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        <title>Frontiers in Lupus | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/lupus</link>
        <description>RSS Feed for Frontiers in Lupus | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-04-16T14:29:55.507+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2026.1788752</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2026.1788752</link>
        <title><![CDATA[Postpartum challenges in women with systemic autoimmune diseases]]></title>
        <pubdate>2026-04-02T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Dina Zucchi</author><author>Chiara Tani</author><author>Giancarlo Cascarano</author><author>Elena Elefante</author><author>Marta Mosca</author>
        <description><![CDATA[The postpartum period represents a critical and underexplored phase in the reproductive course of women with systemic autoimmune diseases (SAD). While advances in disease management have substantially improved pregnancy outcomes, the weeks and months after delivery remain associated with a significant burden of maternal complications. Abrupt immunological and hormonal changes, together with treatment modifications during pregnancy and breastfeeding, may predispose women with SAD to disease reactivation and other adverse outcomes after delivery. This Mini Review summarizes the available evidence on postpartum complications in women with SAD, with a focus on disease flares, thrombotic and infectious events, mental health and quality of life, and therapeutic challenges during lactation. Despite its clinical relevance, postpartum outcomes remain insufficiently investigated, with limited prospective data, heterogeneous endpoints, and gaps between clinical recommendations and real-life practice. Recognizing the postpartum period as a distinct and integral component of reproductive health is essential to improve maternal outcomes and optimize long-term care for women with SAD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2026.1466123</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2026.1466123</link>
        <title><![CDATA[Evaluating the efficacy of SK1217 in attenuating pristane-induced lupus in mice]]></title>
        <pubdate>2026-03-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Swetha Kakkerla</author><author>Sridhar Kavela</author><author>Sathvika Chintalapani</author>
        <description><![CDATA[IntroductionSystemic lupus erythematosus (SLE) is a multifactorial autoimmune disorder characterized by aberrant immune activation, autoantibody production, immune complex deposition, and progressive organ damage, particularly lupus nephritis. Developing therapies that can simultaneously modulate immune dysregulation and inflammation remains a major clinical need.MethodsIn the present study, we evaluated the therapeutic efficacy of the antimicrobial and immunomodulatory peptide SK1217 in a pristane-induced lupus mouse model. Disease progression and therapeutic effects were assessed through measurement of serum autoantibodies, proinflammatory cytokines, complement levels, renal function markers, and immune cell populations. Molecular mechanisms were investigated by analyzing MAPK and NF-κB signaling pathways in renal tissues.ResultsSK1217 treatment significantly reduced serum autoantibody levels, including anti-dsDNA, anti-ssDNA, anti-chromatin, anti-ANA, and anti-nRNP antibodies. The peptide also suppressed proinflammatory cytokines TNF-α, IL-1β, IL-6, and IL-17. Mechanistically, SK1217 attenuated activation of inflammatory signaling pathways, as demonstrated by reduced phosphorylation of JNK and p38 MAPK and downregulation of NF-κB p65. SK1217 further modulated humoral immune responses by decreasing serum BAFF levels and altering splenic CD40+ activated B cells and CD138+ plasma cell populations, accompanied by reduced total serum IgG levels. Complement balance was restored through normalization of serum C3 levels. Functionally, SK1217 improved renal parameters by reducing urinary protein excretion, serum creatinine, and blood urea nitrogen levels, and ameliorated glomerular pathology. Additionally, the peptide modulated immune cell dynamics by reducing Ly6Chi monocytes and regulating peritoneal macrophage and granulocyte populations.DiscussionCollectively, these findings demonstrate that SK1217 exerts multi-target immunomodulatory and renoprotective effects through coordinated suppression of BAFF-driven B cell activation, inflammatory cytokine production, complement activation, and MAPK/NF-κB signaling pathways. These results highlight SK1217 as a promising therapeutic candidate for SLE and lupus nephritis, warranting further translational investigation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2026.1800946</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2026.1800946</link>
        <title><![CDATA[Safety and efficacy of novel therapeutics in lupus: a narrative review]]></title>
        <pubdate>2026-03-25T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Michael F. Loncharich</author><author>Brenna E. Cafeo</author><author>Evan B. Noble</author>
        <description><![CDATA[Systemic lupus erythematosus (SLE) poses diagnostic and management challenges to physicians given its protean manifestations and complex immune dysregulation. Numerous drugs are used in the management of lupus with a plethora under investigation for more effective, safe, and targeted therapies. This narrative review explores recent literature on the safety and efficacy multiple drug classes and gene therapy under investigation in the management of SLE. The findings in this review detail which new candidate drug and gene therapies are showing efficacy and safety in SLE management, and which are not.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2026.1747204</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2026.1747204</link>
        <title><![CDATA[The urgent need for randomized controlled trials in pregnant women with antiphospholipid antibodies—protecting women through research]]></title>
        <pubdate>2026-02-04T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Christine Graversgaard Adams</author><author>Jullie Rudnicki</author><author>Berit Fabricius Petersen</author><author>Søren Jacobsen</author><author>Karen Schreiber</author>
        <description><![CDATA[IntroductionObstetric antiphospholipid syndrome (OAPS) is an autoimmune disorder associated with pregnancy morbidity, including recurrent pregnancy loss, preeclampsia and fetal growth restriction. Despite standard of care (SoC) with low-dose aspirin (LDA) and low-molecular-weight heparin (LMWH), 20%–30% of pregnancies still result in adverse outcomes. The 2023 ACR/EULAR classification criteria have improved research standardisation, yet robust clinical evidence, including randomised controlled trials (RCTs), remains limited and current management largely relies on empirical practice and RCTs performed nearly two decades ago.MethodsIn this mini-review, with a particular focus on refractory OAPS, we summarise the quality of evidence and methodological limitations underpinning current therapeutic strategies. This included existing SoC and potential adjuvant treatments, such as hydroxychloroquine (HCQ), corticosteroids, statins, intravenous immunoglobulin (IVIG) and biologics.ResultsLDA and LMWH remain the cornerstone of OAPS care. Observational data suggest that HCQ may enhance live birth rates in refractory cases, while glucocorticoids offer limited benefit and pose maternal risks. Evidence for IVIG, statins, and biologics is sparse and primarily derived from small uncontrolled studies. With the exception of a few trials reported almost two decades ago, no RCTs have been conducted specifically in OAPS.DiscussionImproved management of OAPS requires higher-quality evidence. Trials in other high-risk pregnancy populations demonstrate that RCTs are feasible. Progress will depend on standardised pregnancy outcome measures, international collaboration with coordinated leadership and increased societal and regulatory recognition of the urgent need for research and funding.This mini-review synthesizes current knowledge on the treatment of refractory OAPS, identifies critical research gaps, and outlines key strategic elements needed to advance evidence-based care for this high-risk population.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1737535</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1737535</link>
        <title><![CDATA[Case Report: Biologic-free clinical remission following anifrolumab discontinuation in systemic lupus erythematosus—two-case reports]]></title>
        <pubdate>2026-01-14T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Takako Hashimoto</author><author>Hidekata Yasuoka</author>
        <description><![CDATA[BackgroundAnifrolumab, a monoclonal antibody against the type I interferon receptor, has shown efficacy in systemic lupus erythematosus (SLE). However, sustained remission after drug discontinuation has been rarely reported.Case presentationWe reported two females with SLE who achieved biologic-free clinical remission after discontinuation of anifrolumab, with no major adverse events observed during or after treatment. Case 1: A 25-year-old woman with newly diagnosed SLE presented with active disease (SLEDAI-2K 14), including arthritis, facial rash, alopecia, mucosal ulcers, hypocomplementemia, and anti–double-stranded DNA antibody positivity. She was initially treated with prednisolone (PSL) and hydroxychloroquine (HCQ); however, a flare occurred during glucocorticoid (GC) tapering, and anifrolumab was initiated with concomitant methotrexate (MTX). The patient achieved clinical remission according to the Definition of Remission In SLE (DORIS) criteria, despite persistent hypocomplementemia and anti–dsDNA antibody positivity. After sustained remission, PSL was discontinued, MTX was tapered, and anifrolumab was discontinued after 25 months due to sustained clinical remission according to the DORIS criteria and patient preference related to work-related difficulty with long-term regular follow-up. She has remained in clinical remission for 6 months on HCQ and low-dose MTX. Case 2: A 22-year-old woman with SLE diagnosed at age 16 presented after disease relapse following GC withdrawal at age 21. At relapse, her disease activity was moderate (SLEDAI-2K 11), characterized by facial rash, alopecia, mucosal ulcers, leukopenia, hypocomplementemia, and anti–dsDNA positivity. She was treated with anifrolumab in combination with HCQ. Her disease activity achieved and maintained clinical remission according to the DORIS criteria, despite persistent hypocomplementemia and anti–dsDNA antibody positivity. Dose spacing and subsequent discontinuation of anifrolumab were attempted because of patient preference related to work-related limitations to long-term follow-up, and future pregnancy plans, and sustained remission was maintained. Even after switching to tacrolimus (Tac), she has maintained remission without anifrolumab for 12 months.ConclusionThese cases suggested that clinical remission could be maintained after discontinuation of anifrolumab in selected patients with SLE.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1679564</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1679564</link>
        <title><![CDATA[Scavenger receptors: key players in the immunological puzzle of lupus]]></title>
        <pubdate>2025-10-29T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Sabine Hahn</author><author>Monika Chitre</author><author>Dominique Shepard</author><author>Romana Rashid</author><author>Zaida G. Ramirez-Ortiz</author>
        <description><![CDATA[Scavenger receptors (SRs) play an important role in the innate immune response by recognizing and binding a variety of ligands to initiate the removal of both altered self- and non-self-antigens. Over the last two decades, SRs have become a forefront for their role influencing and contributing to inflammatory disease pathways. The findings discussed in this review show that the immunological role SRs play is (1) found in multiple organ systems and not limited to one disease or subset of symptoms; (2) part of both the innate and adaptive immune response in addition to influencing inflammatory signaling via non-immune cell subtypes; (3) both pro- or anti-inflammatory depending on which SR class or cell signaling pathway is being observed; (4) potentially useful for the development of therapeutics and diagnostic or prognostic biomarkers for autoimmune disease pathology. Understanding the role of SRs in the context of inflammation and autoimmunity will shed some light on the comprehension of heterogeneous diseases, such as Systemic Lupus Erythematosus.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1600768</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1600768</link>
        <title><![CDATA[Sjögren's disease and systemic lupus erythematosus overlap: immunological insights and therapeutic implications]]></title>
        <pubdate>2025-09-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Giovanni Fulvio</author><author>Gaetano La Rocca</author><author>Chiara Tani</author><author>Marta Mosca</author><author>Chiara Baldini</author>
        <description><![CDATA[Sjögren's disease (SjD) and systemic lupus erythematosus (SLE) are distinct autoimmune disorders and their clinical overlap presents a unique immunological entity with specific challenges. While the clinical manifestations of the SjD-SLE overlap have been extensively characterised, its underlying pathogenetic mechanisms remain less understood. This review underscores the immunological features of the overlap, highlighting the roles of genetic predisposition, interferon pathway activation and B-cell dysregulation. Key genetic factors, particularly those associated with HLA and cytokine signaling, underpin disease susceptibility by promoting aberrant immune responses. The consequent and persistent interferon pathway activation drives chronic inflammation and establishes a feedback loop with autoantibody production. Furthermore, Extrafollicular B-cell responses are central to generating hallmark autoantibodies, such as anti-dsDNA and rheumatoid factor, which are frequent in the overlap. Finally, the continuous activation of interferons and B-cells not only increase disease activity but also contributes to lymphoproliferative complications. Despite progress in elucidating these mechanisms, patients with SjD-SLE overlap remain underrepresented in clinical trials, limiting therapeutic advancements. Emerging strategies, including interferon receptor inhibitors, BAFF-blocking antibodies, and advanced B-cell depletion therapies, may offer promising options to hit the distinct immunological abnormalities of these patients.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1645416</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1645416</link>
        <title><![CDATA[Evaluating CXCR6 and its ligand CXCL16 as biomarkers for lupus organ involvement: a mini review and brief research report]]></title>
        <pubdate>2025-08-29T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Faradia Kernizan</author><author>Himanee Dave</author><author>Victoria Rossetti</author><author>Cheri Frey</author><author>Jillian M. Richmond</author>
        <description><![CDATA[Cutaneous lupus erythematosus (CLE) is a group of skin disorders where the immune system attacks skin cells. CLE can affect people who have systemic lupus erythematosus, or can occur independently. In prior studies, CXCL16 and its primary receptor, CXCR6, have been shown to be elevated at the RNA or protein level in different organs that are affected by lupus. In this systematic review, we sought to understand whether CXCR6 and its ligand CXCL16 could serve as biomarkers for lupus skin or other organ involvement. Our search strategy and protocol are registered on Prospero under # CRD42024583076. CXCL16 was shown to be a biomarker of lupus nephritis and disease activity in both urine and serum samples in multiple studies. CXCL16 was also elevated in cerebrospinal fluid in neuropsychiatric lupus patients as well as other autoimmune brain conditions. Last, we queried publicly available datasets and our own datasets to evaluate expression of CXCR6 and CXCL16 in lupus skin. CXCR6 but not CXCL16 was enriched in lupus skin across multiple datasets and model organisms. Taken together, our study corroborates the CXCR6 chemokine family as a potential biomarker of lupus organ involvement.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1473368</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1473368</link>
        <title><![CDATA[Differences in gestational age at preterm birth can predict future cardiovascular events in systemic lupus erythematosus (SLE)]]></title>
        <pubdate>2025-06-27T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>May Ching Soh</author><author>Catherine Nelson-Piercy</author><author>Magnus Westgren</author><author>Lesley McCowan</author><author>Dharmintra Pasupathy</author>
        <description><![CDATA[IntroductionPregnancy complications from maternal placental syndrome (MPS) are associated with the accelerated development of cardiovascular events (CVE) in the parous cohort with systemic lupus erythematosus (SLE). Preterm birth may result from MPS, which is more common in SLE. This study aimed to determine if preterm birth stratified by gestational age increases the risk of CVE in SLE.MethodsUtilizing Swedish population databases between 1973 and 2011, those who had been pregnant with SLE were identified and stratified into three groups: term (≥37 + 0 weeks), late preterm 34 + 0–36 + 6 weeks, and early preterm <34 + 0weeks births. The primary outcome was CVE or death from CVE. The risk of CVE was calculated and adjusted for SLE-related morbidity and cardiovascular risk factors.ResultsOver the 38-year interval, there were 3,963 subjects, and the prevalence of preterm birth was 20.9%. The prevalence of CVE was 10.4% (n = 411), being highest in those who had given birth <34 + 0 weeks. After multivariable adjustment, the risk of CVE was 1.8 [adjusted hazards ratio (HR) 95% CI: 1.3–2.5] in those who birthed <34 + 0 weeks compared with others who had birthed at term. They also developed CVE earlier than those who birthed at later gestational ages.ConclusionsEarly preterm birth <34 + 0 weeks conferred a two-fold increased hazard for accelerated development of CVE. Reassuringly, those who delivered at a later gestation did not exhibit a similar risk of premature CVE. Therefore, birth <34 + 0 weeks, regardless of an underlying cause, may be a useful screening question to identify parous persons with SLE who are at greater risk of early CVE.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1607792</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1607792</link>
        <title><![CDATA[Immune dysregulation and lipid interactions in systemic lupus erythematosus-associated atherosclerosis: mechanisms and pathogenesis]]></title>
        <pubdate>2025-06-25T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Philippe Bilodeau</author><author>Konstantinos Tselios</author>
        <description><![CDATA[Atherosclerosis is increasingly recognized as a chronic inflammatory process, involving intricate interactions among the endothelium, lipids, coagulation system, and components of both the innate and adaptive immune systems. In the context of systemic lupus erythematosus (SLE), these interactions are even further disrupted, contributing to accelerated atherosclerosis. This narrative review explores how immune system dysregulation plays a central role in the development of atherosclerosis in SLE patients, where cardiovascular disease remains the leading cause of mortality despite recent advancements. We aim to present a model based on current scientific evidence that compares the immune mechanisms driving atherosclerosis in the general population with the accelerated form observed in SLE patients, highlighting the key immunological distinctions that set SLE-associated atherosclerosis apart. Particular emphasis was given to the interactions between interferon, lipid alterations and adaptive immunity as mediators of atherogenesis. This model may help identify gaps in our understanding and generate new hypotheses for potential therapeutic targets to modulate immune responses within atherosclerotic plaques.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1604644</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1604644</link>
        <title><![CDATA[Clinical and histopathological features of lupus nephritis and the risk of long-term kidney outcomes in Indonesia]]></title>
        <pubdate>2025-06-19T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ni Made Hustrini</author><author>Endang Susalit</author><author>Monik Ediana Miranda</author><author>Meilania Saraswati</author><author>Y. K. Onno Teng</author><author>Merel van Diepen</author><author>Joris I. Rotmans</author>
        <description><![CDATA[ObjectiveRace and region-specific variables influence lupus nephritis clinical features and prognosis. We examined the clinicopathological presentation and long-term kidney outcomes of lupus nephritis in Indonesia.MethodsThis was a retrospective cohort study conducted from 1 January 2011 to 31 December 2021 on biopsy-proven lupus nephritis patients, corresponding to the International Society of Nephrology/Renal Pathology Society 2018 classification. Patients were followed until death, development of end-stage kidney disease, initiation of kidney replacement therapy, or end of study. The association between lupus nephritis class and kidney outcomes was analyzed using cumulative incidence plots. A linear mixed-model analysis was performed to assess the association between lupus nephritis class and kidney function decline.ResultsThis study included 268 patients, with a mean age of 28.7 + 8.5 years, and 94.8% were female. The main histopathological diagnosis was class IV (39.6%). The prescription rate of renin–angiotensin–aldosterone system (RAAS) inhibitors ranged from 0.5% in class VI to 37.4% in class IV (p = 0.138), while that of hydroxychloroquine usage ranged from 0% in class VI to 37.7% in class IV (p = 0.845). Class IV was associated with higher chronic and active lesions, including global (42.6%, p = 0.073) and segmental (41.1%, p = 0.009) glomerulosclerosis; segmental (43.1%, p < 0.001) and global (74.1%, p = 0.004) endocapillary hypercellularity; and sub-endothelial deposit (59.5%, p = 0.007). Over a median follow-up of 26 (IQR = 6.0–48.0) months, 16.4% of patients died, and 3.7% developed end-stage kidney disease or initiated kidney replacement therapy. Infection, including tuberculosis (9.1%), was the leading cause of death. Class IV was associated with a high mortality risk (HR 1.94, p = 0.028), a lower baseline estimated glomerular filtration rate (eGFR) compared with class I/II (β = −51.3, SE = 12.3, p < 0.001), and a less steep decline or even an increase in eGFR over time (β = 15.7, SE = 7.0, p = 0.026).ConclusionsThis cohort demonstrated a high prevalence of chronic lesions, low use of renin–angiotensin–aldosterone system inhibitors and immunosuppressive medications, and notable mortality. This study highlights the importance of timely detection on kidney involvement in SLE patients, routine use of renin–angiotensin–aldosterone system inhibitors, optimal prescription of immunosuppressive medications, and aggressive screening and prophylactic measures of infectious diseases should be encouraged to improve kidney outcomes in lupus nephritis patients in Indonesia.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1553510</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1553510</link>
        <title><![CDATA[Rheumatic autoimmune disease in relation to post-traumatic stress disease and traumatic brain injury]]></title>
        <pubdate>2025-04-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>R. Hal Scofield</author><author>Stephanie Lawrence</author><author>Biji T. Kurien</author><author>Tim Gross</author><author>Kristin Sorocco</author><author>Calin Prodan</author><author>Valerie M. Lewis</author>
        <description><![CDATA[BackgroundPost traumatic stress disorder (PTSD) is associated with traumatic brain injury (TBI) and autoimmune disease, including systemic lupus erythematosus (SLE). We sought to determine whether the association was related to only PTSD or the combination of PTSD and TBI.MethodsWe studied rheumatic disease autoantibodies in a cohort of 40 patients, 20 of whom had TBI without PTSD and 20 had both PTSD and TBI. None had diagnosed rheumatic autoimmune disease. We also examined a cohort of 229 TBI patients, of whom 60% had PTSD, for diagnosis of rheumatic autoimmune disease.ResultsAmong the 20 subjects with PTSD and TBI, 8 had autoantibodies [1 each with anti-Ro (or SSA), anti-RNP and anti-RNP plus anti-dsDNA, the remainder with a positive ANA]. Only 1 of 20 subjects with TBI alone had autoantibodies (p = 0.0088 by Fisher's Exact test). In the cohort of 229 subjects, there were 92 with TBI but no PTSD, of whom 4 (4.3%) had a diagnosed rheumatic autoimmune disease. Of the 137 with TBI and PTSD, 17 (13.3%) had an autoimmune rheumatic disease (p = 0.02 by Fisher's exact test).ConclusionWe found more autoantibodies in the sera of patients with TBI and PTSD than in TBI alone. In addition, we found a 3-fold increased prevalence of autoimmune rheumatic disease in patients with TBI and PTSD compared to those with TBI alone. TBI is strongly associated with PTSD but we conclude that TBI does not contribute to the increased risk of autoimmune disease in PTSD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2024.1511382</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2024.1511382</link>
        <title><![CDATA[Altered hemostatic balance in favor of a procoagulant state in pregnant women with systemic lupus erythematosus]]></title>
        <pubdate>2025-01-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Aleksandra Antovic</author><author>Daniele Lini</author><author>Nida Soutari</author><author>Sanja Lalic-Cosic</author><author>Agneta Zickert</author><author>Andrea Mc Nicholas</author><author>Katarina Bremme</author><author>Maria Sennström</author><author>Franco Franceschini</author><author>Elisabet Svenungsson</author><author>Laura Andreoli</author><author>Iva Gunnarsson</author>
        <description><![CDATA[ObjectivesThis study aimed to investigate hemostatic parameters in pregnant patients with systemic lupus erythematosus (SLE) in relation to the use of antithrombotic prophylaxis, preeclampsia (PE), and antiphospholipid antibody status.Patients and methodsIn total, 34 pregnant patients with SLE and 80 pregnant healthy controls (HC) without PE were included. Patients with SLE were sampled during the first and third trimester of gestation. We analyzed fibrinogen, D-dimer, and global hemostatic parameters including the overall coagulation potential (OCP), overall hemostatic potential (OHP), and the overall fibrinolysis potential (OFP). Fibrin structure was visualized using scanning electron microscopy.ResultsThe median age of the patients with SLE was 33 (range 23–42) years and 31 (26–38) years in the HC. The median disease duration was 10 (range 0–26) years. All but two patients with SLE received prophylaxis with low-dose acetylsalicylic acid (LDASA) and 11 received low-molecular-weight heparin (LMWH). OCP and OHP were significantly increased in the patients with SLE compared to HC (p < 0.01). The levels of fibrinogen and D-dimer increased throughout the pregnancies in the patients with SLE, but no differences were found in the third trimester compared to controls. Among the patients treated with LMWH, OCP, OHP, and OFP were undetectable in two, both of whom were on high prophylactic dosage, and one developed PE. OCP, OHP, and OFP levels were not affected by low prophylactic doses of LMWH. Despite LDASA, preeclampsia occurred in four patients with SLE (12.5%); of whom two received a high prophylactic LMWH dose. Five of 32 (15.6%) patients had major bleeding complications at delivery. There were no thromboembolic complications.ConclusionsIn this pilot study, pregnant patients with SLE developed a hypercoagulable state throughout pregnancy, as demonstrated by the global hemostatic parameters OCP and OHP, except for two patients who were treated with a full dosage of LMWH. The alterations in the coagulation system in SLE pregnancy need to be further studied with the aim of optimizing treatment strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1480867</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1480867</link>
        <title><![CDATA[Postnatal health of infants born to mothers with autoimmune diseases when treated with hydroxychloroquine]]></title>
        <pubdate>2025-01-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Viviana Matys</author><author>Francesca Rizzo</author><author>Maria Pia De Carolis</author><author>Salvatore Barresi</author><author>Anna Maria Serio</author><author>Antonio Lanzone</author><author>Ester Garufi</author><author>Sara De Carolis</author><author>Cristina Garufi</author>
        <description><![CDATA[IntroductionThis retrospective cohort study aimed to observe the postnatal health of infants born to mothers with systemic autoimmune rheumatic diseases treated with hydroxychloroquine (HCQ) during pregnancy.MethodsA total of 312 pregnancies of patients who suffered from different systemic autoimmune rheumatic diseases were considered. Pregnancy data were collected; a telephone follow-up questionnaire was successfully completed in 182 infants to detect the long-term pediatric outcome. The women who took hydroxychloroquine during pregnancy were defined as “HCQ group” and were compared to women who did not take hydroxychloroquine, “non-HCQ group”.ResultsA higher prevalence of women with multiple maternal diseases was detected in the HCQ group, in comparison to that of non-HCQ group (p = 0.0015). Despite HCQ group consisting of more complicated maternal conditions, the obstetrical and neonatal outcomes were similar between the two groups. Regarding postnatal health, 40% of infants in HCQ group revealed no pathologies versus 25% of the children in non-HCQ group (p = 0.0368).DiscussionThe protective role of HCQ on infants should be further evaluated in prospective multicenter long-term studies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2025.1540588</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2025.1540588</link>
        <title><![CDATA[Editorial: Rheumatology education without borders—a global approach to basic instruction on the complex disease of SLE]]></title>
        <pubdate>2025-01-22T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Cindy Flower</author><author>Chak Sing Lau</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2024.1471435</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2024.1471435</link>
        <title><![CDATA[Insights into pregnancy risks associated with active juvenile idiopathic arthritis]]></title>
        <pubdate>2024-12-04T00:00:00Z</pubdate>
        <category>Opinion</category>
        <author>Maryam Yeganegi</author><author>Reza Bahrami</author><author>Seyedeh Elham Shams</author><author>Hossein Neamatzadeh</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2024.1449390</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2024.1449390</link>
        <title><![CDATA[High fetal risk in pregnancies of myositis patients—a Hungarian cohort study]]></title>
        <pubdate>2024-12-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Melinda Nagy-Vincze</author><author>Dorottya Szinay</author><author>Katalin Szabó</author><author>Sarolta Molnár Deliné</author><author>László Balkay</author><author>Tibor Béldi</author><author>Zoltán Griger</author>
        <description><![CDATA[BackgroundSeveral systemic autoimmune rheumatic diseases may affect both fetal and maternal outcomes during pregnancy. However, little information is available regarding pregnancy outcomes in women with idiopathic inflammatory myopathy. Previously published articles stated that the activity of maternal disease may worsen pregnancy outcomes. A former multicenter study suggested that anti-Jo1 antibody positivity and joint involvement could distinguish a more vulnerable group regarding pregnancy complications. Our aim was to identify prognostic factors among clinical symptoms at disease onset and auto-antibody profiles for identifying a high-risk group for poor pregnancy outcome.MethodsThe clinical data of the myositis cohort of the Division of Clinical Immunology, University of Debrecen, Hungary, were reviewed retrospectively. IIM diagnoses were made by Bohan and Peter's criteria or European Alliance of Associations for Rheumatology/American College of Rheumatology (EULAR/ACR) criteria. Disease activity was evaluated based on physician opinion. Gynecological definitions were used to evaluate fetal outcomes.ResultsReviewing clinical data of overall 763 patients (542 women and 221 men) revealed that 5.2% of female patients had pregnancies in the same time or after myositis onset. Among these, 71.4% of the mothers suffered from polymyositis (PM) and 28.6% suffered from dermatomyositis (DM). Their mean age at the time of myositis diagnosis was 25.28 years, and the average interval between myositis diagnosis and first pregnancy was 55.4 months. Maternal complications included preeclampsia in one case and pregnancy-induced myositis in 25% of cases. All cases of pregnancy-induced myositis improved after immunosuppressive treatment. Twenty-eight patients reported 60 pregnancies overall, with multiple pregnancies occurring in 57% of cases. Early or late fetal loss was detected in 41.7% of the pregnancies, and stillbirth occurred in 18.3% of deliveries. Although late fetal loss was observed mainly due to placental insufficiency in patients with anti-Jo1 positivity and complications seemed more frequent in PM cases, logistic regression analysis only confirmed that multiple pregnancies could be an independent risk factor for fetal (p = 0.0112) and interstitial lung disease of maternal complications (p = 0.02).ConclusionInternal organ involvement and the number of pregnancies could influence pregnancy outcomes in myositis patients. Patients’ family planning should be well organized and counseled by myositis experts. Prospective, multicenter collaborations are needed to precisely identify high-risk groups and state managing guidelines.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2024.1461739</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2024.1461739</link>
        <title><![CDATA[Sub-optimal use of anti-malarial therapy for SLE in the Asia Pacific region: observations from the Asia Pacific lupus cohort]]></title>
        <pubdate>2024-11-22T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Rangi Kandane-Rathnayake</author><author>Alberta Hoi</author><author>Worawit Louthrenoo</author><author>Yi-Hsing Chen</author><author>Jiacai Cho</author><author>Aisha Lateef</author><author>Laniyati Hamijoyo</author><author>Shirley Chan</author><author>Shue Fen Luo</author><author>Yeong-Jian Jan Wu</author><author>Sandra Navarra</author><author>Leonid Zamora</author><author>Zhanguo Li</author><author>Haihong Yao</author><author>Sargunan Sockalingam</author><author>Yasuhiro Katsumata</author><author>Masayoshi Harigai</author><author>Yanjie Hao</author><author>Zhuoli Zhang</author><author>BMDB Basnayake</author><author>Madelynn Chan</author><author>Jun Kikuchi</author><author>Tsutomu Takeuchi</author><author>Shereen Oon</author><author>Sang-Cheol Bae</author><author>Sean O’Neill</author><author>Fiona Goldblatt</author><author>Kristine (Pek Ling) Ng</author><author>Annie Law</author><author>Nicola Tugnet</author><author>Sunil Kumar</author><author>Naoaki Ohkubo</author><author>Michael L. Tee</author><author>Cherica Tee</author><author>Yoshiya Tanaka</author><author>Chak S. Lau</author><author>Vera Golder</author><author>Mandana Nikpour</author><author>Eric F. Morand</author>
        <description><![CDATA[IntroductionThe guidelines for management of patients with systemic lupus erythematosus (SLE) recommend the use of anti-malarial (AM) drugs [commonly hydroxychloroquine (HCQ)] in all patients, unless contraindicated. We evaluated the prevalence of AM use in patients with SLE in countries across the Asia Pacific region.MethodsWe used data from the Asia Pacific Lupus Collaboration (APLC) cohort, collected prospectively from SLE patients meeting ACR or/and SLICC criteria, between 2013 and 2020. Demographic factors were collected at enrolment; disease activity indicators (SLEDAI-2K, PGA, SFI) and medication (glucocorticoids (GC), immunosuppressants (IS) and AM) details were captured at enrolment and at routine visits, and organ damage was assessed at enrolment and at annual visits using SLICC/ACR Damage Index. We examined medication use in relation to clinical and serological activity, defined based on SLEDAI-2K.ResultsWe analyzed 4,086 patients and 41,653 visits of data; 3,222 (79%) patients used AM at least once during observation (AM-ever users), but this proportion varied significantly between countries (31%–95%). Overall, the total number of visits with AM use was 27,474 (66%). AM-never users were older and had lower disease activity at study enrolment when compared with AM-ever users. AM-ever users had lower GC and IS exposure; experienced fewer severe flares, and less organ damage.DiscussionAM use was suboptimal and varied significantly across countries, highlighting disparities between current practice and SLE management guidelines. This study further reiterates that patients who used AM during the study period had lower exposure to GC and IS and experienced fewer severe flares and organ damage.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2024.1497518</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2024.1497518</link>
        <title><![CDATA[Motherhood and rheumatic disease – a balancing act. A qualitative study on the challenges of mothers with inflammatory arthritis]]></title>
        <pubdate>2024-11-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ingrid Rekaa Nilssen</author><author>Hege Svean Koksvik</author><author>Bente Jakobsen</author><author>Kjersti Grønning</author>
        <description><![CDATA[ObjectiveInflammatory arthritis (IA) often come with symptoms of pain, stiffness and fatigue, as well as fluctuating and unpredictable disease patterns. All of these symptoms can cause challenges in the role as a mother for women with IA. The main objective of this study is to gain a broader understanding of how mothers with IA experience motherhood and the challenges they encounter within a biopsychosocial framework.MethodsThe participants in this study were recruited through RevNatus, a Norwegian nationwide quality register. The sample consisted of women with IA who had given birth within the last 5 years. The data consisted of written answers to an open-ended question: “Is there anything, in particular, you have experienced as challenging with being a mother and having a rheumatic disease at the same time”? The data were analysed following Brinkmann and Kvale's qualitative content analysis.Results186 women answered the open-ended question. The responses consisted of a total of 9,000 words. Motherhood with IA was described as a difficult balancing act, with practical and physical challenges affecting day-to-day life, medical dilemmas, as well as challenges on a deeper emotional level and worries for the future.ConclusionThe main finding in this study is that the challenges these women meet are multifactorial and complex, including physical, mental and social issues that have a large impact on their everyday life. Focusing solely on improving medical treatment will not solve the challenges these women face. A multidisciplinary approach and focus on patient education and self-management strategies is important to help these women thrive in their role as mothers with IA.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/flupu.2024.1484352</guid>
        <link>https://www.frontiersin.org/articles/10.3389/flupu.2024.1484352</link>
        <title><![CDATA[Case Report: Crosstalk between systemic lupus erythematosus and sickle cell syndromes—two cases from eastern India]]></title>
        <pubdate>2024-11-06T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Dhriti Sundar Das</author>
        <description><![CDATA[Autoimmune diseases and sickle cell abnormalities have been reported to share some common pathogenic pathways. Here, we describe two cases of individuals with sickle cell trait (SCT) who presented with antibodies to antinuclear antigens and clinical features consistent with systemic lupus erythematosus (SLE). These patients were from the eastern state of India, i.e., Odisha. Both patients had documented sickle cell trait and tested positive for anti-double-stranded DNA antibodies. They presented with lupus nephritis without any obvious features of sickle cell hemoglobinopathies. Crosstalk between SLE and SCT may explain this association, which needs validation in future large-scale studies.]]></description>
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