Clinical significance of serum TNFα and -308 G/A promoter polymorphism in rheumatoid arthritis

Gheita, Tamer A.; Azkalany, Ghada S.; Gaber, Wafaa; Mohey, Abeer

doi:10.1016/j.ejr.2014.07.001

Cited by 36 publications

(14 citation statements)

References 33 publications

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“…However, IL-33 level showed a significant negative correlation with disease duration in years (r =-0.537, P=0.006) where no correlation occurred with TNF-α (r=-0.250, P=0.228). This was in contrast to Gheita et al 21 who reported that the disease duration would predict the TNF-α level (P=0.006).…”

Section: Discussioncontrasting

confidence: 98%

“…This was in agreement with Xu et al 27 who stated that IL-33 may amplify autoantibody induced arthritis by accelerating mast cell maturation and activation, promoting mast cell degranulation in the joints and driving the expression of articular proinflammatory cytokines (IL-1b and TNF-α) 28 . However, such correlation was not noticed with TNF-α level (r=0.011, P=0.959) which was in agreement with Gheita et al 21 who showed that no correlation between TNF-α polymorphism and morning stiffness duration existed.…”

Section: Discussionsupporting

confidence: 88%

“…On comparing the TNF-α level between the three groups, there was a highly statistically significant difference of TNF-α level between RA and control group (P<0.001) and between SLE and control group (P<0.001). Studies done by Klimiuk et al 20 and Gheita et al 21 showed that there was a significant elevation in serum TNF-α level in RA in comparison with controls. Also Sabry et al 9 and Weckerle et al 11 showed that serum TNF-α was significantly higher in SLE than in non-autoimmune controls.…”

Section: Discussionmentioning

confidence: 93%

“…However, Matsuyama et al 8 stated that serum IL-33 level was significantly higher in high disease activity group than in moderate and low activity groups. While Gheita et al 21 showed that patients with GA genotype of TNF-α polymorphism showed a significant negative correlation of the serum TNF-α level with the DAS28 (r=-0.66, P=0.038 )…”

Section: Discussionmentioning

confidence: 95%

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Does Novel IL-33 Correlates with TNF-α in RA and SLE ?

Dwedar

Awad

Raafat³

2015

EJMM

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Background: Production of high amounts of inflammatory cytokines plays direct role in disease pathogenesis, including that of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Objectives: To investigate whether serum levels of novel IL-33 and TNF-α are higher in Egyptian RA and SLE patients than controls and to compare serum levels of the novel IL-33 with TNF-α in RA and SLE with assessing their correlation to clinical disease activity and laboratory findings. Methodology: 24 SLE, 25 RA and 25 controls were enrolled in this study. Disease activity was evaluated using SLEDAI for SLE patients and DAS 28 for RA patients. IL-33 and TNF-α serum levels were determined using sandwich enzyme immunoassay. Results: A significant statistical difference of IL-33 level between SLE & RA groups (P=0.002) and between SLE & control groups existed (P<0.001). However, a non-significant difference existed between RA & control groups (P=0.340). There was a significant statistical difference of TNF-α level between SLE & control groups (P<0.001) and between RA & control groups (P<0.001), which didn't exist between RA & SLE groups (P=0.070). A significant positive correlation of serum IL-33 level with serum TNF-α level in SLE patients occurred (r=0.505, P=0.012), which was not found in RA (r=-0.023, P=0.912) or in the controls (r=-0.168, P=0.601). A significant positive correlation was found between TNF-α level and SLE patients with high disease activity (r=0.446 , P=0.029), which didn't exist with IL-33 (r=0.227, P=0.286). There was no correlation between serum IL-33 and DAS 28 (r=0.205, P=0.326), however a negative correlation occurred with TNFα (r=-0.404, P=0.045). Conclusion: Serum levels of TNF-α and novel IL-33 were higher in RA and SLE Egyptian patients than controls. A significant positive correlation occurred between serum IL-33 and serum TNF-α in SLE but not in RA patients. Most clinical and laboratory variables in RA and SLE patients did not correlate with either serum IL-33 or TNF-α levels.

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Section: Discussioncontrasting

confidence: 98%

Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 95%

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Does Novel IL-33 Correlates with TNF-α in RA and SLE ?

Dwedar

Awad

Raafat³

2015

EJMM

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“…Rheumatoid arthritis (RA) is a chronic disease characterized by synovitis, increased inflammatory markers and progressive bone and cartilage erosion [1]. Cytokine imbalance has been considered to play a role in the pathogenesis of RA in several Egyptian studies [2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-34 in the Serum and Synovial Fluid of Rheumatoid Arthritis Patients: Relation to Disease Activity and Radiographic Damage

et al. 2018

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Background Interleukin 34 (IL-34) is a recently discovered proinflammatory cytokine that can promote inflammation and osteoclastogenesis in arthritic joints. In this study, we tried to assess the serum and synovial fluid (SF) levels of IL-34 in rheumatoid arthritis (RA) patients, and to determine its relationship with disease activity and radiographic damage. Patients and methods ELISA was used to evaluate IL-34 levels in the serum of RA patients (n=50), osteoarthritis (OA) patients (n=28), and healthy control subjects (n=20) and in SF isolated from RA and OA patients. Disease activity in RA patients was assessed using the disease activity score-28 (DAS 28). The extent of radiographic joint damage, narrowing, and erosions was assessed. Results Serum IL-34 level was significantly elevated in RA patients compared to that in OA patients and healthy controls (P<0.0001). Synovial IL-34 level was also significantly elevated in RA patients compared to that in OA patients (P=0.0004). Serum and synovial IL-34 levels were significantly higher in cases that were rheumatoid factor (RF) positive (n=28) compared to the levels in RF-negative RA cases (n=22) (P=0.03 and P=0.04, respectively). Serum and synovial IL-34 levels were positively correlated with RF (r=0.43, P=0.02 and r=0.39, P=0.03, respectively), and with the extent of radiological damage (SENS) (P=0.0002 and P<0.0001, respectively). However, no significant correlation between IL-34 levels and disease activity was found. Conclusion IL-34 appears to play a key role in the pathogenesis of RA and contribute to bone destruction, making it a potential therapeutic target in the management armamentarium of the disease.

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