Cardiovascular (CV) disease is the leading cause of mortality in systemic lupus erythematosus (SLE). The risk of myocardial infarction (MI) in SLE is twice the incidence and ten years earlier in onset than in the general population. We present the first known case in the Philippines of acute MI from triple vessel coronary artery disease (CAD) in a young female patient with SLE. This aims to increase recognition and improve preventive strategies for this rare lupus complication. A 31-year-old female with SLE for thirteen years, antiphopspholipid syndrome (APS) and controlled hypertension (HTN) presented with acute chest pain, diaphoresis, and dyspnea. She was a non-smoker with quiescent lupus and nephritis, maintained on low-dose aspirin, mycophenolate mofetil and hydroxychloroquine for the past four years. The physical examination revealed hypertension, bradycardia, normal heart sounds without murmurs, and no signs of lupus flare. The troponin level was elevated, and the electrocardiogram showed inferior wall ST-segment elevation myocardial infarction (STEMI). Coronary angiography revealed triple-vessel disease, with 80-90% stenosis of the left circumflex artery, and total occlusion of the left anterior descending and right coronary artery. There were segmental wall motion abnormalities and a low ejection fraction of 44% on echocardiography. The complete blood count, urinalysis, and serum C3 were within normal range. The anti-dsDNA was low and lipid levels were abnormal. The patient refused coronary artery bypass grafting (CABG). Medical management consisting of anti-platelets, beta-blockers, statin, and warfarin was maximized. The patient completed one year of follow-up without any lupus flares or cardiovascular events. This case illustrates the complex interaction of disease-related and traditional cardiovascular risk factors leading to premature coronary artery disease in a young female with SLE. The case demonstrates favorable one-year outcomes after optimized post-MI medical management. Aside from optimized lupus control and reduced glucocorticoid use, proactive screening and aggressive management of modifiable CV risk factors and antiphospholipid antibodies (aPL), are necessary.
Human ; Female ; Adult: 25-44 Yrs Old ; Lupus Erythematosus, Systemic ; Myocardial Infarction ; Literature ; Infarction ; Female

Abstract An 18-year-old female with Systemic Lupus Erythematosus (SLE) presented with bilateral thigh pain, fever, and diarrhea three days before admission. Diagnosed with SLE one month earlier, she reported prior symptoms, including joint pain, malar rash, hair loss, and hyperpigmented lesions. Initial investigations revealed elevated transaminase levels (AST 355, ALT 132), positive ANA, decreased complement levels (C3 68, C4 16.8), and raised creatine kinase (619). A muscle biopsy confirmed myositis. The patient was treated with immunosuppressant (a combination of steroids and hydroxychloroquine) and supportive therapy. By the eighth day of hospitalization, her symptoms, especially thigh pain, resolved. Electromyocardiography was done, and the results were normal, indicating therapeutic success. This case highlights the importance of prompt diagnosis and management of myositis as a rare SLE manifestation to achieve favorable outcomes.
Systemic Lupus Erythematosus (SLE) ; Myositis ; Muscle Biopsy ; Electromyocardiography

BACKGROUND : Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder that impacts several organ systems. Regulatory T cells (Tregs) are essential for maintaining immunological tolerance, and their dysregulation has been found linked to the pathogenesis of SLE. This study aimed to evaluate the correlation between CD4⁺CD25⁺FOXP3⁺ Treg levels and disease activity, as measured by the MEX-SLEDAI score, in patients with SLE. METHODS : A cross-sectional study was conducted involving 40 SLE patients treated in the Allergy and Immunology outpatient clinic and inpatient ward of Mohammad Hoesin Hospital from June 1, 2024 to August 31, 2024. Inclusion criteria were adults (≥18 years) diagnosed with SLE who provided informed consent. Exclusion criteria included other history autoimmune or immunocompromised conditions, pregnancy or lactation, hormonal contraceptive use, and active severe infection. CD4⁺CD25⁺FOXP3⁺ Treg cell levels were measured by flow cytometry. Disease activity was assessed using the MEX-SLEDAI score. Spearman’s correlation test was used to analyze the association between Treg levels and disease activity. RESULTS : Of 40 enrolled subjects (39 women, 1 man), 75% were aged 20–44 years. Mucocutaneous manifestations were the most common clinical feature (95%). Nephritis and hematologic involvement were most frequently observed in patients with severe disease activity. A strong negative correlation was identified between CD4⁺CD25⁺FOXP3⁺ Treg cell levels and MEX-SLEDAI scores (R = –0.72, p<0.001), indicating that lower Treg levels were associated with higher disease activity. CONCLUSIONS CD4⁺CD25⁺FOXP3⁺ Treg levels show a significant negative correlation with MEX-SLEDAI disease activity in SLE. Lower Treg cell levels reflect more severe disease activity.
disease progression ; flow cytometry ; systemic lupus erythematosus ; Treg cells

Objective To investigate the common molecular features of immunothrombosis, thus enhancing the comprehension of thrombosis triggered by immune and inflammatory responses and offering crucial insights for identifying potential diagnostic and therapeutic targets. Methods Differential gene expression analysis and functional enrichment analysis were conducted on datasets of systemic lupus erythematosus (SLE) and venous thromboembolism (VTE). The intersection of differentially expressed genes in SLE and VTE with those of neutrophil extracellular traps (NET) yielded cross-talk genes (CG) for SLE-NET and VTE-NET interaction. Further analysis included functional enrichment and protein-protein interaction (PPI) network assessments of these CG to identify hub genes. Venn diagrams and receiver operating characteristic (ROC) curve analysis were employed to pinpoint the most effective shared diagnostic CG, which were validated using a graft-versus-host disease (GVHD) dataset. Results Differential expression genes in SLE and VTE were associated with distinct biological processes, whereas SLE-NET-CG and VTE-NET-CG were implicated in pathways related to leukocyte migration, inflammatory response, and immune response. Through PPI network analysis, several hub genes were identified, with matrix metalloproteinase 9 (MMP9) and S100 calcium-binding protein A12 (S100A12) emerging as the best shared diagnostic CG for SLE (AUC: 0.936 and 0.832) and VTE (AUC: 0.719 and 0.759). Notably, MMP9 exhibited good diagnostic performance in the GVHD dataset (AUC: 0.696). Conclusion This study unveils the common molecular features of SLE, VTE, and NET, emphasizing MMP9 and S100A12 as the optimal shared diagnostic CG, thus providing valuable evidence for the diagnosis and therapeutic strategies related to immunothrombosis. Additionally, the expression of MMP9 in GVHD highlights its critical role in the risk of VTE associated with immune system disorders.
Humans ; Computational Biology/methods* ; Lupus Erythematosus, Systemic/immunology* ; Protein Interaction Maps/genetics* ; Venous Thromboembolism/therapy* ; Matrix Metalloproteinase 9/genetics* ; Extracellular Traps/metabolism* ; Gene Regulatory Networks ; Thrombosis/immunology* ; Graft vs Host Disease/genetics* ; Gene Expression Profiling

Systemic lupus erythematosus (SLE) is a complex autoimmune disease with diverse clinical symptoms, which involves multiple systems and organs such as the kidney, cardiovascular system, and nervous system. The main characteristic of SLE is the mistaken attacks on self-tissues by the immune system, but the specific pathogenesis is still unclear. This paper reviews and compares the modeling mechanisms and main pathological manifestations of spontaneous and experimental mouse models of SLE, which can provide evidences for selecting appropriate mouse models in studies on the pathogenesis, clinical diagnosis and treatment of SLE.
Animals ; Lupus Erythematosus, Systemic/immunology* ; Disease Models, Animal ; Mice ; Humans

Objective To explore the effects of S100 calcium-binding protein A9 (S100A9) gene knockout on the phenotype of systemic lupus erythematosus (SLE) in mice and to clarify the role of S100A9 in the pathogenesis of SLE. Methods Ten female C57BL/6 wild-type and S100A9 knockout (S100A9-KO ) mice were selected, with five wild-type and five S100A9-KO B6 mice receiving imiquimod (IMQ) cream to establish SLE mouse model. The other five wild-type and five S100A9-KO B6 mice were treated as control groups by wiping the skin of the right ear with a cotton swab. After 8 weeks, the mice were sacrificed. The serum was collected from each mouse to detect the levels of anti-double-stranded DNA (dsDNA) antibodies, immunoglobulin G (IgG), B cell activating factor (BAFF), and interleukin 6 (IL-6) using ELISA. The levels of serum creatinine were determined using a sarcosine oxidase method. Urine was collected to measure urinary protein concentration. Kidneys were collected and stained with hematoxylin and eosin (H&E) for evaluating histological changes. Results After IMQ treatment, the length and weight of spleen, levels of serum creatinine, anti-dsDNA antibodies, IgG, BAFF, IL-6, and urinary protein in the IMQ B6 group and IMQ S100A9-KO B6 group were significantly higher than those of the control groups. Lupus-like changes including increased glomerular volume and tubular epithelial swelling were observed in kidneys from the IMQ and IMQ S100A9-KO groups. However, compared with the IMQ B6 group, the IMQ S100A9-KO B6 group exhibited milder levels of serum and urine indicators as well as the lupus-like symptoms. Conclusion IMQ could induce lupus-like symptoms in both wild-type B6 mice and S100A9-KO B6 mice, but the lesions in S100A9 knockout mice are milder. Theses results suggested that S100A9 is involved in and promotes the pathogenesis of SLE.
Animals ; Lupus Erythematosus, Systemic/chemically induced* ; Female ; Calgranulin B/genetics* ; Mice, Knockout ; Mice, Inbred C57BL ; Phenotype ; Mice ; Interleukin-6/blood* ; Disease Models, Animal ; Antibodies, Antinuclear/blood* ; B-Cell Activating Factor/blood* ; Immunoglobulin G/blood* ; Kidney/pathology*

Autophagy is a fundamental biological metabolic process involved in immune defense, material metabolism, and homeostasis and closely linked to immune regulation. Systemic lupus erythematosus (SLE) is a widespread connective tissue disorder primarily resulting from immune system imbalance. Due to the immune system's failure to recognize its own substances, it generates autoantibodies that can affect various tissues and organs, leading to diverse clinical manifestations. The pathogenesis and treatment of SLE are currently under extensive investigation. In normal metabolic processes, autophagy engages in both innate and adaptive immunity, regulates the immune response, and is crucial for maintaining normal immune function and the body's internal homeostasis. Research has indicated that SLE patients exhibit immune dysfunction and altered autophagy levels. Modulating autophagy expression can influence immune system functionality and alleviate SLE symptoms. Additionally, autophagy aids in the innate immune response and adaptive immunity by clearing metabolites and regulating the life cycle of immune cells. Studies suggest that drugs targeting autophagy can positively influence the progression of SLE. This article reviews advancements in research regarding the impact of autophagy on the pathogenesis of SLE through the regulation of immune system functions.
Lupus Erythematosus, Systemic/pathology* ; Autophagy/immunology* ; Humans ; Animals ; Immunity, Innate ; Adaptive Immunity ; Disease Progression ; Immune System/immunology*

The patient was a girl aged 10 years and 10 months, with weakness, pale complexion, and rash as the initial presentation. She had the manifestations of anemia, thrombocytopenia, hematuria-proteinuria with renal insufficiency, hypocomplementemia, polyserositis, and positive anti-nuclear antibody and anti-dsDNA antibody. The girl was initially diagnosed with systemic lupus erythematosus and lupus nephritis. She demonstrated a suboptimal response to methylprednisolone pulse therapy, intravenous immunoglobulin administration, and therapeutic plasma exchange. She had persistent anemia, thrombocytopenia, abnormal renal function, elevated lactate dehydrogenase, decreased complement factors H and I, increased antibodies to C3 converting enzyme, and normal ADAMTS13 activity. She was diagnosed with complement-mediated hemolytic thrombotic microangiopathy secondary to systemic lupus erythematosus. The patient's condition improved after treatment with two doses of eculizumab (600 mg per dose). Patients with systemic lupus erythematosus complicated by thrombotic microangiopathy often have a severe disease course and poor prognosis; therefore, early recognition and aggressive intervention are crucial for improving outcomes.
Humans ; Female ; Lupus Erythematosus, Systemic/drug therapy* ; Thrombotic Microangiopathies/etiology* ; Antibodies, Monoclonal, Humanized/therapeutic use* ; Child

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder affecting multiple systems, characterized by the development of harmful autoantibodies and immune complexes that lead to damage in organs and tissues. Chinese medicine (CM) plays a role in mitigating complications, enhancing treatment effectiveness, and reducing toxicity of concurrent medications, and ensuring a safe pregnancy. However, CM mainly solves the disease comprehensively through multi-target and multi-channel regulation process, therefore, its treatment mechanism is often complicated, involving many molecular links. This review introduces the research progress of pathogenesis of SLE from the aspects of genetics, epigenetics, innate immunity and acquired immunity, and then discusses the molecular mechanism and target of single Chinese herbal medicine and prescription that are commonly used and effective in clinic to treat SLE.
Lupus Erythematosus, Systemic/immunology* ; Humans ; Medicine, Chinese Traditional ; Drugs, Chinese Herbal/pharmacology* ; Animals

Systemic lupus erythematosus (SLE) is the most common form of lupus and a chronic autoimmune disorder that can affect multiple organ systems including the joints, skin, the cardiovascular system and even the central and peripheral nervous system. Although rare, these patients may present with neuropsychiatric symptoms. This patient presented initially with an SLE flare associated with sudden focal to generalized tonic-clonic seizures. Further rheumatologic workup was done which revealed that the patient also has scleroderma, an autoimmune connective tissue that causes inflammation of the skin and other key internal organs. Due to the seizure occurrence, cranial magnetic resonance imaging (MRI) was done which showed incidental mesial temporal sclerosis, which is the scarring of the medial part of the said lobe of the brain. Her overlap syndrome was managed with Hydrocortisone and she was given Valproic acid as her anti-epileptic drug with no recurrence of seizure afterwards.