The potential use of serum interleukin-21 as biomarker for lupus nephritis activity compared to cytokines of the tumor necrosis factor (TNF) family

Lupus ◽  
2022 ◽  
pp. 096120332110637
Author(s):  
Hend Shater ◽  
Mary Fawzy ◽  
Alyaa Farid ◽  
Azza El-Amir ◽  
Salwa Fouad ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
B Lymphocyte ◽  
Activity Index ◽  
Characteristic Curve ◽  
Serum Levels ◽  
Potential Biomarker ◽  
Necrosis Factor

Objective Lupus nephritis (LN) is a significant consequence of systemic lupus erythematosus (SLE). To the best of our knowledge, this is the first work that focuses on evaluation of serum interleukin (IL-) 21 as a diagnostic biomarker of LN activity, compared to B lymphocyte stimulator (BlyS), tumor necrosis factor ligand superfamily member 13 (TNF-SF13), and traditional techniques of active LN attempting to compare their diagnostic usefulness. Methods Serum levels of IL-21, BlyS, and TNF-SF13 during LN were investigated. Twenty-five biopsy-proven, active LN female patients and 15 SLE patients without active LN and 20 healthy controls (HCs) joined this work. Results Serum IL-21 level was significantly higher in active LN group than in inactive LN group. Correlation analysis showed that serum IL-21 levels were significantly correlated with total SLEDAI (r = 0.41, p = 0.03), renal-SLEDAI (r = 0.48, p = 0.04), renal activity index (AI) (r = 0.93; p < 0.001), and 24-h proteinuria (r = 0.51; p > 0.008). Receiver operating characteristic curve (ROC) revealed the ability of serum IL-21 to discriminate between active and inactive LN with 70% sensitivity at >240 pg/ml cutoff point (AUC 0.809). Conclusion For Egyptian SLE patients, serum levels of IL-21 were superior to TNF-SF13 and BlyS and correlated significantly with the activity indexes of LN, indicating a promising role as a potential biomarker of active LN.

scholarly journals Serum tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and IL-17 levels are associated with disease activity in systemic lupus erythematosus patients with and without nephritis

2019 ◽  
Vol 8 (3) ◽  
pp. 204-210
Author(s):  
Mohammadreza Nakhjavani ◽  
Sima Abediazar ◽  
Amir Ghorbanihaghjo ◽  
Niloofar Esmaeili ◽  
Tala Pourlak ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Disease Activity ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Activity Index ◽  
Renal Involvement ◽  
Clinical Manifestations ◽  
Serum Levels ◽  
Systemic Lupus ◽  
Necrosis Factor

Introduction: Lupus nephritis (LN) is one of the most severe signs of systemic lupus erythematosus (SLE) and rapid diagnosis of kidney damage remains an important concern for LN. Objectives: The aim of this study was to investigate the association of the serum levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and interleukin 17 (IL-17) with SLE severity, renal involvement, and other clinical manifestations in lupus patients. Patients and Methods: In order to determine a better biomarker for the detection of renal damage, this study evaluated the ability of serum TWEAK (sTWEAK) and IL-17 in lupus patients with (n=25) and without (n=25) nephritis and healthy controls (n=39). Moreover, it compared the levels of these cytokines with disease activity and chronicity as well as traditional serum markers including complement C3 and C4, creatinine, and proteinuria in lupus patients. Results: Increased levels of sTWEAK and IL-17 were observed in SLE and LN groups compared to healthy controls and non-LN groups, respectively. Significant positive associations were observed between serum TWEAK and IL-17 levels and systemic lupus erythematosus disease activity index (SLEDAI), proteinuria, nephritis activity index, and some clinical manifestations (P<0.05). Discriminating the ability of the studied cytokines were not better than the utility of any markers individually. Conclusion: The serum levels of TWEAK and IL-17 in the SLE and LN groups were significantly higher than the control group and both markers were indicative of the renal disease severity; therefore, they could possibly indicate renal involvement in the lupus patients.

scholarly journals Oligoclonal bands and levels of interleukin 4, interleukin 10, and tumor necrosis factor alpha in idiopathic intracranial hypertension Egyptian patients

2019 ◽  
Vol 55 (1) ◽  
Author(s):  
Mohamed S. El-Tamawy ◽  
Maha A. Zaki ◽  
Laila A. Rashed ◽  
Eman H. Esmail ◽  
Shaimaa Shaheen Mohamed ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Intracranial Hypertension ◽  
Idiopathic Intracranial Hypertension ◽  
Tumor Necrosis ◽  
Serum Levels ◽  
Interleukin 4 ◽  
Oligoclonal Bands ◽  
Control Groups ◽  
And Control ◽  
Necrosis Factor

Abstract Background Idiopathic intracranial hypertension (IIH) is a neurological disorder of unknown pathophysiology with many proposed theories that involve CSF dynamics but recently, involvement of inflammatory and autoimmune processes has been postulated. Objectives To investigate presence of oligoclonal bands (OCB) in cerebrospinal fluid (CSF) and serum cytokine level in patients with IIH. Methods This study was conducted on 27 IIH female patients and 21 age- and sex-matched control groups. Patient and control groups were subjected to measurement of interleukin-4 (IL-4), IL-10, and tumor necrosis factor α (TNF-α) levels in serum, and CSF oligoclonal bands was measured in the IIH patient group. Body mass index (BMI) was measured to both patients and control. Results Serum levels of IL-4, IL-10, and TNF alpha were significantly higher in IIH patients than controls (p <  0.001); 22% of IIH patients had positive OCB in CSF. There was a statistically significant difference regarding TNF-α level in OCB-positive and OCB-negative patients being higher in positive patients. No statistically significant correlation was found between serum levels of IL-4, IL-10, TNF-α, and BMI. Conclusion Autoimmune inflammatory process may play a role in pathophysiology of IIH.

scholarly journals Low BASDAI score alone is not a good predictor of anti-tumor necrosis factor treatment efficacy in ankylosing spondylitis: a retrospective cohort study

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Bora Nam ◽  
Bon San Koo ◽  
Tae-Han Lee ◽  
Ji-Hui Shin ◽  
Jin-Ju Kim ◽  
...  
Keyword(s):  
Cohort Study ◽  
Ankylosing Spondylitis ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Retrospective Cohort Study ◽  
Retrospective Cohort ◽  
Tumor Necrosis ◽  
Activity Index ◽  
Rank Test ◽  
Necrosis Factor

Abstract Background The purpose of this study was to determine the prevalence of high disease activity as measured using the Ankylosing Spondylitis Disease Activity Score (ASDAS) in ankylosing spondylitis (AS) patients who nonetheless have low Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) scores after anti-tumor necrosis factor (TNF) treatment. Its clinical impact on anti-TNF survival was also investigated. Methods We conducted a single-centre retrospective cohort study of AS patients having low BASDAI scores (< 4) and available ASDAS-C-reactive protein (CRP) data after 3 months of first-line anti-TNF treatment. Patients were grouped into high-ASDAS (≥ 2.1) and low-ASDAS (< 2.1) groups according to the ASDAS-CRP after 3 months of anti-TNF treatment. Their characteristics were compared. And survival analyses were carried out using Kaplan–Meier curves and log-rank test with the event being discontinuation of anti-TNF treatment due to lack/loss of efficacy. Results Among 116 AS patients with low BASDAI scores after 3 months of anti-TNF treatment, 38.8% were grouped into the high-ASDAS group. The high-ASDAS group tended to have greater disease activity after 9 months of treatment (BASDAI 2.9 ± 1.1 vs. 2.3 ± 1.4, p=0.007; ASDAS-CRP 1.8 ± 0.6 vs. 1.5 ± 0.7, p=0.079; proportion of high ASDAS-CRP 27.8% vs. 13.8%, p=0.094) and greater risk of discontinuing anti-TNF treatment due to lack/loss of efficacy than the low-ASDAS group (p=0.011). Conclusions A relatively high proportion of AS patients with low BASDAI scores had high ASDAS-CRP. These low-BASDAI/high-ASDAS-CRP patients also had a greater risk for discontinuation of anti-TNF treatment due to low/lack of efficacy than the low-ASDAS group. The use of the ASDAS-CRP alone or in addition to the BASDAI may improve the assessment of AS patients treated with anti-TNF agents.

Tumor necrosis factor receptor II and PTPN22 genes polymorphisms and the risk of systemic lupus erythematosus in Egyptian children

Lupus ◽  
2021 ◽  
pp. 096120332110203
Author(s):  
Riham Eid ◽  
Ayman Hammad ◽  
Maha Abdelsalam ◽  
Aya Ahmed Fathy ◽  
Dena M Abd-El Ghafaar ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Tumor Necrosis Factor ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Tyrosine Phosphatase ◽  
Tumor Necrosis Factor Receptor ◽  
Clinical Manifestations ◽  
Systemic Lupus ◽  
Egyptian Children ◽  
Necrosis Factor

Background Many genes have been implicated in the pathogenesis of systemic lupus erythematosus (SLE). Tumor necrosis factor (TNF) is a potent cytokine stimulator acting through 2 cell surface receptors (TNFR I and II). TNFRII gene which controls expression of these receptors has been linked to SLE susceptibility through promoting apoptosis. Also; Protein tyrosine phosphatase non receptor 22 (PTPN22) gene enhances intrinsic phosphatase activity of T lymphocytes leading to their dysregulation and stimulates autoimmune process of lupus and its rs2476601 has been linked to susceptibility to thyroiditis in SLE patients in few studies. Objectives (i) to investigate the correlation between 2 SNPs of TNFR II and PTPN22 genes and SLE susceptibility in a cohort of Egyptian children compared to controls (ii) and to investigate their possible association with different clinical presentations of the disease in children. Subjects and methods Typing of TNFR II rs1061622 and PTPN22 rs2476601 SNPs were done using polymerase chain reaction-restriction fragment length polymorphism for 74 children with SLE and 100 matched healthy controls. Results Children with SLE had more frequent G allele and GG genotype of TNFR II rs1061622 ( p < 0.001) and more T allele and TT genotype of PTPN22 rs2476601 ( p = 0.012 and <0.001, respectively) compared to controls. Only 6 patients (8%) had thyroiditis (hypothyroidism) with T allele and TT genotype of PTPN22 1858 T more prevalent in those patients versus those without thyroiditis ( p ≤ 0.001). Apart from, thyroiditis, no significant association was found between genotypes and alleles frequencies of the 2 studied SNPs and other clinical manifestations of the disease. Conclusion The G allele and GG genotype of TNFR II rs1061622 and T allele and TT genotype of PTPN22 rs2476601 genes polymorphism can be considered as risk factors for the development of SLE. The presence of the T allele of PTPN22 rs2476601 may increase the risk of concomitant thyroiditis in Egyptian children with SLE but further studies are required to confirm this finding as thyroiditis was reported only in few cases in this study.

scholarly journals Increased Serum Levels of Tumor Necrosis Factor-Alpha, Resistin, and Visfatin in the Children with Autism Spectrum Disorders: A Case-Control Study

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Mohammad Ali Ghaffari ◽  
Elham Mousavinejad ◽  
Forough Riahi ◽  
Masoumeh Mousavinejad ◽  
Mohammad Reza Afsharmanesh
Keyword(s):  
Autism Spectrum Disorders ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Serum Levels ◽  
Autism Spectrum ◽  
Necrosis Factor Alpha ◽  
Children With Asd ◽  
Factor Alpha ◽  
Spectrum Disorders ◽  
Necrosis Factor

Background. Autism spectrum disorders (ASDs) are complex disorders where the pathogenesis is not fully understood. Several proinflammatory and immunoinflammatory disturbances have been observed in the etiology of ASD. There is, however, limited knowledge on variations of adipokines in ASD. The present study aimed to analyze the serum levels of resistin, visfatin, and tumor necrosis factor-alpha (TNF-α) in children with ASD in relation to body weight, gender, and ASD severity level. Method. In total, 30 children with ASD (mean age: 7.72±2.65 y; range; 4–12 y) and 30 healthy children (mean age: 8.4±2.66 y; range: 4–12 y), including males and females, were matched for age, gender, and body mass index (BMI). Serum samples were collected, and visfatin, resistin, and TNF-α serum levels were measured using an enzyme-linked immunosorbent assay (ELISA) kit. Result. Serum visfatin, resistin, and TNF-α levels in children with ASD were significantly higher than that in the healthy patients (p<0.05). Two significant correlations were found: a correlation between resistin and visfatin with TNF-α in children with ASD (R = 0.8 and R = 0.62, resp.) and a correlation between resistin and visfatin in children with ASD (R = 0.66). Conclusion. Higher TNF-α, resistin, and visfatin levels were found in children with ASD in comparison with controls, suggesting that elevated levels of serum proinflammatory agents may be implicated in the pathophysiology of ASD.

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