Autoimmune Diseases Research Articles

Phytochemical characterization and anti-arthritic potential of green-synthesized CuO nanoparticles derived from the Bistorta amplexicaulis root extract

IntroductionRheumatoid arthritis is an autoimmune disease that mainly causes joint damage. The patient experiences loss of appetite, pain, fever, and fatigue. The present study was designed to phytochemically characterize and evaluate the anti-arthritic activity of green-synthesized copper oxide (CuO) nanoparticles (NPs) using the hydroalcoholic extract of Bistorta amplexicaulis roots in an adjuvant-induced arthritic rat model.Material and MethodsFor this purpose, crude powdered plant material was used for proximate analysis, and the plant extract was assessed for qualitative phytochemical analysis, mineral contents, and flavonoid and phenolic contents, as well as quantitative phytochemical analysis through reversed-phase high-performance liquid chromatography (RP-HPLC) and Fourier-transform infrared (FTIR) spectroscopy. The in vitro antioxidant activity of both extracts was determined by the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay. The biosynthesized CuO NPs from the Bistorta amplexicaulis extract showed anti-arthritic activity due to the presence of flavonoids and phenols, which showed a pain reliever effect by blocking the cyclo-oxygenase enzyme and has immune suppressant activity, thus securing the joint from destruction. The nanoparticles were characterized by zeta size, zeta potential, scanning electron microscopy (SEM), and FTIR spectroscopy. Forty-eight albino rats were divided randomly into six treatment groups.Results and DisscussionThe zeta size and zeta potential of the nanoparticles were 186.8 nm and −9.23 mV, respectively. Joint stiffness, spleen weight, thymus weight, and paw thickness showed a significant decrease after treatment with NPs. The hematological parameters such as red blood cells (RBCs) and hemoglobin showed a significant increase, while platelets and white blood cells (WBCs) showed a significant decrease in NP-treated groups. C-reactive protein (CRP), rheumatoid factor (RF), liver and kidney function biomarkers, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels showed a significant decrease at both low and high doses of green-synthesized CuO nanoparticles from the Bistorta amplexicaulis root extract. The final data were analyzed by one way and two-way analysis of variance (ANOVA) and Tukey’s multi-comparison test.ConclusionSo, from this study, it was concluded that both the plant root extract and green-synthesized CuO nanoparticles have anti-arthritic potential, but CuO NPs showed remarkable results.

Understanding and Using Animal Models of Hepatotoxicity.

Hepatotoxicity is a critical health hazard, primarily contributing to the increased incidence of deaths globally. The liver is one of the major and extremely vital organs of the human body. Autoimmune diseases, viruses, exposure to toxicants such as carcinogens, and changes in eating habits can all cause liver problems, among other things. Free radical generation, together with raised enzyme levels including SGOT, SGPT, and total bilirubin, are among the pathological changes set off by liver injury. Hepatotoxicity causes changes in cells, such as eosinophilic cytoplasm, nuclear pyknosis, fatty degeneration, too many liver lesions, and hepatic centrilobular necrosis due to lipid peroxidation. Researchers have used animal models to investigate liver diseases and toxicities. Drugs such as azathioprine, alcoholism, paracetamol intoxication, and anti-tuberculosis drugs are some of the most common causes of liver toxicity. These toxins cause calcium ions (Ca2+), reactive oxygen species (ROS), and inflammatory mediators to be released inside cells. This activates immune cells like NK cells, NKT cells, and Kupffer cells. These signaling pathways also play roles in hepatotoxicity. Due to its pathogenesis, no effective drug is currently available for hepatotoxicity due to a lack of understanding related to the signaling factors involved in it. The paper primarily examines different experimental models of hepatotoxicity, including non-invasive and invasive methods, as well as genetic models. As such, these models are crucial tools in advancing our understanding of hepatotoxicity, thus paving the way for new therapeutic interventions.

Reduced durability of hybrid immunity to SARS-CoV-2 in immunocompromised children

BackgroundIn endemic COVID-19, immunocompromised children are vulnerable until vaccinated but the optimal primary vaccination regime and need for booster doses remains uncertain.MethodsWe recruited 19 immunocompromised children (post-solid organ transplantation, have autoimmune disease or were on current or recent chemotherapy for acute lymphoblastic leukemia), and followed them from the start of primary vaccination with BNT162b2 mRNA SARS-CoV-2 until 1-year post-vaccination. We investigated the quality of vaccine immunogenicity, and longevity of hybrid immunity, in comparison to healthy children.ResultsImmunocompromised children failed to produce T cell and memory B cell (MBC) responses reaching thresholds of protection after 2 doses; a third dose however improved both responses. Initially robust hybrid immunity demonstrated significantly more decline in T cell and MBC responses in immunocompromised compared to healthy children, to levels below the protective threshold by month 12.DiscussionImmunocompromised children may benefit from a 3-dose primary vaccination regime, with yearly or twice-yearly booster doses for sustained immunity.

A Narrative Review of Molecular, Immunohistochemical and In-Situ Techniques in Dermatopathology

Skin disorders pose a significant health burden globally, affecting millions of individuals across diverse demographics. Advancements in molecular techniques have revolutionised our understanding of the underlying mechanisms of skin disorders, offering insights into their pathogenesis, diagnosis, and potential targeted treatment. Furthermore, the integration of molecular diagnostics into clinical practice has enhanced the accuracy of skin disorder diagnoses. Polymerase chain reaction (PCR), next-generation sequencing (NGS), and other molecular assays have allowed for the detection of infectious agents, assessment of genetic mutations, and profile gene expression patterns with unequalled precision. These techniques have proven instrumental in distinguishing between subtypes of skin cancers, aiding treatment strategies and prognostic assessments. Moreover, molecular profiling is increasingly guiding the selection of therapeutic agents, ensuring a personalised and effective approach to managing skin disorders. The application of PCR has revolutionised the field by enabling the identification of microbial DNA (i.e., Mycobacterium tuberculosis and Epstein-Barr Virus) in skin infections and detecting specific genetic mutations associated with dermatological disorders (e.g., BRAF). DNA sequencing technologies, such as next-generation sequencing, have facilitated the elucidation of genetic variations and mutations in skin diseases (i.e., bullous disorders), paving the way for personalised treatment approaches. Gene expression profiling techniques, such as microarrays and RNA sequencing, have provided insights into dysregulated pathways and molecular signatures associated with conditions ranging from inflammatory skin disorders to cutaneous malignancies. Immunohistochemistry and fluorescence in situ hybridization have proven invaluable in determining protein expression patterns and detecting chromosomal abnormalities, respectively, aiding in the characterization of skin lesions in conjunction with the molecular data. Proteomic studies have contributed to understanding the intricate protein networks involved in dermatological conditions (i.e., psoriasis), while epigenetic analyses have shed light on the role of epigenetic modifications in gene regulation within skin cancer (i.e., Malignant Melanoma). Together, these molecular techniques have laid the groundwork for targeted therapies and precision medicine in dermatology, with implications for improved diagnostics and treatment outcomes. This review focuses on the routinely employed molecular techniques within dermatopathology, with a focus on cutaneous malignancies, autoimmune diseases, infectious diseases, and neonatal screening which can be implemented in the diagnosis and contribute to improved patient care.

Statistical and Clustering Analysis of Safety Profiles of FDA-Approved Protein Kinase Inhibitors

Protein kinases are vital regulators in cell biology, modifying protein functions through phosphorylation. Protein kinase inhibitors (PKIs), which impede these kinases’ activities, have broadened their therapeutic scope from cancer treatment to autoimmune and viral diseases. Despite their clinical success, challenges such as drug resistance and tolerability of adverse events persist. This article used the Protein Kinase Inhibitor Database (PKIDB) and major pharmacovigilance databases to assess the adverse events (AEs) linked to FDA-approved protein kinase inhibitors. Methods were adopted to statistically identify outliers and construct a prototypical profile to generalize AE occurrences. A total of 66 inhibitors were analyzed, revealing substantial variability in the safety profiles. Cluster analysis identified distinct patterns of AEs based on kinase target classes, highlighting the importance of tailored therapeutic approaches. Statistical methods such as Tukey’s fences were used to identify drugs with unusual safety profiles, offering insights into both frequent and rare severe reactions. Real-world evidence complements clinical trial data, capturing AEs that might not be fully identified pre-approval.

Immunotherapy for Type 1 Diabetes: Mechanistic Insights and Impact of Delivery Systems.

Type 1 Diabetes is an autoimmune disease characterized by the destruction of insulin-producing pancreatic β-cells, leading to hyperglycemia and various complications. Despite insulin replacement therapy, there is a need for therapies targeting the underlying autoimmune response. This review aims to explore the mechanistic insights into T1D pathogenesis and the impact of delivery systems on immunotherapy. Genetic predisposition and environmental factors contribute to T1D development, triggering an immune-mediated attack on β-cells. T cells, particularly CD4+ and CD8+ T cells, play a central role in β-cell destruction. Antigen- specific immunotherapy is a unique way to modify the immune system by targeting specific antigens (substances that trigger the immune system) for immunotherapy. It aims to restore immune tolerance by targeting autoantigens associated with T1D. Nanoparticle-based delivery systems offer precise antigen delivery, promoting immune tolerance induction. Various studies have demonstrated the efficacy of nanoparticle-mediated delivery of autoantigens and immunomodulatory agents in preclinical models, and several patents have been made in T1D. Combining antigen-specific immunotherapy with β-cell regeneration strategies presents a promising approach for T1D treatment. However, challenges remain in optimizing delivery systems for targeted immune modulation while ensuring safety and efficacy.

PF4 Silencing Promotes Trophoblast Cell Proliferation, Migration, Invasion and EMT by Regulating SOCS3/STAT3 Signaling Pathway.

Recurrent Miscarriage (RM) is a chronic and heterogeneous autoimmune disease. Platelet factor 4 (PF4) has been found to be involved in the pathogenesis of RM. We aimed to explore the role and mechanism of PF4 on trophoblasts in RM in vitro. In this study, the expression of PF4 and PF4 receptor CXC chemokine receptor 3 (CXCR3) in the placentas of patients with RM were analyzed by RT-qPCR and western blotting. Serum PF4 level was tested by ELISA. Following PF4 silencing and SOCS3 overexpression in HTR-8/SVneo cells, cell proliferation was detected by CCK-8, colony formation, and EDU assays. Wound healing and transwell assays separately evaluated cell migration and invasion. Immunofluorescence assay determined E-cadherin expression. Tube formation assay was used to measure the angiogenesis. Western blotting examined the expression of metastasis, epithelial-mesenchymal transition (EMT) and suppressor of cytokine signaling 3 (SOCS3)/signal transducer and activator of transcription 3 (STAT3) signaling-associated proteins. The results revealed that PF4 displayed increased expression in placental villus tissues of RM patients. Serum PF4 level was also elevated in RM patients. PF4 silencing promoted the proliferation, migration, invasion, EMT, and angiogenesis of HTR-8/SVneo cells. Additionally, PF4 knockdown downregulated SOCS3 expression to activate STAT3 signaling. SOCS3 overexpression countervailed the effects of PF4 deficiency on HTR-8/SVneo cells. In summary, PF4 participated in the proliferation, migration, invasion, EMT and angiogenesis of trophoblast cells by modulating the SOCS3/STAT3 signaling pathway, indicating that targeting the PF4/SOCS3/STAT3 pathway could be a novel therapy for RM.

From trials to practice: Immune checkpoint inhibitor therapy for melanoma patients in Norway.

Norway has one of the highest rates of cutaneous melanoma (CM) incidence and mortality globally. Immune checkpoint inhibitor (ICI) therapy for CM was introduced between 2014 and 2017 to improve treatment and patient prognosis, but knowledge about its clinical usage is limited. This study investigates patient's characteristics and treatment patterns in real-world practice compared to clinical trial results. All adult (≥18) CM patients treated with ICI therapy in Norway from 2014 to 2021 were included, utilizing high-coverage data from multiple national registries to describe patients' health, socioeconomic factors, and treatment management, stratified by first ICI therapy. We compared patient and tumour characteristics with findings from five randomized controlled trials (RCTs). Among 2,083 patients receiving ICI therapy, 975 (47%) received nivolumab as their first treatment in the metastatic setting. Patients on combination therapy were younger and had higher education and income levels compared to those on monotherapy. Overall, real-world patients were older and had a higher incidence of brain metastases than those in RCTs. Approximately, 1 in 5 patients would have been excluded from RCTs due to pre-existing autoimmune diseases. Targeted therapy was the most common secondary systemic treatment after first-line PD-1 inhibitors. This study details ICI therapy in Norway, highlighting differences between real-world ICI users and clinical trial participants, raising questions about the effectiveness of this treatment for patients not eligible for trials.

Retrospective analysis of health and economic burden among commercially-insured individuals diagnosed with invasive meningococcal disease in the United States

ABSTRACT Invasive meningococcal disease (IMD) is a life-threatening yet vaccine-preventable disease, with vaccines approved and recommended in the United States by the Centers for Disease Control and Prevention. This study assessed complications, mortality, healthcare resource utilization (HCRU), and healthcare costs among a sample of commercially-insured individuals living in the United States who experienced IMD. We used retrospective data from large claims databases limited to individuals with IMD covered by commercial health plans between January 2010–March 2022. Health outcomes, HCRU, and healthcare costs were analyzed during the acute (index date to 30 days post-hospital discharge) and post-acute (end of acute phase to end of follow-up period) phases. Among 618 IMD cases identified, the most common acute phase complications were severe brain damage, renal failure, and autoimmune disease. The most common post-acute phase complications were autoimmune disease, arthralgia, and renal failure. Acute phase HCRU ranged from 72.7 (95% confidence interval [CI] 19.81–186.12) intensive care unit (ICU) stays to 12,102.9 (95% CI 11,201.07–13,058.00) surgeries per 1,000 patient-years. Post-acute phase HCRU ranged from 3.6 (95% CI 1.18–8.50) ICU stays to 7,808.3 (95% CI 7,661.22–7,957.54) specialty physician visits per 1,000 patient-years. Patients with IMD incurred average healthcare costs of $60,866.23 and $145,883.65 during the acute and post-acute phases, respectively. Negative health outcomes and high HCRU and costs were observed among commercially-insured patients with IMD. Our findings suggest that IMD immunization efforts and healthcare interventions targeting education on vaccine recommendations to healthcare providers and patients could help prevent IMD and reduce disease burden.

Upper arm deep vein thrombosis in a patient with active lupus

Upper extremity deep vein thrombosis (UEDVT) is relatively rare, and much less as an initial presentation of systemic lupus erythematosus (SLE). Primary UEDVT should be considered in individuals with unilateral arm swelling where the brachial, axillary, and subclavian veins are frequently involved. SLE is a chronic autoimmune disease that predominantly affects women of childbearing age and of African descent. Patients present with clinical features ranging from arthritis and arthralgias (over 90% of patients with SLE) to life-threatening hematologic, or central nervous system involvement. Individuals have an increased risk of arterial and/or venous thrombosis where the most important risk factor is the presence of antiphospholipid antibodies. Even within this condition, thrombotic events are typically seen in the legs, and UEDVT remains an unusual presentation. Here, we present a case of a 36-year-old female of African descent with a recent medical history of small joint arthralgia and vaginal bleeding due to uterine fibroids, for which she was prescribed a short course of prednisolone and norethisterone, respectively. She presented with a 2-week history of unilateral swelling in the left arm. Doppler ultrasound and later computed tomography scan with contrast indicated left UEDVT. Further investigations throughout her admission led to the diagnosis of SLE, while antiphospholipid syndrome - a common contributor to thrombosis in SLE - was notably ruled out. The patient was initiated on anticoagulants. The patient went on to later rapidly develop lupus nephritis and started on high-dose prednisolone. Given the high risk of bleeding, the decision to postpone the kidney biopsy was taken. There is limited data available about UEDVT when compared to lower extremity DVT and even fewer studies on SLE patients with thrombosis in the absence of antiphospholipid syndrome. Keeping this in mind, clinicians need to recognize idiopathic UEDVT as a potential early sign of SLE and maintain a high level of suspicion.

Basic immunization against diphtheria, tetanus and pertussis within the at-risk population of oncological patients: cross-sectional data from the Berlin Metropolitan area

Abstract Aim Oncological patients are susceptible to severe infectious complications, some of which may be preventable through vaccination. Vaccination rates among oncological patients are generally considered low. While prevalence data on basic immunization for diphtheria, tetanus and pertussis among the general population is available in Germany, such data remains lacking for oncological patients. With this publication, we aim to present the first data. Subject and methods In this study, we examined data collected during the EVO intervention study to assess participants’ vaccination status against DTP. Our analysis focused on the baseline data of all participants and the follow-up data of the control group, thereby excluding data affected by the intervention. We used Pearson’s chi-squared test to explore factors potentially associated with higher or lower vaccination rates (e.g. sex, diagnosis). Results Of the 370 patients included in the study, 78.9% had a solid and 21.1% a haematological tumour; 47.3% were vaccinated against tetanus, 44.9% against diphtheria and 39.7% against pertussis. Patients with haematological cancer had a higher vaccination rate against diphtheria compared to those with solid tumour (55.1% vs. 42.1%). On the other hand, women had higher rates compared to men against tetanus (53.7% vs. 40.7%) and diphtheria (50.0% vs. 39.4%). Additional positive factors included the presence of autoimmune diseases and a diagnosis of multiple myeloma. Conclusion Oncological patients seem to have significantly lower vaccination rates for diphtheria and tetanus compared to the German general population. For pertussis, on the other hand, the vaccination rate is higher than in the general population.

Interactive Antibacterial Activity and Toxicity Profiles of Selected Pure Plant Compounds and Conventional Antibiotics Against Bacterial Triggers of Some Autoimmune Diseases

Interactive Antibacterial Activity and Toxicity Profiles of Selected Pure Plant Compounds and Conventional Antibiotics Against Bacterial Triggers of Some Autoimmune Diseases

Cordycepin ameliorates autoimmunity by promoting STING degradation via autophagy pathway.

Stimulator of interferon response cGAMP interactor 1 (STING), a central hub protein of cyclic GMP-AMP synthase (cGAS)-STING signalling pathway, has a crucial role in regulating type I interferons (IFNs) production and response. Recent studies indicate that excessive activation of STING is strongly associated with autoimmune diseases, including systemic lupus erythematosus (SLE). Searching immunomodulators that negatively regulate STING might greatly contribute to the suppression of autoimmunity. The peripheral blood mononuclear cells (PBMCs) of SLE patients, Hela cells, L929 cells and bone marrow-derived macrophages (BMDMs) from mice were used as in vitro models. While, Trex1 KO mouse autoimmune disease model was used as in vivo model. After treatment with cordycepin, a nucleoside from Cordyceps mushrooms, type I IFNs production and response were determined by western blotting, real-time polymerase chain reaction (PCR), dual-luciferase assay, enzyme-linked immunosorbent assay (ELISA), haematoxylin-eosin staining and RNA-seq. Cordycepin inhibited type I IFNs production and response in human and murine systems following cGAS-STING signalling activation. Importantly, cordycepin markedly attenuates the autoinflammatory and autoimmune responses in Trex1 KO BMDMs and Trex1 KO mice. Furthermore, cordycepin effectively suppressed the production of type I IFNs and interferon-stimulated genes (ISGs) in the PBMCs of SLE patients. Mechanistically, cordycepin promoted STING degradation via autophagy pathway upon DNA stimulation. This study shows that cordycepin promotes STING autophagic degradation to alleviate autoimmunity upon DNA stimulation. Cordycepin might be a potential therapeutic candidate for alleviating aberrant type I IFNs in autoimmune and autoinflammatory diseases.

Assessment of the Expression Levels of USP27X and DDX3X genes in Systemic Lupus Erythematosus (SLE) Patients

Introduction: Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease influencing numerus tissues in body. Ubiquitin carboxyl-terminal hydrolase 27 (USP27X) is a deubiquitinating enzyme involved in the type I interferons (IFNs) generation, apoptosis and production of proinflammatory mediators. DEAD-box helicase 3 X-linked (DDX3X) is a ribonucleic acid (RNA) helicases and contributes to the generation of type I IFNs, and proinflammatory mediators. Considering the involvement of IFN type I, apoptotic cell death and proinflammatory mediators in the pathogenesis of SLE, the expression levels of USP27X and DDX3X genes were assessed in SLE patients. Methods: Two groups, including SLE patients and healthy subjects, were included in the study and the expression levels of USP27X and DDX3X genes in their peripheral blood mononuclear cells (PBMC) were quantified by the real-time polymerase chain reaction (PCR). Results: The results demonstrated the expression level of DDX3X gene was 5.9-fold higher in the SLE patients compared to the healthy subjects ( P < .01). No significant difference in the expression level of USP27X gene was detected between both groups ( P > .05). Conclusion: A significant elevation in the level of DDX3X gene in SLE patients prepossess the potential involvement of DDX3X in SLE pathogenesis possibly through the induction of proinflammatory mediators. In spite of the potential involvement of USP27X in SLE through the induction of type 1 IFNs, and apoptotic cell death, our finding did not provide evidence in the contribution of USP27X in SLE pathogenesis.

Diseases of the Gallbladder and the Biliary Tree in Systemic Lupus Erythematosus: Review of Clinical Presentation, Diagnosis and Management

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterised by multi-system involvement and diverse clinical manifestations. Among the systems affected, the gastrointestinal and hepatobiliary systems are notable taragets of the autoimmune response. Although gastrointestinal and hepatic syndromes commonly reported, gallbladder dysfunction is rare and not included in the diagnostic criteria for the disease. Biliary complications in SLE can present as a spectrum of conditions, ranging from acalculous cholecystitis and Salmonella infection to more uncommon manifestations such as primary biliary cirrhosis, autoimmune cholangiopathy, and primary sclerosing cholangitis. These complications frequently occur in the context of heightened lupus disease activity, with vasculitis identified as a key underlying mechanism, and are associated with significant morbidity. Thus, biliary involvement should be considered in the differential diagnosis of abdominal pain and related symptoms in patients with SLE. This review article explores the spectrum of gall bladder and the biliary manifestations in SLE and discusses the corresponding diagnostic and treatment strategies.

Antithrombotic Treatment in Antiphospholipid Syndrome: A Review

Antiphospholipid syndrome (APS) is a thrombo-inflammatory disease propelled by circulating autoantibodies that recognize cell surface phospholipids and phospholipid-binding proteins. APS is an autoimmune disorder associated with recurrent thrombosis of arterial or venous vessels and/or recurrent obstetric complications as miscarriages. APS can be divided into primary or secondary clinical syndrome because of the possible association with other autoimmune systemic diseases as systemic lupus erythematosus (SLE). Vitamin K antagonists remain the mainstay of treatment for most patients with APS and, based on current data, appear superior to the more targeted direct oral anticoagulants. However, the choice of the type of antithrombotic drug is based on the anamnesis of affected patients: patients with previous arterial or venous thrombosis may benefit from anticoagulants, while patients with previous obstetric diseases may benefit from aspirin, but several clinical exceptions may be evaluated. This short review is dedicated to underlining the main clinical evidence for patients affected by APS or CAPS (catastrophic antiphospholipid syndrome) in order to prevent recurrent thrombosis.

Epidemiology of myositis.

This review aims to synthesize recent developments in the epidemiology of idiopathic inflammatory myopathies (IIMs), focusing on incidence, prevalence, disease classification, and clinical outcomes. IIM is a rare group of autoimmune diseases characterized by muscle weakness and systemic involvement, with incidence rates ranging from 0.2 to 2 cases per 100 000 person-years. The role of myositis-specific autoantibodies (MSAs) in stratifying disease risk and prognosis is increasingly recognized, such as in anti-MDA5 positive DM, which is associated with a high risk of rapidly progressive interstitial lung disease. Furthermore, patients with IIM exhibit elevated risks of comorbidities, including cardiovascular disease and malignancy. IIM diseases are complex disorders with significant health impacts, necessitating enhanced awareness and research. Improved classification and understanding of MSAs are crucial for earlier diagnosis and tailored therapeutic strategies. Continued epidemiological research is essential to elucidate underlying mechanisms and inform future interventions, ultimately aiming to enhance the quality of life and clinical outcomes for affected patients.

Unraveling the Pathways: A Meta-Analysis Exploring the Biopsychosocial Mechanisms Linking Psychosomatic Symptoms and Systemic Lupus Erythematosus

Background: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a complex interplay of biological, psychological, and social factors. Psychosomatic symptoms, such as depression, anxiety, and stress, are common in individuals with SLE and can significantly impact disease activity and overall well-being. This meta-analysis aims to explore the biopsychosocial mechanisms linking psychosomatic symptoms and SLE. Methods: A systematic search of PubMed, Embase, PsycINFO, and Web of Science databases was conducted from January 2013 to December 2024. Studies examining the relationship between psychosomatic symptoms and SLE were included. Data were extracted and analyzed using random-effects models to calculate pooled effect sizes. Results: Six studies met the inclusion criteria. The meta-analysis revealed a significant association between psychosomatic symptoms (depression, anxiety, and stress) and SLE disease activity (pooled effect size: r = 0.42, 95% CI: 0.31-0.53, p < 0.001). Furthermore, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, pro-inflammatory cytokine activity, and impaired coping mechanisms emerged as key biopsychosocial pathways linking these factors. Conclusion: This meta-analysis highlights the significant impact of psychosomatic symptoms on SLE and identifies potential underlying mechanisms. These findings underscore the need for integrated biopsychosocial interventions in SLE management, targeting both physical and psychological well-being to improve patient outcomes.

Higher risk profile among patients with TET2-mutated giant cell arteritis: a cluster analysis

ObjectiveWe aimed to assess the prevalence of clonal haematopoiesis (CH) in patients with giant cell arteritis (GCA) compared with controls and individuals with other autoimmune diseases (AIDs) and to identify...

Neurologic Outcomes in People With Multiple Sclerosis Treated With Immune Checkpoint Inhibitors for Oncologic Indications.

Immune checkpoint inhibitors (ICIs) are increasingly used against various cancers but are associated with immune-related adverse events (irAEs). Risk of irAEs may be higher in patients with certain preexisting autoimmune diseases, and these patients may also experience exacerbation of the underlying autoimmune disease following ICI initiation. People with multiple sclerosis (MS) have mostly been excluded from clinical trials of ICIs, so data on the safety of ICIs in MS are limited. This study aims to assess the rate of MS activity, as well as neurologic and nonneurologic irAEs in persons with MS treated with ICIs for cancer. Participating sites were invited to this retrospective observational study through the Medical Partnership 4 MS+ listserv. Seven large academic centers participated in the study, each conducting a systematic search of their electronic medical record system for patients with MS and history of ICI treatment. The participating neurologist reviewed each chart individually to ensure the inclusion criteria were met. Demographics and data on MS and cancer history, treatments, and outcomes were abstracted from patient charts using a structured instrument. We identified 66 people with MS (median age 66 years, 73% female, 68% not on disease-modifying therapy for MS) who were treated with ICIs for lung cancer (35%), melanoma (21%), or another oncologic indication. During post-ICI follow-up (median: 11.7 months, range 0.2-106.3 months), 2 patients (3%) had relapse or MRI activity, 3 (5%) had neurologic irAEs, and 21 (32%) had nonneurologic irAEs. At the last follow-up, 25 (38%) participants had partial or complete remission of their cancer, while 35 (53%) were deceased. In this multi-institutional systematic retrospective study of predominantly older patients with MS, most of whom were not on disease-modifying therapy, MS activity and neurologic irAEs following ICI treatment were rare. These data suggest that preexisting MS should not preclude the use of ICIs for cancer in older patients, but the results may not be generalizable to younger patients with active MS. Prospective studies of ICI safety that enroll younger patients with MS are needed.