scholarly journals Complement Consumption in Systemic Lupus Erythematosus Leads to Decreased OpsonophagocytosisIn Vitro

2018 ◽  
Vol 45 (11) ◽  
pp. 1557-1564 ◽  
Author(s):  
Amanda Mitander ◽  
Ying Fei ◽  
Estelle Trysberg ◽  
Majd Mohammad ◽  
Zhicheng Hu ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Infection Risk ◽  
Human Neutrophils ◽  
High Dose ◽  
Healthy Individuals ◽  
Systemic Lupus ◽  
Healthy Human ◽  
Infection Incidence ◽  
Host Immune Responses

Objective.Infections remain a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). The high prevalence of infections in SLE is attributed to both the disease and its treatments. The complement system plays an important role in host immune responses against invading microorganisms. We sought to provide the experimental and clinical evidence supporting the hypothesis that low levels of complement factors cause defective complement-mediated opsonization in patients with SLE.Methods.Staphylococcus aureuswas opsonized with sera from healthy individuals (n = 16), SLE patients with normal (n = 5) or low complement (n = 8) levels. Phagocytosis ofS. aureusby healthy human neutrophils was analyzed by an imaging flow cytometry-based method. We retrospectively examined the infection incidence in relation to complement levels in a cohort of 165 patients with SLE during a 1.5-year period. The association was analyzed for infection incidence and disease-related variables.Results.Uptake ofS. aureusby neutrophils was decreased whenS. aureuswas opsonized with sera from SLE patients with low complement levels compared to sera from healthy individuals and SLE patients with normal complement. In our SLE cohort, 44% of patients had at least 1 infection during the 1.5 years. No significant association was observed between complement levels and infection risk. Importantly, high-dose glucocorticoids (GC; prednisone ≥ 10 mg/day) were the most important predictive factor for infections in patients with SLE.Conclusion.Low complement levels affect bacterial opsonization in SLE blood and lead to downregulated phagocytosis by neutrophils. High-dose GC increase the infection risk in patients with SLE.

scholarly journals Serum levels and gene polymorphisms of angiopoietin 2 in systemic lupus erythematosus patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jia-Min Wang ◽  
Wang-Dong Xu ◽  
Zhi-Chao Yuan ◽  
Qian Wu ◽  
Jie Zhou ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Gene Polymorphisms ◽  
Serum Levels ◽  
Healthy Individuals ◽  
Systemic Lupus ◽  
Potential Biomarker ◽  
Angiopoietin 2 ◽  
Inflammatory Autoimmune Diseases

AbstractThis study aimed to discuss association between serum Angiopoietin2 (Ang2) levels, Ang2 gene polymorphisms and systemic lupus erythematosus (SLE) susceptibility. It was carried out by 235 SLE, 342 other inflammatory autoimmune diseases patients and 380 healthy individuals. Serum Ang2 levels was examinated by ELISA, and Ang2 rs12674822, rs1823375, rs1868554, rs2442598, rs3739390 and rs734701 polymorphisms were genotyped using KASP. Increased Ang2 concentrations in SLE patients were observed compared with healthy controls and patients with other inflammatory autoimmune diseases. For allelic contrast, except for rs1823375 (P = 0.058) and rs2442598 (P = 0.523), frequencies of alleles for other polymorphisms were significantly different between SLE patients and controls. Genotypes for rs12674822 (TT), rs1868554 (TT, TA and TT+TA), rs734701 (TT) were negatively correlated with SLE susceptibility (OR = 0.564 for rs12674822; OR = 0.572, OR = 0.625, OR = 0.607 for rs1868554; OR = 0.580 for rs734701). Patients carrying rs1868554 T allele and rs3739390 G allele were more likely to develop hematuria (P = 0.039; P = 0.003). The G allele frequencies of rs12674822 and rs2442598 were higher in SLE patients with proteinuria (P = 0.043; P = 0.043). GC genotype frequency of rs3739390 was higher in patients with ds-DNA (+) (P = 0.024). In summary, SLE had increased serum Ang2, which may be a potential biomarker, and the polymorphisms correlated with SLE.

Increased Serum Soluble OX40 in Patients with Systemic Sclerosis

2008 ◽  
Vol 35 (12) ◽  
pp. 2359-2362 ◽  
Author(s):  
KAZUHIRO KOMURA ◽  
AYUMI YOSHIZAKI ◽  
MASANARI KODERA ◽  
YOHEI IWATA ◽  
FUMIHIDE OGAWA ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Systemic Sclerosis ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Disease Duration ◽  
Tumor Necrosis Factor Receptor ◽  
Healthy Individuals ◽  
Systemic Lupus ◽  
Clinical Associations ◽  
Necrosis Factor

ObjectiveTo determine levels of serum soluble OX40 (also termed CD134, a member of the tumor necrosis factor receptor superfamily) and their clinical associations in patients with systemic sclerosis (SSc).MethodsSerum soluble OX40 levels were examined by ELISA in 53 patients with SSc, 15 patients with systemic lupus erythematosus (SLE), and 32 healthy individuals.ResultsOX40 levels were significantly elevated in SSc patients (125.7 ± 5.7 pg/ml) compared to patients with SLE (80.7 ± 1.7 pg/ml; p < 0.005) and controls (88.2 ± 3.0 pg/ml; p < 0.0001). Elevated OX40 levels were found to be associated with disease duration of less than 2 years (p < 0.05).ConclusionOur results suggest that serum soluble OX40 levels correlate with the early-onset of SSc disease.

Missed hypereosinophilic syndrome in a critically ill patient with systemic lupus erythematosus

2021 ◽  
Vol 14 (1) ◽  
pp. e236592
Author(s):  
Ying Ling ◽  
Mary Jane Bell ◽  
Lisa Chodirker ◽  
Shirley Lake
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Hypereosinophilic Syndrome ◽  
Clinical Manifestations ◽  
Critically Ill Patient ◽  
Total Leucocyte Count ◽  
High Dose ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Systemic Lupus

A high functioning 74-year-old man with systemic lupus erythematosus presented to the emergency department with acute anxiety. He was found to have elevated cardiac enzymes and admitted to the cardiology service for investigation. In hospital, he developed an erythematous papular rash, and deteriorated to being somnolent and bedridden. He was found to have new multiterritory ischaemic strokes. It was eventually noted that he had persistent eosinophilia, present even on admission, which had been overlooked as the total leucocyte count was normal. Serology for antiphospholipid antibody syndrome (APS) was positive. He was diagnosed with hypereosinophilic syndrome (HES) secondary to new APS, and responded to high-dose steroids. This case highlights the importance of fully evaluating a leucocyte differential to make a diagnosis of HES. We discuss the definition, clinical manifestations, diagnostic approach and management of this important condition.

Juvenile-onset systemic lupus erythematosus

2013 ◽  
pp. 948-956
Author(s):  
Louise Watson ◽  
Michael W. Beresford
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Family Involvement ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Juvenile Onset ◽  
Host Immune Responses ◽  
American College Of Rheumatology ◽  
Organ Manifestations ◽  
New Treatment ◽  
Onset Systemic Lupus Erythematosus

Paediatric or juvenile-onset systemic lupus erythematosus (JSLE) is a rare autoimmune condition, differing from the adult form in terms of severity, organ manifestations, and a less striking female predominance. The diagnosis relies on the adult-derived American College of Rheumatology SLE classification criteria. Genetic, autoantibody, and host immune responses, characteristic of this disease, result in a clinically heterogeneous phenotype. A proportion of paediatric SLE patients will have evidence of a genetic deficiency known to be associated with SLE, such as C1q deficiency, and screening for these is required. A challenging diagnosis to make in the younger age group, the management of JSLE compared to adult-onset SLE requires special consideration towards the significant long-term consequences of the disease and treatment toxicity, combined with an onset during a fundamental time with regards to growth and development. A comprehensive, multidisciplinary team approach to the management of JSLE is essential. With a more severe phenotype and limited comorbidities, patients with JSLE represent an invaluable opportunity for investigating the pathogenesis. To date, clinical trials informing interventions in JSLE are very limited and treatment choices rely on the outcome of adult trials. Patient and family involvement in research to improve outcomes and understanding is essential. New treatments, including biological therapies, are becoming available for clinical use and new treatment combinations have been used to induce and maintain clinical remission.

Systemic Lupus Erythematosus and Related Disorders

2014 ◽  
pp. 257-270
Author(s):  
Bonnie L. Bermas
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Central Nervous System ◽  
Nervous System ◽  
Lupus Erythematosus ◽  
Immunosuppressive Agents ◽  
Future Research ◽  
High Dose ◽  
Childbearing Age ◽  
Systemic Lupus ◽  
Multisystem Disease

Systemic lupus erythematosus (SLE) is a multisystem disease that preferentially affects women of childbearing age. This disorder is both more common and more severe in individuals of African and Asian ancestry. The etiology of SLE is not well understood, although genetics and environmental stimuli clearly are involved. Whether this disease is caused by a T-cell, B-cell, or other immunologic malfunction is debated, but all would agree that clearly autoantibodies such as antinuclear antibodies and anti–double-stranded DNA contribute to the pathophysiology of this disorder. This multisystem disease can affect the skin, joints, lungs, heart, kidneys, and central nervous system. Most of the morbidity and mortality is from renal and central nervous system (CNS) involvement, although accelerated atherosclerosis has recently been appreciated as a major contributor to disease burden. The treatment of SLE has improved over the past decade with less reliance on high-dose corticosteroids and more emphasis on immunosuppressive agents. It is our hope that future research into the pathophysiology of this disorder and the development of more specific therapy, such as biologics, will improve the outcome of this disease.

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