Faculty Bibliography

OBJECTIVE:The objective of this scoping review was to synthesize evidence on the proportion of individuals living with Sjögren's disease who experience central nervous system (CNS) manifestations. METHODS:We searched MEDLINE (via PubMed) and Embase from 1980 through January 29, 2026, and the ECRI Guidelines Trust from 2020 through January 29, 2026. Title and abstract screening, followed by full-text review, were performed in duplicate using prespecified inclusion and exclusion criteria. One reviewer extracted data, with an independent audit completed by one of the project co-leads. Meta-analyses of proportions were conducted. Sensitivity analyses were planned a priori to evaluate the influence of statistical outliers. RESULTS:We identified 22,857 citations, of which 108 met the inclusion criteria. Pooled proportion estimates were generated for 23 CNS manifestations. Several manifestations occurred at frequencies exceeding those reported in the general population, including depression, migraine, insomnia, cognitive dysfunction, psychosis, movement disorders, aseptic meningoencephalitis, neuromyelitis optica spectrum disorder, optic neuritis, multiple sclerosis, cerebral vasculitis, cerebellar syndrome, spinal cord involvement, and non-localizing somatosensory complaints. The degree of increased frequency differed substantially across manifestations, and several estimates were highly influenced by individual studies, as indicated by sensitivity analyses. CONCLUSION/CONCLUSIONS:The spectrum of CNS involvement in Sjögren's disease is broad and heterogeneous. Attributing CNS manifestations to direct SjD involvement or coexisting conditions remains unclear and cannot be assumed to be causally linked. Our findings underscore the complexity of CNS manifestations in Sjögren's disease and highlight the need for evidence-informed guidance to support accurate diagnosis, attribution, and management of neurologic manifestations.

Although previously B cells had been underestimated in comparison to T cells in their role in autoimmunity, now, their impact is well established. Via secretion of autoantibodies, presentation of autoantigens, regulation of antigen processing and presentation, and release of inflammatory cytokines, B cells can mediate cytotoxicity and lead to organ damage. B cell depletion via CD20 targeting effectively eliminates B cells in the blood and primary lymph organs and has found an effective role in the treatment of both rheumatological and neurological diseases. The neonatal Fc receptor (FcRn) is a key component of immune regulation that prevents IgG (produced by B cells) from degradation by lysosomes, sending it back into the extracellular compartment, thereby extending its half-life. This abundance of pathogenic IgG can lead to the development of autoimmune disease. The interplay between these two mechanisms of autoimmunity provides the great potential for combination therapy to reduce existent pathogenic IgG as well as prevent the production of new autoantibodies, though further investigation is needed to determine the risks, particularly of infection. This paper will explore existing B cell depleting treatments and FcRn inhibitors, and consider the potential impact for autoimmune disease as well as for the treatment of atherosclerosis.

High plasma cholesterol levels substantially contribute to cardiovascular disease. Hepatic delivery of the microRNA-30c analog C2 decreased plasma cholesterol in apoB-containing lipoproteins in hypercholesterolemic C57BL/6 mice, in African green monkeys that spontaneously developed diabetes and hyperlipidemia and prevented diet-induced hypercholesterolemia in mice with humanized livers. Furthermore, C2 significantly reduced plasma cholesterol and atherosclerosis in LDL receptor knockout mice. C2 did not affect hepatic triglyceride and cholesterol, plasma ALT, AST, CK-MB, ALP, IL-6, TNF-α, and INF-ϒ, thus indicating an absence of tissue lipid accumulation and inflammatory response. In contrast, MTP inhibitor lomitapide significantly reduced plasma lipids and caused hepatic steatosis. Mechanistic studies revealed that C2 reduced hepatic microsomal triglyceride transfer protein expression, secretion of apolipoprotein B-containing lipoproteins and FA synthesis and increased hepatic FA oxidation, plasma bile acids and fecal cholesterol excretion. C2 is a first-in-class microRNA therapeutic that decreases plasma cholesterol and atherosclerosis, without causing hepatic injury and inflammatory response.

OBJECTIVES/OBJECTIVE:Sjögren's disease is an autoimmune disorder that can impact multiple organ systems, including the peripheral nervous system (PNS). PNS manifestations, which can exist concurrently, include mononeuropathies, polyneuropathies, and autonomic nervous system neuropathies. To help patients and providers in the decision-making process, we developed an evidence-based clinical practice guideline for the evaluation and management of peripheral nervous system manifestations in patients with Sjögren's disease. METHODS:A Topic Review Group (TRG), comprised of experts in rheumatology, neurology, and guideline methodology, developed Patient, Intervention, Comparison, and Outcome (PICO) questions and conducted a systematic review to identify current best evidence on management of PNS manifestations of Sjögren's disease. PubMed and Embase were searched for evidence published up to July 22, 2025. Literature screening, data extraction, and critical appraisal were performed in duplicate. Six case series, one retrospective cohort, and two prospective cohort studies lacking a comparison group met the inclusion criteria. RESULTS:We developed an aligned nomenclature of PNS terms that can be used across disciplines, 31 good practices for evaluation of suspected PNS manifestations, and 20 evidence-based treatment recommendations, the latter of which were rated as conditional or strong based on Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology. Due to the scarcity of high-level evidence, this guideline predominantly derives from expert opinion. CONCLUSION/CONCLUSIONS:This clinical practice guideline on PNS manifestations of Sjögren's disease provides clinicians a rigorous, evidence-based resource, developed through an expert consensus-based process, for the assessment, diagnosis, and treatment of peripheral neuropathy in Sjögren's patients. Recommendations were rated as strong when the benefits significantly outweighed potential harms, creating a scenario in which the majority of patients would prefer the advised action.

Sjögren's disease (SjD) exemplifies the intricate relationship between oral health and overall systemic wellness. Characterized by autoimmune-mediated destruction of exocrine glands, it commonly manifests as xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eyes), yet its reach extends well beyond the salivary and lacrimal glands to involve musculoskeletal, renal, pulmonary, and neurological systems. Insights from national patient surveys underscore considerable unmet needs in SjD management, emphasizing the importance of early recognition of oral health challenges. Concurrently, advances in clinical and translational research deepen our understanding of SjD's underlying mechanisms, revealing novel diagnostic and therapeutic strategies that target immunological pathways, foster glandular regeneration, and may alter disease progression. By providing a cohesive synthesis of state-of-the-art evidence, this review aims to expand clinicians' and researchers' understanding of SjD pathogenesis, address new research areas and key gaps, highlight the critical role of medical partnerships in addressing both systemic and oral manifestations, and advance patient-centered strategies to improve detection, treatment, and long-term disease management of this multifaceted autoimmune disorder. We discuss immune-mediated tissue damage, the potential of emerging biomarkers, and innovative treatments, including biologic agents and regenerative techniques. Patient perspectives further illuminate the daily challenges posed by SjD, underscoring the need for interdisciplinary care models that integrate oral medicine, rheumatology, and other medical specialties. Taken together, these insights underscore the pressing need for heightened awareness and collaborative approaches to pave the way for precision medicine interventions that can transform current management paradigms and ultimately improve the lives of individuals affected by Sjögren's disease.

Nomenclature for the disease widely known as Sjögren syndrome has proven unsatisfactory. Patients have perceived 'syndrome' as indicative of a vague collection of symptoms, prompting the Sjögren's Foundation to abandon the term. Furthermore, the traditional distinction between 'primary' and 'secondary' forms fails to account for the complex interplay between overlapping autoimmune diseases. Following a bibliometric analysis, systematic literature review and a Delphi consensus process with equal involvement of professional and patient representatives, five recommendations are now issued. First, the term 'Sjögren disease' should replace 'Sjögren syndrome'. Second, the acronym 'SjD' should be used as an abbreviation for 'Sjögren disease'. Third, the descriptor 'associated' should be used in lieu of 'secondary' for Sjögren disease occurring in association with a second systemic autoimmune disease for which classification criteria are fulfilled. Fourth, Sjögren disease is the preferred terminology in common parlance and in clinical diagnosis, without differentiation as to primary and associated forms. Fifth, the differentiation between primary and associated Sjögren is recommended for scientific studies to define a homogeneous population. In conclusion, the consensus endorses 'Sjögren disease' as the official nomenclature to acknowledge the distinct pathogenesis of this disorder and to improve clarity in both clinical practice and research.

OBJECTIVES/UNASSIGNED:Outside of the association of SS-A antibody with congenital heart block, little is known about adverse maternal and neonatal outcomes, in patients with Sjogren's disease (SjD). Our study involved collaboration with maternal-fetal medicine (MFM). METHODS/UNASSIGNED:-test and Fisher's exact test. RESULTS/UNASSIGNED:48 patients were included: 12 SjD patients and 36 controls. APO was significantly increased in SjD with one preterm birth, one fetal growth restriction, and one limb anomaly; non-SjD had one cardiac anomaly. There were no cases of CHB. SjD patients were more likely to be delivered by cesarean delivery. CONCLUSION/UNASSIGNED:There was an increased risk of APO in SjD patients compared with controls. No significant difference in neonatal outcomes was found. We speculate that placental pathology may play a role in pathophysiology and future studies should be performed. KEY POINTS/UNASSIGNED:There was an increased risk of APO in SjD patients compared with controls.No significant difference in neonatal outcomes was found.We speculate that placental pathology may play a role in pathophysiology, prompting future studies.