients with a predominantly centromere pattern (p < 0.05) and elevated titers ranging between 1:640 and 1:1280 (p < 0.05). Tumors were diagnosed a mean of 3.2 years before SSc diagnosis in some patients and a mean of 11 years after SSc diagnosis in others. DISCUSSION:Our findings reveal a distinctive malignancy profile characterized by a higher preva-lence of genitourinary, head, and neck, and gastrointestinal tumors compared to international co-horts, and an earlier average age of tumor onset highlighting unique regional characteristics. CONCLUSION:The study is the first to describe tumor burden in the UAE's SSc population and highlights the need to tailor malignancy screening and management.
Background: Acute myocarditis is an inflammatory disorder of the myocardium that can lead to severe cardiac dysfunction, arising from a broad spectrum of infectious and noninfec-tious etiologies. Ankylosing spondylitis, which primarily affects the axial skeleton, can involve the heart due to its systemic inflammatory nature, occasionally resulting in severe complications such as myocarditis. Case Presentation: We report an unusual case of acute myocarditis in a 49year-old male with an-kylosing spondylitis presenting with chest pain and systemic inflammatory symptoms. Diagnostic workup using the 2018 Lake Louise Criteria among cardiac MRI confirmed myocarditis in the absence of coronary artery disease or infectious etiology. The patient also demonstrated extra-articular manifestations with pulmonary and ocular involvement, consistent with an active anky-losing spondylitis flare. Management combined beta blockers, physical activity restriction, and re-introduction of anti-TNF alpha therapy, leading to both clinical and biological improvement. Conclusion: Acute myocarditis represents a rare yet severe cardiac manifestation of ankylosing spondylitis, requiring a high clinical suspicion to prevent heart failure and dilated cardiomyopathy.
INTRODUCTION:To perform a two-sample Mendelian randomization (MR) analysis to explore the potential causal relationship between polymyalgia rheumatica (PMR) and hypothyroidism. METHODS:Genome-wide association study (GWAS) data for PMR and hypothyroidism were obtained from publicly available databases. The inverse variance weighted (IVW) method was primarily used to evaluate the potential causal effect of PMR-related traits on the risk of hypothyroidism. To assess the robustness of the findings, additional methods, including the weighted median (WME), MR-Egger (ME), simple mode (SM), and weighted mode (WM), were employed. Sensitivity analyses were performed using the MR-PRESSO method and Cochran's Q test to detect potential heterogeneity and horizontal pleiotropy. Furthermore, a reverse MR analysis was performed to investigate the possibility of reverse causality. RESULTS:IVW analysis demonstrated a significant causal relationship between PMR and hypothyroidism (OR=1.373, 95%CI:1.287-1.465, P=5.84×10⁻²²). In contrast, ME produced a non-significant result (OR=0.880, 95%CI:0.602-1.286, P=0.577). WME supported IVW findings (OR=1.373, 95%CI:1.280-1.480, P=8.97×10⁻¹⁸), as did WM (OR=1.410, 95%CI:1.243-1.599, P=0.013) and the SM (OR=1.398, 95%CI:1.240-1.575, P=0.012). Collectively, these findings provide evidence supporting a causal effect of PMR on the risk of hypothyroidism. Reverse MR analysis using the IVW method also indicated a significant causal association (OR=1.195, 95%CI:1.135-1.258, P=9.35×10-12). However, both ME regression and IVW heterogeneity tests showed evidence of heterogeneity (P=3.16×10⁻³⁸; P=4.11×10⁻³⁸). The ME analysis revealed no evidence of horizontal pleiotropy (P=0.615). DISCUSSION:A study suggested that hypothyroidism-induced myopathic changes may mimic or exacerbate PMR symptoms, potentially leading to misdiagnosis or overtreatment with corticosteroids. Importantly, recurrence of PMR symptoms has been observed after thyroid hormone replacement, even in the presence of normalized thyroid function. These findings underscore a potential bidirectional relationship between PMR and hypothyroidism. In addition, some researchers held that HLA-B8 and DR3 may be a significant indicator to assess the association between these diseases; however, some observations suggest that it may not serve as a specific risk marker for PMR or its complications. CONCLUSION:PMR is closely associated with the development of hypothyroidism; the risk of hypothyroidism increases as PMR progresses; on the other hand, advancing hypothyroidism may also raise the likelihood of developing PMR.
INTRODUCTION:Systemic sclerosis (SSc) is a severe autoimmune disease marked by immune dysregulation and progressive fibrosis, yet reliable blood biomarkers remain limited. Ferroptosis, an iron‑dependent lipid peroxidation-driven cell death pathway, links iron/redox imbalance to inflammation and fibrotic remodeling, but its role in SSc is poorly defined. To profile Ferroptosis‑Related Genes (FRGs) in Peripheral Blood Mononuclear Cells (PBMCs) from SSc patients and assess their clinical significance. METHODS:Transcriptional profiles from four SSc patients and six Healthy Controls (HCs) were analyzed using the Arraystar Human LncRNA Microarray to identify Differentially Expressed Genes (DEGs). Ferroptosis-related DEGs in SSc (Ferr-DEGs) were obtained by intersecting DEGs with a ferroptosis database, and key Ferr-DEGs were prioritized using bioinformatic analyses. Immune cell infiltration was estimated using single-sample gene set enrichment analysis (ssGSEA). The expression of selected genes was validated by quantitative real-time polymerase chain reaction (RT-qPCR) in an expanded cohort (SSc = 36, HC = 36), and correlations with clinical indicators were assessed. Diagnostic performance was evaluated using ROC curves. RESULTS:Microarray analysis revealed 397 upregulated and 637 downregulated DEGs in the SSc group. Bioinformatic analyses identified eight ferroptosis-associated key genes in SSc: MAPK14, SRC, ATF3, CYBB, ACSL1, STK11, PLIN2, and NCF2. MAPK14, SRC, ATF3, and CYBB were significantly upregulated in SSc compared with HCs, whereas ACSL1 was downregulated. Notably, SRC showed good diagnostic performance for SSc, with an AUC of 0.891 (95% CI, 0.819-0.964). DISCUSSION:Given the emerging link between ferroptosis and autoimmune diseases, exploring its role in the pathogenesis of Systemic Sclerosis (SSc) could open new avenues for improving diagnostic and therapeutic strategies. CONCLUSIONS:Our findings indicate significant dysregulation of FRGs in PBMCs from SSc patients, suggesting their potential involvement in inflammation, immune cell infiltration, and fibrosis; notably, SRC may serve as a candidate diagnostic marker for SSc.
Background: Fibromyalgia is a chronic condition characterized by a wide range of clinical presentations, making it well-suited for an integrated medicine approach that includes complementary therapies. This study aimed to evaluate the effectiveness of an Integrated Medicine (IM) protocol in treating fibromyalgia patients. Methods: In this retrospective cohort study, we examined a group of 75 fibromyalgia patients treated with an IM protocol that included homeopathy, acupuncture, and nutritional advice. We assessed the protocol's effectiveness using data collected from the SF-12 (Quality of Life) questionnaire, the Edmonton Symptom Assessment System (ESAS), and the reduction in the use of conventional drugs. Results: The results demonstrated that the application of the IM protocol led to statistically significant improvements (p < 0.001) in pain and mobility symptoms. Additionally, there was a reduction in the use of conventional pharmacotherapy by 60% to 90%. Conclusion: The findings suggest that the IM protocol is effective in improving the quality of life for fibromyalgia patients and reducing their reliance on conventional drugs. The authors recommend expanding the case series and promoting the paradigm of Integrated Medicine, especially for diseases with multifactorial causes and comorbidities.
INTRODUCTION:Tocilizumab biosimilars offer an innovative therapeutic option for pa-tients with rheumatoid arthritis (RA); however, their safety and efficacy compared with the refer-ence product remain undefined. This systematic review and meta-analysis aim to synthesize data from all randomized clinical trials (RCTs) comparing the efficacy and safety of tocilizumab bio-similars with reference tocilizumab for RA treatment. METHODS:Following PRISMA guidelines, we searched PubMed, the Cochrane Library, and Web of Science up to March 2026. We included RCTs comparing biosimilars of tocilizumab to refer-ence tocilizumab in adult RA patients. Primary efficacy outcomes included ACR20 response and DAS28-ESR; secondary outcomes were ACR50/70, DAS28-CRP, and safety outcomes. RESULTS:Four Phase 3 double-blind RCTs enrolling 2160 patients were included in the analysis. No statistically significant differences were found between biosimilars and reference tocilizumab for ACR20, ACR50, or ACR70 DAS28-CRP responses at 12, 24 weeks, and approximately 1 year. Similarly, no difference was observed in DAS28-ESR change from baseline at 12 (MD, -0.07; P = 0.26) or 24 weeks (MD, -0.04; P = 0.60). However, at approximately 1 year (48-52 weeks), biosimilars showed a statistically significantly greater reduction in DAS28-ESR (MD -0.24, 95% CI: -0.44 to -0.05; P = 0.01) but did not reach the minimal clinically important differ-ence (MCID). Safety profiles were comparable, with no significant differences in safety out-comes. DISCUSSION:Our results indicate that tocilizumab biosimilars are therapeutically equivalent to the reference product in terms of clinical response and safety. However, a primary limitation of this meta-analysis is the small number of included RCTs. Future research should prioritize long-term surveillance and cost-effectiveness analysis in diverse settings to facilitate widespread clinical adoption and ensure sustained patient safety. CONCLUSION:Our meta-analysis shows that tocilizumab biosimilars have efficacy and safety pro-files equivalent to those of reference tocilizumab for the treatment of RA. These findings support the use of biosimilars as an effective therapeutic alternative.
INTRODUCTION:Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation and progressive destruction of cartilage and bones. In the world, RA affects 0.2-1.2% of the population, and the highest percentage of those affected is women. Depression has been identified as a comorbid condition of RA. This condition tends to increase pain as well as the intensity of RA. The objective of this study is to systematically analyse the prevalence rates, risk factors, and effects of depression among RA patients and establish the knowledge gaps that should inform improved comprehensive management. METHODS:This systematic review adhered to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) protocol. Electronic databases PubMed, Google Scholar, and Scopus database from 2015 to 2025. Cross-sectional studies involving adults aged 18 years and above diagnosed with rheumatoid arthritis (RA) and assessed using validated measures of depression. Data analysis of the results was performed using SPSS version 26.0. A forest plot was generated through meta-analysis to calculate the pooled prevalence within the study population. Heterogeneity among studies was examined using the I2 statistic and the Cochran's Q test. The protocol for this systematic review and meta-analysis was registered with PROSPERO (International Prospective Register of Systematic Reviews) with registration no. CRD420261287407. RESULTS:Out of 9,950 initially identified records, only 19 studies were included. The pooled prevalence of depression was high and varied depending on the diagnostic instrument used and the age group considered. The highest prevalence was observed among the subjects aged 50-60 years. Higher detection rates were reported with the Hospital Anxiety and Depression Scale (HADS) and the Patient Health Questionnaire -9 (PHQ-9). Depression was found to be associated with greater disease activity, fatigue, pain, lower quality of life, and treatment non-adherence. DISCUSSION:This meta-analysis highlights that depression is a highly prevalent comorbid condition among RA patients, with a pooled prevalence of 39.31%. Substantial heterogeneity across studies (I2 = 96.9%) suggests that variation exists in diagnostic tools, population characteristics, and regional contexts. Higher prevalence rates were observed in Middle Eastern and South Asian populations; this might be influenced by socioeconomic factors, healthcare accessibility, and cultural stigma in mental health reporting. CONCLUSION:Depression has been found to have a high prevalence among RA patients across diverse populations. The interpretation is limited by the inclusion of cross-sectional studies and high heterogeneity. The findings support the routine depression screening and management in RA patients. Future research should investigate the development of RA in depression patients to understand the possible bidirectional relationship.
INTRODUCTION:Clinical evidence suggests the presence of comorbidity between Autoimmune diseases (ADs) and secondary Idiopathic thrombocytopenic purpura (ITP), whereas the underlying causal relationship remains to be established. This study employed Mendelian Randomization (MR) analysis to investigate potential causal relationships between multiple common ADs and the risk of ITP. METHODS:Using criteria of P<5×10-8 , P<5×10-6 , and F-statistic>10, and excluding single nucleotide polymorphisms (SNPs) with confounding, palindromic sequences, and linkage disequilibrium as instrumental variables (IVs). The primary analysis was conducted using the inverse-variance weighted (IVW) method, supplemented by MR-Egger regression, weighted median estimator (WME), simple mode, and weighted mode approaches to assess robustness. Multiple sensitivity analyses were conducted to assess the robustness of the findings. RESULTS:SNPs significantly associated with each autoimmune disease were identified as IVs, including 6 SNPs for systemic lupus erythematosus (SLE), 5 for rheumatoid arthritis (RA), 6 for ankylosing spondylitis (AS), 5 for Sjögren's syndrome (SS), 7 for polymyositis (PM), 13 for primary sclerosing cholangitis (PSC), 4 for primary biliary cirrhosis (PBC), 16 for psoriatic arthritis (PsA), and 25 for adult-onset Still's disease (AOSD). IVW analysis indicated no genetic association between SLE, RA, AS, PBC, PsA, or AOSD and ITP. Significant associations were observed for PM (OR=0.807, 95% CI=0.742-0.876, P=3.93×10⁻⁷), PSC (OR=0.831, 95% CI=0.742-0.933, P=0.002), and SS (OR=1.589, 95% CI=1.375-1.835, P=3.05×10⁻¹⁰). WME analysis yielded consistent results for PM, PSC, and SS. Most sensitivity analyses supported the robustness of these findings. DISCUSSION:This study preliminarily explored the genetic relationship between ADs and ITP, but it is subject to several limitations, such as the limited number of IVs. Larger-scale genome-wide association study (GWAS) datasets will be needed for further validation. CONCLUSIONS:MR analysis suggested that there might be no significant causal associations between SLE, RA, AS, PBC, PsA, or AOSD and ITP, whereas PM, PSC, and SS might potentially show causal associations with ITP.
INTRODUCTION/OBJECTIVE:Etanercept is a tumor necrosis factor inhibitor used widely for rheumatoid arthritis. Because patients respond differently, clinicians have increasingly explored whether measuring drug levels and antidrug antibodies could help guide treatment. This review brings together what is currently known about etanercept immunogenicity, serum concentrations, and the role of therapeutic drug monitoring, with a particular focus on practice in resource-limited settings such as Iraq. METHODS:Major databases were searched (January 2010-June 2025) for clinical trials, observational studies, and systematic reviews of adults with rheumatoid arthritis receiving originator or biosimilar etanercept that reported antidrug antibodies, serum levels, or outcomes related to monitoring. RESULTS:Across randomized and real-world studies, etanercept generally showed low immunogenicity, with reported antidrug antibodies mostly below 15% and neutralizing antibodies rarely detected. Serum levels varied considerably between patients, and no robust therapeutic range could be defined. In most studies, etanercept concentrations did not consistently predict clinical response, and originator and biosimilar products appeared similar in terms of effectiveness and safety. DISCUSSION:Overall, these findings suggest that immunogenicity is not a major reason for etanercept treatment failure and that routine therapeutic drug monitoring is unlikely to help most patients. However, the evidence is heterogeneous, and real-world data from low- and middleincome countries, including Iraq, are still limited. CONCLUSION:Current evidence supports etanercept and its biosimilars as low-immunogenic options for rheumatoid arthritis, where routine monitoring is usually unnecessary. A more practical strategy may be to reserve targeted testing for selected non-responders while strengthening pharmacovigilance and local real-world research.
INTRODUCTION:Data on Tocilizumab (TCZ) efficacy and safety among RA patients in the Middle East in clinical practice remains limited. We aimed to evaluate the safety and efficacy of TCZ, as monotherapy or in combination with disease-modifying antirheumatic drug (DMARDs), in patients with moderate to severe active RA. METHODS:A regional, multicenter, descriptive, and prospective study conducted among 62 adults with moderate to severe active RA (DAS-28 ≥3.2) initiating treatment with TCZ after inadequate response to ≥1 conventional DMARD. TCZ treatment was for 24 weeks with a follow-up period of 6 months after the last injection. RESULTS:Clinical improvement, as measured by the DAS-28 score, was observed in 83.0% at Week 12 compared to 96.3% at Week 48. Low disease activity was achieved in 61.9% of patients at Week 12 and 81.50% at Week 48. Remission was reported in 42.9% at Week 12 compared to 55.6% at Week 48. During the 24-week treatment, 24/62 (38.7%) patients experienced 47 adverse events (AEs), infections being the most common, with 11 serious AEs. DISCUSSION:Our results were similar to those reported from developed countries. The significant drop in mean DAS-28 score in RA patients treated with TCZ comes in line with data from the U-Act-Early and CAMERA-II trials. No specific safety concern was reported with an AE rate of 42%, similar to another open-label phase-4 study done in the Middle East. CONCLUSION:Short-course treatment with TCZ was effective and safe for patients with moderate to severe active RA with inadequate response to DMARDs.
BACKGROUND:Acquired factor X deficiency (AFXD) is considered a rare but clinically significant cause of coagulation disorders, predominantly associated with systemic AL amyloidosis. Autoimmune-mediated AFXD is very rare, and a clear, well-documented association with Sjögren's syndrome has not yet been reported. CASE PRESENTATION:A 60-year-old woman with hypertension presented with chest pain. Despite normal liver function and absence of monoclonal gammopathy, she was found to have significantly prolonged PT/INR and severe factor X deficiency (3%). During follow-up, she developed symptoms of dry eyes, and autoimmune serology was positive for ANA, anti-SSA, and anti-SSB, meeting the 2016 ACR/EULAR criteria for Sjögren's syndrome. After ruling out alternative causes, she was diagnosed with autoimmune-mediated AFXD. Despite the severe deficiency, she did not present with any significant bleeding symptoms. Prednisone treatment (1 mg/kg/day) led to partial biochemical improvement. CONCLUSION:This report describes the first known association between Sjögren's syndrome and AFXD. Furthermore, the case highlights the importance of considering autoimmune etiologies in cases of unexplained coagulopathy and demonstrates the disconnect between laboratory abnormalities and bleeding phenotypes.
Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent systemic inflammation that extends far beyond the joints, giving rise to a wide range of comorbidities, including metabolic disorders, neurodegenerative conditions, osteoporosis, and various malignancies. These complications not only accelerate disease progression but also profoundly impair patient quality of life and overall survival. Understanding the molecular mechanisms that connect RA with its comorbidities is therefore essential for advancing risk prediction, enabling early diagnosis, and developing personalized therapeutic strategies. Traditional observational studies have provided valuable epidemiological evidence, yet they are frequently hampered by confounding variables and reverse causation. In recent years, rapid progress in computational methodologies has transformed RA research, offering more precise and unbiased approaches to dissect disease mechanisms. Large-scale retrospective analyses strengthen statistical associations, whereas bioinformatics pipelines and machine learning algorithms contribute to biomarker discovery, disease classification, and risk stratification. Mendelian Randomization has emerged as a powerful genetic tool for identifying causal relationships between RA and its comorbidities by employing genetic variants as instrumental variables. Furthermore, the integration of multi-omics layers-including genomics, transcriptomics, proteomics, and epigenomics-has greatly expanded insights into shared pathogenic pathways and unveiled promising therapeutic targets. Artificial intelligence-driven predictive models further enhance disease risk estimation and enable patient stratification based on molecular signatures, paving the way toward precision medicine in RA management. Collectively, this review highlights recent computational advances, underscoring their role in refining predictive models, elucidating mechanistic links between RA and comorbidities, and guiding the development of targeted therapeutic interventions to improve long-term patient outcomes.
INTRODUCTION:Methotrexate (MTX) is a cornerstone therapy for rheumatoid arthritis (RA), yet its hematological toxicity remains a significant clinical concern. This systematic review synthesizes evidence on MTX-induced hematological side effects to inform safer management. METHODS:A comprehensive search of Medline/PubMed (1991 to 2024), SCOPUS (1995 to 2024), and the Cochrane Library identified 108 studies reporting hematological adverse events associated with MTX in RA patients. Search terms included "RA," "MTX," and "hematologic side effects". Exclusion criteria included the use of biologics or other DMARDs, other rheumatic diseases, and studies focusing on non-hematological side effects. RESULTS:Hematological disorders represent the second most prevalent adverse outcome following gastroenterological disorders. The side effects often include complications such as leukopenia, thrombocytopenia, megaloblastic anemia, and pancytopenia. Risk factors were consistently identified across studies and include renal failure, advanced age, hypoalbuminemia, folate deficiency, dosing errors, and concomitant use of medications. Pancytopenia emerges as a potentially fatal complication, requiring careful monitoring and timely intervention with folinic acid (leucovorin). DISCUSSION:Low-dose MTX, though effective for RA, can lead to significant hematologic side effects such as anemia, leukopenia, thrombocytopenia, and pancytopenia, with reported incidence rates of 2.4-5.6%, exceeding earlier estimates. Dosage errors by patients or healthcare providers demonstrate the potential for fatal outcomes. Risk factors include renal impairment, hypoalbuminemia, infections, advanced age, and inadequate folic acid supplementation. Side effects typically resolve after discontinuation, and MTX can be safely resumed under appropriate monitoring and dose adjustment protocols. CONCLUSION:Our study summarizes evidence indicating that hematological disorders are commonly reported adverse events following gastroenterological disorders. Pancytopenia represents a potentially fatal complication requiring careful monitoring and timely intervention. This work provides an integrative clinical synthesis of evidence across diverse study designs to inform risk stratification and clinical management.
Osteoarthritis (OA) is a chronic and progressive joint disease involving the articular cartilage, synovium, subchondral bone, and ligaments, ultimately leading to pain, dysfunction, and, in advanced stages, joint destruction. Several factors contribute to the development and progression of OA, including genetic predisposition, biomechanical stress, metabolic imbalance, and chronic low-grade inflammation. Recently, a novel factor has emerged: the gut microbiome. Gut dysbiosis, defined as an alteration in gut microbiota homeostasis, can disrupt immune, metabolic, and inflammatory pathways, promoting systemic inflammation and accelerating degenerative changes in joint tissues. Conversely, restoration of a balanced gut microbiota may play a protective role and represent a promising avenue for innovative therapeutic strategies. The aim of this review is to analyse the relationship between gut dysbiosis and osteoarthritis, and to discuss potential therapeutic approaches targeting the microbiome to prevent disease progression.
INTRODUCTION:Gout, a highly serious inflammatory disease that is caused by monosodium urate crystals, is becoming an increasingly significant health concern. Artificial Intelligence and multi-omics-based research have made significant gains for the early detection and prevention of gout based on diverse approaches. This review intends to summarize current advances in forecasting gout susceptibility and gout-related symptoms, evaluate the predictive efficacy of different features, and ascertain which clinical and omics characteristics are most effective in these prediction models. METHODS:We explored the PubMed database after 2010 using keywords such as "gout", "predictive model", "risk prediction", and "machine learning", and confined our search to Englishlanguage articles. The original peer-reviewed research articles that developed gout models were selected. Research that was not original or lacked internal validation was excluded. RESULTS:Clinical features, genomics, microbiomics, radiomics, and metabolomics have been utilized to construct models related to gout and have demonstrated excellent predictive performance. Multisource data prediction models usually exhibit better effectiveness. DISCUSSION:Gout-oriented models performed excellently in predictive performance but present limitations in certain clinical and omics domains. However, if they are to affect actual patient care, they must overcome some external confirmation roadblocks and the fiscal and practical implications they will face ahead of time. CONCLUSION:This review indicates that clinical and multi-omics models of gout are significant instruments for clinical decision-making. The models constructed in these studies may be crucial for the treatment of gout and its practical benefits.
INTRODUCTION:Inequities in systemic lupus erythematosus (SLE) care affect outcomes (i.e., flares, damage, mortality), interventions (referrals, advanced therapies), and populations (gender, race/ethnicity, and geographic region). This systematic review highlights themes related to access to care for SLE patients and explores potential solutions to address these disparities. METHODS:In adherence to PRISMA guidelines, we conducted a systematic review of the literature. We searched for articles published in PubMed, Scopus, Web of Science, Cochrane Library, and EBSCO. Publications related to economic burden, barriers and facilitators to access, and potential solutions were included. RESULTS:A total of 77 articles were identified. Five critical issues concerning access to SLE care were revealed from the literature: (1) economic burden, (2) barriers and facilitators to access, (3) utilization, (4) adherence, and (5) possible solutions to improve healthcare access. DISCUSSION:The usual barriers and facilitators involved several social factors related to health (i.e., transportation, insurance, and limited access to mental health services, among others). Utilization of SLE care is influenced by socioeconomic status (SES), ethnicity, and education level. Factors like low education, low SES, rural residency, and depressive symptom adherence contribute to nonadherence. There were various proposals to improve access to SLE care, including peer support, digital platforms (e.g., telemedicine), and community-based programs (such as PALS and WELL). CONCLUSIONS:The SLE care field highlights the inequalities that impact marginalized communities. Emphasizing community-based programs, addressing social determinants of health, acknowledging social exclusion, and adopting digital platforms can help reduce healthcare inequity.
BACKGROUND:It is becoming increasingly recognized that rheumatologic diseases and sensorineural hearing loss (SNHL) are linked. These autoimmune disorders can affect the auditory system through both disease-related immune dysregulation and medication-induced ototoxicity. The latest findings on auditory involvement in patients with autoimmune rheumatologic conditions are summarized in this review. METHODS:This narrative review was conducted using PubMed, focusing on articles published in English between 2010 and 2024. Clinical, experimental, and epidemiological studies describing hearing outcomes in autoimmune conditions were included. MeSH and keywords related to autoimmune diseases, SNHL, auditory dysfunction, and cochlear implantation were used. RESULTS:Autoimmune-mediated SNHL results from immune complex deposition, vasculitis, antibody- mediated cytotoxicity, and inflammatory injury to cochlear structures. Rheumatoid arthritis, systemic lupus erythematosus, primary Sjögren's syndrome, vasculitis, juvenile idiopathic arthritis, IgG4-related disease, and Behçet's disease all demonstrate variable yet significant auditory involvement. Commonly used medications for these diseases, such as calcineurin inhibitors, methotrexate, cyclophosphamide, and antimalarials, may also cause ototoxicity. Cochlear implantation offers effective rehabilitation for severe or refractory SNHL. However, autoimmune- related cochlear fibrosis or ossification may limit outcomes, highlighting the need for prompt diagnosis. CONCLUSION:Hearing is affected in patients with rheumatologic disease and those using immunosuppressants as treatment. Routine audiologic monitoring, early identification of auditory symptoms, and personalized therapeutic planning are essential. Further prospective research is needed to clarify the mechanisms and optimize treatment protocols for autoimmune-associated hearing loss.
INTRODUCTION:Carpal Tunnel Syndrome (CTS) imposes significant occupational and economic burdens, yet data on postoperative work outcomes in Tunisia remain limited. METHODS:This retrospective cross-sectional study (2014-2022) analyzed 118 surgically managed CTS patients from Taher Sfar Mahdia University Hospital using the BCTQ-A (symptom/function severity) and WPAI-GH (work productivity) questionnaires. RESULTS:Key predictors for surgical intervention included bilateral involvement (Adj. OR=22.0, 95%CI:5.5-33.4), thumb opposition loss (p<0.001), and occupational factors like >8h workdays (p=0.04) and >20 years' seniority (p=0.05). Postoperatively, 68.3% required workstation adjustments, while 19.5% underwent job transfers. The cohort demonstrated substantial productivity impairment, with 69.4% overall work productivity loss (WPAI-GH), disproportionately affecting older (>40 years, p=0.02) and less-educated workers (p=0.02). Notably, 84.4% of patients required 30-day medical leave, aligning with global benchmarks (23.4-day average). Multivariate analysis identified nocturnal pain (p<0.001) and difficulty with bottle-opening (p<0.001) as key drivers of productivity decline. DISCUSSION:Operated CTS appears to have a more substantial impact on work quality, likely due to surgical complications and postoperative recovery challenges. This underscores the importance of early conservative management and preventive strategies. These findings underscore the need for early ergonomic interventions, particularly in high-risk sectors like garment manufacturing (81.7% of the cohort) and multidisciplinary prevention strategies combining workplace modifications, health education, and weight management. CONCLUSION:With CTS costing over $2B annually in the U.S. alone, proactive measures targeting long-tenured manual laborers are urgently needed to mitigate its socioeconomic impact.
Introduction The coexistence of psoriatic arthritis (PsA) and crystal-associated joint disease is an important diagnostic problem in clinical treatment. In patients with established PsA, the presence of new inflammatory responses may indicate disease activity or another pathological state, and thus necessitates differential diagnosis of disease processes and/or a diagnosis of a new disease process.Presentation We report the case of a 55-year-old man with chronic PsA who presented with acute monoarticular inflammation of the left wrist that was refractory to standard anti-inflammatory treatment. The discovery of newly observed calcific deposits in the left wrist, observed during sequential plain radiographic evaluation, raised suspicion of a crystal-associated inflammatory process. This discovery provided insight into the treatment regimen and clinical response.Conclusion This case illustrates the need to consider crystal-associated inflammation in patients with PsA who present with atypical or treatment-resistant joint pathology. Sequential imaging, especially plain radiography, might facilitate diagnostic clarification and prevent the inappropriate escalation of immunosuppressive therapy.
