Introduction This study aims to identify the influence of social determinants of health (SDoH) on patients with systemic lupus erythematosus (SLE), emphasizing racial and ethnic disparities in healthcare. Methods A cross-sectional study used the National Institute of Health\'s (NIH) All of Us Research Program (AoU). From 727,000 patients, SLE patients were categorized by race, ethnicity, and responses to the Social Determinants of Health survey from May 2018 until March 2023. Survey questions addressed transportation access, neighborhood safety, provider biases, and food insecurity. JMP Pro 16.0 and R 4.2.2 were used for statistical analysis. Results Significant racial disparities were evident amongst SLE patients for transportation access, neighborhood safety, food security, and respect from healthcare providers (p-value < 0.001). African Americans, Asians, and White participants showed different perceptions regarding neighborhood crime, healthcare provider courtesy, and feeling unheard by providers, with respective p-values of 0.001, 0.010, and 0.023. Hispanic participants perceived higher neighborhood crime rates, felt unsafe during nighttime walks, felt unheard by healthcare providers, and reported worrying about food security compared to non-Hispanic participants, with respective p-values of 0.003, 0.003, 0.009, and <0.001.  Discussion SLE is affected by access to care, treatments, stress, and lifestyle habits. Therefore, identifying SDoH for SLE patients is critical as it impacts disease progression, leading to delays in diagnosis, improper management, and worsening morbidity.  Conclusion Targeted social and community-based interventions may improve access to care, identify implicit biases among providers, and alleviate food insecurity.

Discoid lupus erythematosus (DLE) is an autoimmune skin condition that is typically part of the cutaneous manifestation of systemic lupus erythematosus (SLE). DLE is characterized by erythematous patches that can progress to depigmentation and alopecia, leading to scarring and permanent hair loss if left untreated. Herein, we present a unique case of localized DLE on the scalp in a 46-year-old female with no prior history of autoimmune disorders. The patient underwent several medication trials, including intralesional corticosteroids, topical calcineurin inhibitors, topical corticosteroids, and systemic hydroxychloroquine, with limited success in treating her discoid alopecia. Subsequently, a combination therapy of oral hydroxychloroquine and topical pimecrolimus significantly improved her scalp lesion. This case highlights the efficacy of combination therapy in managing localized DLE, providing valuable insights for future research focused on DLE alopecia management and optimizing treatment strategies for similar cases.

BACKGROUND: Despite accumulating evidence correlating oxidative stress with lupus disease activity, the brain redox pathways are still poorly investigated. Cinnamomum cassia, a widely used spice with powerful antioxidant properties, could be a novel therapeutic candidate in lupus.
METHODS: C57BL/6J female mice were divided into five groups: sham, sham-cinnamon, lupus, lupus-cinnamon starting from induction, and lupus-cinnamon starting two weeks before induction. Lupus was induced by skin application on the right ear with 1.25 mg of 5% imiquimod cream three times per week for six weeks. Cinnamomum cassia was given orally, five days per week, at 200 mg/kg.
RESULTS: Concomitant to TLR7-MYD88 pathway activation, the p-NRF2/NRF2 and p-FOXO3/FOXO3 ratios were increased in the hippocampus and alleviated by cinnamon treatment. BCL-2 positivity was enhanced in hippocampal neurons and reversed only by preventive cinnamon administration. In vitro, exposure of hippocampal cells to the plasma of different groups induced a surge in oxidative stress. This was associated with an increased t-BID/BID ratio. Cinnamon treatment, particularly in the preventive arm, normalized these modifications.
CONCLUSIONS: Our study shows a neuroprotective effect of cinnamon by rescuing brain redox and apoptosis homeostasis in lupus, paving the way for its use as a natural therapeutic compound in the clinical management of lupus.

UNASSIGNED: The safety and efficacy of mycophenolate mofetil (MMF) for lupus nephritis (LN) treatment is established in adults and in some children. MMF is rapidly converted to the biologically active metabolite mycophenolic acid (MPA) whose pharmacokinetics (PK) is characterized by large inter- and intra-individual variability.
UNASSIGNED: This randomized, double-blind, active comparator, controlled clinical trial of pediatric subjects with proliferative LN compares pharmacokinetically-guided precision-dosing of MMF (MMFPK, i.e. the dose is adjusted to the target area under the concentration-time curve (AUC0-12h) of MPA ≥ 60-70 mg*h/L) and MMF dosed per body surface area (MMFBSA, i.e. MMF dosed 600 mg/m2 body surface area), with MMF dosage taken about 12 hours apart. At baseline, subjects are randomized 1:1 to receive blinded treatment with MMFPK or MMFBSA for up to 53 weeks. The primary outcome is partial clinical remission of LN (partial renal response, PRR) at week 26, and the major secondary outcome is complete renal response (CRR) at week 26. Subjects in the MMFBSA arm with PRR at week 26 will receive MMFPK from week 26 onwards, while subjects with CRR will continue MMFBSA or MMFPK treatment until week 53. Subjects who achieve PRR at week 26 are discontinued from study intervention.
UNASSIGNED: The Pediatric Lupus Nephritis Mycophenolate Mofetil (PLUMM) study will provide a thorough evaluation of the PK of MMF in pediatric LN patients, yielding a head-to-head comparison of MMFBSA and MMFPK for both safety and efficacy. This study has the potential to change current treatment recommendations for pediatric LN, thereby significantly impacting childhood-onset SLE (cSLE) disease prognosis and current clinical practice.

Systemic lupus erythematosus (SLE, lupus) is a debilitating, multisystem autoimmune disease that can affect any organ in the body. The disease is characterized by circulating autoantibodies that accumulate in organs and tissues, which triggers an inflammatory response that can cause permanent damage leading to significant morbidity and mortality. Lyn, a member of the Src family of non-receptor protein tyrosine kinases, is highly implicated in SLE as remarkably both mice lacking Lyn or expressing a gain-of-function mutation in Lyn develop spontaneous lupus-like disease due to altered signaling in B lymphocytes and myeloid cells, suggesting its expression or activation state plays a critical role in maintaining tolerance. The past 30 years of research has begun to elucidate the role of Lyn in a duplicitous signaling network of activating and inhibitory immunoreceptors and related targets, including interactions with the interferon regulatory factor family in the toll-like receptor pathway. Gain-of-function mutations in Lyn have now been identified in human cases and like mouse models, cause severe systemic autoinflammation. Studies of Lyn in SLE patients have presented mixed findings, which may reflect the heterogeneity of disease processes in SLE, with impairment or enhancement in Lyn function affecting subsets of SLE patients that may be a means of stratification. In this review, we present an overview of the phosphorylation and protein-binding targets of Lyn in B lymphocytes and myeloid cells, highlighting the structural domains of the protein that are involved in its function, and provide an update on studies of Lyn in SLE patients.

Systemic lupus erythematosus (SLE) is an autoimmune condition more commonly observed in women of childbearing age. The most commonly reported initial presentations were fatigue, arthritis, and skin manifestations. However, due to the involvement of a variety of organs, diagnosis remains a challenge for physicians. Our patient is a 48-year-old lady who presented with severe bilateral lower extremity edema with non-resolving right lower lobe pneumonia and ipsilateral exudative pleural effusion. Her leg swelling was not responding to diuretics, and her pneumonia was not improving following a course of antibiotics. This unusual presentation prompted an autoimmune workup, which later revealed a diagnosis of SLE with class 5 lupus nephritis. Pleuritis, exudative pleural effusion, and lupus nephritis have been associated with autoimmune disorders in the literature, but this is an uncommon initial presentation in SLE without other clinical manifestations. Our case report highlights the challenges in the diagnosis of an atypical case of SLE and the need to maintain high clinical suspicion for SLE, especially in female patients with multiorgan involvement.

UNASSIGNED: To determine the full range of ophthalmological clinical manifestations in systemic lupus erythematosus (SLE) and to compare the systemic features associated with them.
UNASSIGNED: Files of 13 patients with ocular SLE (n = 20 eyes) diagnosed as per the American College of Rheumatology (ACR) 2012 revised criteria were retrospectively reviewed.
UNASSIGNED: The following clinical manifestations were found: keratoconjunctivitis sicca (n = three patients), anterior uveitis associated with an inflammatory pseudo-tumor orbital mass (n = one patient, one eye), episcleritis and periorbital edema (n = one patient, two eyes), posterior scleritis (n = one patient, two eyes), bilateral papillary edema in the context of idiopathic intracranial hypertension (n = one patient, one eye), inflammatory optic neuritis (n = one patient, one eye), and lupus retinopathies with varying degrees of capillary occlusions mainly arteriolar (n = seven patients, 13 eyes) and larger arteries or veins (retinal arteries occlusions and retinal veins occlusions) (n = one patient, two eyes). Some patients presented with combined ophthalmological manifestations.Systemic SLE was discovered by its ophthalmic manifestation in three cases (23%) and was previously known in the other 10 cases (77%). On average, ocular symptoms were seen 8 years after the initial diagnosis of SLE. Other systemic SLE disorders included cutaneous disorders (77%), joint disorders (38%), central nervous system (CNS) disorders (23%), renal disorders (38%), and oral ulcers (23%).Treatment of the ophthalmic system manifestations of lupus included local steroid therapies along with systemic immunosuppression.The most common laboratory ACR criteria were: high levels of antinuclear antibodies (ANA) (100%), positive anti-Sm (64%), anti-dsDNA (27%), low complement levels (27%), and positive antiphospholipid (APL) antibodies (18%).
UNASSIGNED: SLE activity in the ophthalmic system is characterized by its functional severity and the range of involvement can be categorized by anatomical involvement: presence of anterior uveitis, episcleritis, scleritis, periorbital edema, posterior uveitis with retinal vascular ischemia, or papillary edema. Not currently part of the diagnosis criteria of the SLE ACR given its rarity, the ocular localization of the pathology led to the diagnosis of SLE in three cases; thus, developing a greater understanding of ocular lupus may help in identifying and treating systemic manifestations of lupus earlier.

UNASSIGNED: The coronavirus disease 2019 (COVID-19) pandemic has limited healthcare delivery for patients with chronic diseases, including Systemic Lupus Erythematosus (SLE). This study aims to describe the outcomes of patients with SLE in a national COVID-19 referral center in the Philippines.
UNASSIGNED: A review of records of all adult patients with SLE seen in the University of the Philippines-Philippine General Hospital (UP-PGH) from March 2020 to December 2021 was done. Data about patient characteristics, health encounters, and outcomes before and after the first visit during the study period were extracted. Descriptive statistics were employed.
UNASSIGNED: Our population of 403 patients was predominantly young (mean age 34.53 ± 11.14 years), female, and unemployed. This consisted of 370 known cases of SLE, 92 were diagnosed in institutions outside UP-PGH, and 33 new patients. Over the 22-month study period, there were 2,093 medical encounters, most of which were teleconsultations (81.70%). During an average gap of 53.6 ± 26.7 weeks between the last consultation and the first visit within the pandemic study period, 84 patients (22.70%) discontinued at least one of their SLE control medications, 68 (18.38%) patients developed a lupus flare, and 79 (21.35%) were hospitalized for various reasons. On their return to the rheumatology clinic during the pandemic, 37.47% were in lupus flare, 28.29% needed to be hospitalized, and 20 died. However, 86.75% of flares were controlled. During subsequent health encounters, 48 patients had a new flare (43 of these were controlled) and 20 died. The most common reason for hospitalization (n=160) was lupus disease flare and the most common cause of death (n=40) was pneumonia. Sixty patients acquired COVID-19 infection from which most recovered and four died.
UNASSIGNED: Audio teleconsultation was the most common method used by our lupus cohort to interact with their doctors during the pandemic. There was an average of a year-long interruption in medical care for 62.70%. More than a third developed a disease flare and 15% acquired COVID-19 but outcomes were good in more than 85%. Despite the challenges posed by the pandemic, the majority of our lupus cohort who were able to continue their treatment had favorable outcomes.

UNASSIGNED: Systemic Lupus Erythematosus (SLE) can have an insidious onset and a fatal prognosis in children. Patients presenting without typical signs of SLE should undergo further evaluation if they are not responding to the initial diagnosis and treatment. This is especially true for patients with rapidly progressing symptoms and deterioration in spite of treatment.
UNASSIGNED: Pediatric Systemic Lupus Erythematosus is a chronic autoimmune disorder with various organ involvement pulmonary involvement in the course of this disorder is a rare yet potentially life-threatening complication. In this case report we highlight the findings of a 16-year-old girl acutely and initially presenting with cough and fever, eventually complicating to diffuse alveolar hemorrhage and gradual loss of consciousness. Although the patient was started on immunosuppressive treatment after the diagnosis of lupus, based on renal and hematological impairment, was made and initially responded, she eventually deteriorated.

Protein kinase C delta (PKCδ) has emerged as a key protective molecule against systemic lupus erythematosus (SLE or lupus), an autoimmune disease characterized by anti-double stranded (ds) DNA IgGs. Although PKCδ-deficient mice and lupus patients with mutated PRKCD genes clearly demonstrate the requirement for PKCδ in preventing lupus autoimmunity, this critical tolerance mechanism remains poorly understood. We recently reported that PKCδ acts as a key regulator of B cell tolerance by selectively deleting anti-dsDNA B cells in the germinal center (GC). PKCδ\'s tolerance function is activated by sphingomyelin synthase 2 (SMS2), a lipid enzyme whose expression is generally reduced in B cells from lupus patients. Moreover, pharmacologic strengthening of the SMS2/PKCδ tolerance pathway alleviated lupus pathogenesis in mice. Here, we review relevant publications in order to provide mechanistic insights into PKCδ\'s tolerance activity and discuss the potential significance of therapeutically targeting PKCδ\'s tolerance activity in the GC for selectively inhibiting lupus autoimmunity.