tbuckley/cabot-search huggingface dataset:
AB1519 EARLY PREDICTION OF PULMONARY HYPERTENSION IN PATIENTS WITH RHEUMATIC AND MUSCULOSKELETAL DISEASE WITH TRANSTHORACIC ECHOCARDIOGRAPHY AND SPO2 IN 6MWT
Authors: S. Ishigaki, H. Hanaoka, T. Hiraide, Y. Kaneko
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Pulmonary hypertension (PH) is one of the most critical organ involovement in rheumatic and musculoskeletal diseases. The threshold for the diagnosis of PH is defined as 20 mmHg of a mean pulmonary arterial pressure (mPAP) with right heart catherterization (RHC) [1]. The definition of pulmonary hypertension has been updated from a mean pulmonary arterial pressure (mPAP) of 25 mmHg to 20 mmHg, aiming for a better long-term prognosis. However, it is still difficult to predict patients with PH through non-invasive findings. <h3>Objectives:</h3> To identify predictive factors for early PH diagnosis in patients with rheumatic and musculoskeletal diseases. <h3>Methods:</h3> We reviewed consecutive patients with rheumatic and musculoskeletal diseases who underwent RHC from December 2020 to May 2023. Right heart catheterization was performed who showed tricuspid regurgitation pressure gradient (TRPG) was ≥ 30 mmHg with signs of right heart overload in transthoracic echocardiography. PH was diagnosed based on mPAP &gt; 20mmHg with RHC. We divided the patients into two groups according to the presence of PH and compared their clinical characteristics. <h3>Results:</h3> Thirty-nine patients including 14 with overlap syndrome, 7 with mix connective tissue disease, 9 with systemic sclerosis, 2 with systemic lupus erythematosus, 1 with Sjögren syndrome, and 6 with others were included in the analysis. Among them, 22 (56.4%) patients were diagnosed as having PH. Patients with PH showed significantly higher TRPG (48.4 mmHg vs 31.3mmHg, p=0.0004), lower saturation of percutaneous oxygen (SpO2) in 6-min walk test (6MWT) (86.7% vs 90.5%, p= 0.0421), and higher positive rate for anti-SSA antibody (66.7% vs 21.3%, p= 0.0489). A receiver operating characteristic curve identified 33.5 mmHg as a cut-off value of TRPG and 90% of lowest SpO2 in 6MWT to discriminate patients with PH from those without. Compared to evaluation using TRPG alone (sensitivity of 86.4% and a specificity of 76.5%), using TRPG in combination with either 6MWT or anti-SSA yielded higher specificity (sensitivity 82.4%, specificity 92.3%). <h3>Conclusion:</h3> TRPG higher than 33.5 mmHg with transthoracic echocardiography, SpO2 lower than 90% in the 6MWT, and anti-SSA positivity can predict the presence of PH in patients with rheumatic and musculoskeletal diseases. <h3>REFERENCES:</h3> [1] European heart journal 43.38 (2022): 3618-3731. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
AB1597-HPR THE PATIENTS’ WITH SYSTEMIC VASCULITIS JOURNEY FROM SYMPTOMS ONSET TO DIAGNOSIS AND DAILY LIVING: DATA FROM A CONTEMPORARY PATIENT COHORT
Authors: E. Mavrea, C. Koutsianas, C. Tsalapaki, D. Vassilopoulos
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Systemic vasculitides are rare but often organ- or life-threatening diseases where delays in diagnosis and treatment may have significant impact on patients' morbidity and mortality. Contemporary data regarding patients' journey from symptom onset to living with vasculitis are limited. <h3>Objectives:</h3> We aimed to explore the experiences of patients with systemic vasculitides regarding their journey from symptom onset to diagnosis and daily living. <h3>Methods:</h3> Patients with systemic vasculitides who were seen and followed at a tertiary referral center (Clinical Immunology- Rheumatology Unit, General Hospital of Athens "Hippocration", Greece) were included in the study. All patients answered a special questionnaire, regarding their journey from their initial symptoms until their last site visit. Demographic and clinical characteristics of the patients were collected through both the medical record and questionnaires. <h3>Results:</h3> 30 patients with a median age of 57 years, 66% females with systemic vasculitides (GPA 53%, MPA 6%, ΕGPA 26%, GCA 10%, TAK 3%) were included. The mean interval from symptoms' onset to final diagnosis was 7 months. The main presenting symptoms were fatigue/weakness (56%), arthralgias (53%), cough/dyspnea (53%), fever (46%), rashes (33%), headache (20%), asthma (20%), visual disturbances (10%), rhinorrhea (10%), serositis (6%) and jaw claudication (3%). The initial patient assessment was performed mainly by an Internist or General Practitioner (36%) followed by other specialties (Pulmonary: 16%, ENT: 10%, Neurologist: 10%, Orthopedic: 6%, Gastroenterologist: 6%, Cardiologist: 6%, Endocrinologist: 3%) while only 3% were seen initially by a Rheumatologist. Immediate referral to a rheumatologist was made by the 1<sup>st</sup> evaluating physician in only 20% of cases. Ultimately, the diagnosis was made by a rheumatologist in 74% of cases. Almost half of the patients (53%, 16/30) reported that they had to stop work because of their disease (23%, 7/30 permanently) while 40% reported that their health-related expenses were quite high. <h3>Conclusion:</h3> Patients with systemic vasculitides still experience significant delays in their diagnosis mainly due to delayed referral to the specialist (rheumatologist) while the disease. impact on their daily life is significant. These preliminary data emphasize the unmet needs for earlier recognition-diagnosis and better management of systemic vasculitides. <h3>REFERENCES:</h3> <b>NIL.</b> <h3>Acknowledgements:</h3> Supported in part by the Special Account for Research Grants (S.A.R.G.), National and Kapodistrian University of Athens, Athens, Greece (DV #12085, 12086). <h3>Disclosure of Interests:</h3> <b>None declared.</b>
POS0372 TNFRSF11A AS A CAUSATIVE GENE IN SYSTEMIC AUTOINFLAMMATORY DISEASES: A CASE SERIES OF 12 PATIENTS
Authors: V. Papatheodorou, C. Gerodimos, A. Dimitrakopoulos, E. Lada, M. G. Tektonidou, A. Germenis, P. P. Sfikakis, K. Laskari
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Limited evidence suggests that <i>TNFRSF11A</i> as a causative gene in systemic autoinflammatory diseases (SAIDs) [1,2]. <h3>Objectives:</h3> To estimate the prevalence of <i>TNFRSF11A</i> variants in a cohort of patients with SAIDs and describe their disease phenotypic expression. <h3>Methods:</h3> Consecutive patients (n=167) with confirmed SAIDs who underwent screening by next generation sequencing targeting 26 SAID-associated genes, including <i>TNFRSF11A,</i> were included in this study. The demographic, clinical and laboratory parameters of those carrying at least one <i>TNFRSF11A</i> gene variant were recorded. <h3>Results:</h3> A total of 12 out of 167 patients, 7 males, aged (median) 38 years at disease onset, yielded at least one <i>TNFRSF11A</i> rare variant. All patients carried a coexisting variant in at least one of 10 other SAID-related genes, most frequently <i>MEFV</i> (6 patients), but also <i>TNFRSF1A</i>, <i>NOD2</i>, <i>NLRP3</i>, <i>NLRP7</i>, <i>MVK</i>, <i>IL36RN</i>, <i>RBCK1</i>, <i>PLCG2</i> and <i>PSMB8</i>. Disease episodes lasting (median) 9 days manifested most frequently with high grade fever (91%), myalgias (75%), malaise (67%), serositis (58%), arthralgias/arthritis (58%), gastrointestinal involvement (33%), and rash (25%), and responded well to corticosteroids. The most common initial clinical diagnosis was TNF-associated periodic fever syndrome (TRAPS), nevertheless, genetic testing was consistent with this diagnosis in only one patient. The emergence of <i>MEFV</i> variations supported the diagnosis of Familial Mediterranean Fever in two cases, albeit with atypical clinical features, whereas the diagnosis of Yao syndrome was considered in two patients with <i>NOD2</i> variants. The presence of atypical disease in these patients as well as the inability to define diagnosis in the remaining 7 cases, raised thoughts about the possible involvement of <i>TNFRSF11A</i> variants in the phenotypic expression of SAIDs. <h3>Conclusion:</h3> Herein, we provide first evidence in a case series that <i>TNFRSF11A</i> gene variants, occurring in 7% of SAID patients, contribute to the development of an autoinflammatory syndrome resembling to TRAPS. Additional studies to confirm new pathogenic SAID pathways are clearly warranted. <h3>REFERENCES:</h3> [1] Jéru I, et al. Brief Report: Involvement of TNFRSF11A molecular defects in autoinflammatory disorders. Arthritis Rheumatol (Hoboken, NJ). 2014;66(9):2621–7. [2] De Jesus AA, Goldbach-Mansky R. Newly recognized Mendelian disorders with rheumatic manifestations. Curr Opin Rheumatol. 2015 Sep 1;27(5):511–9. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
POS1383 RISK OF CANCERS ACCORDING TO THE USE OF BIOLOGICAL AGENTS IN PATIENTS WITH ANKYLOSING SPONDYLITIS: A NATIONWIDE POPULATION-BASED COHORT STUDY
Authors: M. C. Park, O. C. Kwon, H. S. Lee, J. Yang
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> As the duration of use of biological disease-modifying anti-rheumatic drugs (bDMARDs) in patients with ankylosing spondylitis (AS) accumulates over time, long-term real-world safety data on cancer risk are needed. <h3>Objectives:</h3> This study assessed the association between tumor necrosis factor inhibitors (TNFis) and interleukin-17 inhibitors (IL-17is) exposures and cancer risk in patients with AS. <h3>Methods:</h3> From the Korean nationwide database, we assembled 41,889 patients without prior history of cancer who were diagnosed with AS from 2010 onwards. Patients were followed-up through 2021. Multivariable time-dependent Cox models were performed to estimate the adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) of (i) overall cancers and (ii) cancer subtypes according to TNFis exposure vs. bDMARDs non-exposure, IL-17is exposure vs. bDMARDs non-exposure, and IL-17is exposure vs. TNFis exposure. <h3>Results:</h3> The incident rates of overall cancers during bDMARDs non-exposure, TNFis exposure, and IL-17is exposure were 53.81, 37.63, and 67.27 per 10,000 person-years, respectively. TNFis exposure vs. bDMARDs non-exposure was not associated with an increased risk of overall cancers (aHR=0.919, 95% CI=0.775–1.090). IL-17is exposure was not associated with an increased risk of overall cancers compared with bDMARDs non-exposure (aHR=1.233, 95% CI=0.510–2.984) or TNFis exposure (aHR=1.342, 95% CI=0.551–3.272). Similarly, no significant associations were observed between exposure to bDMARDs with the risk of cancer subtypes. <h3>Conclusion:</h3> In patients with AS, there was no evidence of increased cancer risk with TNFis and IL-17is exposures compared with bDMARDs non-exposure, suggesting that the use of bDMARDs is safe with respect to cancer risk in patients with AS. <h3>REFERENCES:</h3> <b>NIL.</b> <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
AB1564-HPR DETERMINANTS OF BIOPSYCHOSOCIAL STATUS IN INDIVIDUALS WITH AXIAL SPONDYLOARTHRITIS
Authors: N. B. Karaca, G. I. Kinikli, S. Buran, C. Boström, O. Tüfekçi, L. Kiliç, E. Ünal, Ş. A. Bilgen
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Biopsychosocial (BPS) problems such as pain, fatigue, loss of physical function, and psychosocial issues are observed in patients with axial spondyloarthritis (axSpA) [1]. BETY-Biopsychosocial Questionnaire (BETY-BQ), created with the feedback of individuals with rheumatism, was recently validated for individuals with Ankylosing Spondylitis [2]. This instrument holistically evaluates biopsychosocial characteristics such as pain, functionality and fatigue, emotional state, social participation, sexuality, and sleep [3]. Therefore, it is important to identify determinants of BPS status in individuals with axial axSpA. <h3>Objectives:</h3> This study was conducted to investigate the determinants of BPS status in individuals with axSpA. <h3>Methods:</h3> Forty-one individuals (28 female, 13 male) with axSpA were recruited in this cross-sectional study. BETY-BQ, disease activity (Bath Ankylosing Spondylitis Disease Activity Index (BASDAI)), subjective and objective functional level (Bath Ankylosing Spondylitis Functional Index (BASFI) and Ankylosing Spondylitis Performance Index (ASPI)), spinal mobility (Bath Ankylosing Spondylitis Metrology Index (BASMI)), mood (Hospital Anxiety and Depression Scale (HADS)) and quality of life (Ankylosing Spondylitis Quality of Life Scale (ASQoL)) of the individuals whose demographic information was obtained was recorded. <h3>Results:</h3> Participants' demographic and clinical features are shown in Table 1. Correlations between BETY-BQ and other measurement parameters can be observed in Table 2. The multiple regression analysis revealed that BASFI, rate of perceived exertion in the ASPI Bending (pick up 6 pencils), HADS anxiety score, and ASQoL score explained 82.8% of the variance in the BETY-BQ (p&lt;0.001, R<sup>2</sup>=0.86, AR<sup>2</sup>=0.82). <h3>Conclusion:</h3> Functionality, anxiety, and quality of life were found as determinants of BPS in individuals with axSpA. Addressing these parameters in the disease management of individuals with axSpA may contribute to improving the BPS condition. <h3>REFERENCES:</h3> [1] Wilk, Mateusz et al. "Pain catastrophizing in rheumatoid arthritis, psoriatic arthritis and axial spondyloarthritis: biopsychosocial perspective and impact on health-related quality of life." Rheumatology international vol. 42,4 (2022): 669-682. doi:10.1007/s00296-021-05070-4. [2] Verep U, Unal E, Oksuz S, Soy M, Önen F, Kiraz S. A New Biopsychosocial Questionnaire (BETY-BQ) for Patients with Ankylosing Spondylitis. Eur J Integr Med. 2023;102267; https://doi.org/10.1016/j.eujim.2023.102267. [3] Ünal E, Arin G, Karaca NB, Kiraz S, Akdoğan A, Kalyoncu U, et al. Development of a quality of life measurement for rheumatic patients: item pool construction. Journal of Exercise Therapy and Rehabilitation. 2017;4(2): 67-75. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
POS0165 MACHINE LEARNING-BASED APPROACHES TOWARDS STRATIFICATION OF DISEASE SEVERITY AND ORGAN DAMAGE IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
Authors: P. Garantziotis, D. Nikolopoulos, C. Adamichou, A. Fanouriakis, A. Repa, D. Boumpas, P. Sidiropoulos, G. K. Bertsias
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Organ damage is a key determinant of unfavorable long-term prognosis and increased mortality, thus being reflective of disease severity in SLE patients. <h3>Objectives:</h3> To develop a clinical, machine learning based model for the prediction of early organ damage in SLE towards disease severity stratification. <h3>Methods:</h3> Using a cohort of 914 adults with SLE [1], panels of deconvoluted classification criteria [ACR 1997 (ACR), SLICC 2012 (SLICC) and EULAR/ACR 2019 (EULAR)] and non-criteria features present at any timepoint throughout the first five years since SLE diagnosis were assessed. Permanent organ damage was evaluated using the SLICC/ACR Damage Index (SDI). We randomly divided the patient cohort into a training (70%) and a test (30%) set. Employing feature selection algorithms, the smallest set of clinical features that most accurately predicted early organ damage accrual (defined as SDI increase within the first 5 years since SLE diagnosis) was selected. Five different prediction models (random forest (RF), logistic regression (glm), linear discriminant analysis (LDA), k-nearest neighbors (KNN), extreme gradient boosting (XGBoost)) were adopted. The best model in 10-fold cross-validation was tested in the test set. Accuracy, sensitivity, specificity, and area under (AUC) the receiver operating curve (ROC) were determined in the test set. <h3>Results:</h3> The LDA model demonstrated the highest performance in predicting early organ damage with an AUC of 0.831 (95% CI: [0.7817, 0.8739]) with sensitivity of 0.955 and specificity of 0.463. The leading predictors included synovitis, non-scarring alopecia, acute cutaneous lupus, SLICC 2012-based neurologic disorder, leukopenia, and the age at the time of SLE diagnosis. The XGBoost model exhibited the highest specificity (0.841) with an accuracy of 0.805 (95% CI: [0.7619 - 0.8241]) and sensitivity of 0.653. Age at the time of diagnosis, the presence of ACR 1997-based neurologic disorder, non-scarring alopecia, and low complement (2012 criteria) emerged as the strongest predictors in this model. <h3>Conclusion:</h3> Machine learning methods using standard disease features may identify SLE patients at risk for early damage accrual. Further validation in external cohorts is warranted. <h3>REFERENCES:</h3> [1] Adamichou C, Genitsaridi I, Nikolopoulos D, Nikoloudaki M, Repa A, Bortoluzzi A, Fanouriakis A, Sidiropoulos P, Boumpas DT, Bertsias GK. Lupus or not? SLE Risk Probability Index (SLERPI): a simple, clinician-friendly machine learning-based model to assist the diagnosis of systemic lupus erythematosus. Ann Rheum Dis. 2021 Jun;80(6):758-766. doi: 10.1136/annrheumdis-2020-219069. Epub 2021 Feb 10. PMID: 33568388; PMCID: PMC8142436. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
POS1405 IDENTIFICATION OF SPATIALLY-RESOLVED IMMUNE POPULATIONS IN LUPUS NEPHRITIS KIDNEY VIA HI-RESOLUTION 20-PLEX IMMUNOHISTOCHEMISTRY SINGLE-CELL SPATIAL ANALYSES
Authors: M. C. Marlin, C. Y. Lee, X. Yang, T. Stephens, A. I. Celia, C. Wright, J. Hodgin, P. Izmirly, H. M. Belmont, R. Furie, J. H. Anolik, J. A. James, M. Petri, J. P. Buyon, D. L. Kamen, C. Putterman, A. Fava, A. Rosenberg, J. M. Guthridge
Journal: Annals of the Rheumatic Diseases (2024)
AB1681-PARE PATIENTS’ PERCEPTION ON DIAGNOSIS DELAY OF AXIAL SPONDYLOARTHRITIS
Authors: A. Fazaa, N. Ben Salem, S. Miladi, Y. Makhlouf, L. Souabni, K. Ouenniche, S. Chekili, S. Kassab, K. Ben Abdelghani, A. Laatar
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> Symptoms of Axial Spondyloarthritis (axSpA) can start in early childhood and may persist throughout a lifespan. The average time to diagnosis is 6,7 years [1]. Understanding patients' perception throughout their diagnostic journey may provide insights into the emotional and socioeconomic burden of axSpA. <h3>Objectives:</h3> The aim of this study was to evaluate patients' perception on their diagnosis journey, how the diagnosis delay of axSpA affects their emotional and socioeconomic well-being and to identify the associated factors. <h3>Methods:</h3> We conducted a cross-sectional study among patients with axSpA (ASAS 2009 classification criteria) and progressing for more than 12 months. Data concerning demographics, disease and patient's journey characteristics was obtained from medical files. Patients' perception of their care pathway was assessed using a survey. <h3>Results:</h3> Sixty patients were enrolled in this study with a mean age of 50.3±13.2 years. Sex ratio was 1.3. The mean age of disease onset was 30,3 ± 11,2 years. Median delay from onset of symptoms to axSpA diagnosis was 49.2 months [0.5-458.8]. Based on patients' self-perception, 55% of patients reported a long delay until their diagnosis. According to these patients, the main reason for the delayed diagnosis was symptom fluctuation (90,9%). Other reported reasons included significant wait times for medical tests and scans (63,6%), delayed doctor appointments (57,6%), economic difficulties (27,3%), lack of time (27,3%) geographical difficulties in accessing health centers (24,2%) and fear of medications (12,1%). Sixty percent of patients experienced stress and anxiety while waiting for their diagnosis and 58,3% reported that their diagnosis journey was stressful for their families. The diagnosis journey resulted in strained social relationships for 15% of patients and led to job loss for 31.7%. Experiencing stress and anxiety was significantly associated with lack of social security affiliation (p=0,02), higher BASDAI at diagnosis (p&lt;0,001) and longer diagnosis delay (p=0,03). Job loss was significantly associated with older age at diagnosis (p=0,02), BASDAI at diagnosis (p=0,01) and longer diagnosis delay (p=0,002). No significant association was found with strained social relationships. <h3>Conclusion:</h3> Diagnosis delay of axSpA has a significant negative impact on patients' emotional and socioeconomic well-being. This highlights the importance of early diagnosis and the need for better strategies in managing axSpA. <h3>REFERENCES:</h3> [1] Zhao SS, Pittam B, Harrison NL, Ahmed AE, Goodson NJ, Hughes DM. Diagnostic delay in axial spondyloarthritis: a systematic review and meta-analysis. Rheumatology. 6 avr 2021;60(4):1620-8. <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>
POS1061 VORINOSTAT AS A DUAL INHIBITOR OF TYPE I IFN PRODUCTION AND ABERRANT B CELL: A NOVEL THERAPEUTIC CANDIDATE FOR SYSTEMIC LUPUS ERYTHEMATOSUS
Authors: T. Hirayama, H. Takamatsu, A. Kumanogoh
Journal: Annals of the Rheumatic Diseases (2024)

<h3>Background:</h3> SLE is a systemic autoimmune disease caused by impaired innate and acquired immune tolerance, resulting in increased Type I IFN (IFN-I) and aberrant B cell development. Upon sensing nucleic acid, IFN-I is produced via multiple pathways, including RIG-I-like receptors-, Toll-like receptors- (TLR), and cGAS-mediated pathway, In particular, TLR7 stimulation lead to autoantibody production via promoting extrafollicular differentiation B cell into the pathological B cell populations, such as active naive B cells, double negative B cells, and short-lived plasmablasts. Increased IFN-I and pathogenic B cell activity are synergistically involved in disease activity at onset and relapse. However, there have been no therapeutic agents that simultaneously inhibit both IFN-I production and abnormal B cell maturation. <h3>Objectives:</h3> We aimed to identify inhibitors from among clinically approved drugs that have the potential to inhibit both IFN-I production and abnormal B cell maturation. We then aimed to elucidate the molecular mechanisms by which they inhibit both IFN-I production and abnormal B cell maturation, and their therapeutic efficacy in mouse models. <h3>Methods:</h3> We screened the candidate compounds using the reporter cell that can monitor IFN-I induction and chemical library consisting of clinically approved drugs. We then examined whether they suppress the expression and phosphorylation of upstream signaling molecules for IFN-I and the differentiation of B cells into plasma cells, and whether they can alleviate disease severity in SAVI mice and NZB/W F1 mice. <h3>Results:</h3> We identified that Vorinostat, a clinically approved pan-HDAC inhibitor, inhibited both IFN-I production and B cell differentiation. Vorinostat inhibited TBK1 phosphorylation and following IRF3 nuclear translocation, and suppressed the expression of both IFN-I–inducing molecules, such as IRF5, and IRF7, and B cell-related genes, such as VpreB. Additionally, Vorinostat suppressed lung inflammation and fibrosis in SAVI mice due to suppressing IFN-I and alleviated the mortality and renal disease of NZB/W F1 mice by suppressing IFN-I and B cells differentiation. Furthermore, Vorinostat suppressed TLR7-mediated plasma cell differentiation from human B cells. <h3>Conclusion:</h3> Vorinostat has a potential to simultaneously inhibit IFN-I production and aberrant B cell development by suppressing TLR7-mediated signaling. Vorinostat would have the advantage of being in clinical use and can be rapidly delivered to SLE patients as a novel agent that selectively affects both IFN-I and B cells. <h3>REFERENCES:</h3> <b>NIL.</b> <h3>Acknowledgements:</h3> <b>NIL.</b> <h3>Disclosure of Interests:</h3> <b>None declared.</b>