Background/Purpose

: Systemic lupus erythematosus (SLE) is characterized by autoantibody production and immune complex deposition which trigger both a local and systemic inflammatory response. The continuation of inflammation could be due to failure of the healing process resulting from insufficiency of the pro-resolution lipid mediators such as lipoxin A4 (LXA4) which might lead to progression and flares of lupus. Thus, we assessed the levels of serum and urinary LXA4 in SLE patients and in healthy controls, and correlated them with various clinical and laboratory data as well as renal biopsy and disease activity indices.

Methods

Forty female SLE patients, diagnosed according to the ACR revised criteria for SLE, were included in this study as well as forty healthy age & sex matched subjects who served as the control group. All patients were subjected to full history taking, clinical examination, assessment of disease activity (SLEDAI and renal SLEDAI), laboratory investigations including serum LXA4 and urinary LXA4/creatinine ratio using Enzyme Linked Immunosorbent Assay (ELISA) and renal biopsy. The SLE patients were divided into 2 groups:  Group I: 20 patients without nephritis and Group II: 20 patients with nephritis. Statistical analysis was done using SPSS computer software package, version 15.0, 2006.

Results

Urinary LXA4/creatinine ratio levels were significantly higher in all SLE patients when compared to healthy controls (p=0.037). The median level of urinary LXA4/ creatinine ratio was lower in SLE patients with nephritis than those without nephritis (0.1, 0.3 ng/ml respectively), but this difference was not statistically significant (p=0.11). The urinary LXA4/creatinine ratio levels were significantly lower in SLE patients with cardiovascular manifestations, as well as those with neuropsychiatric manifestations (p=0.009, 0.04 respectively).There was no significant statistical correlation between serum LXA4 and urinary LXA4/creatinine ratio (r=0.065, p=0.7). There was a positive significant correlation only between urinary LXA4 /creatinine ratio and ESR (p=0.008), but no significant correlation between serum LXA4 and urinary LXA4/creatinine ratio and other laboratory parameters including anti-ds DNA, C3 and C4. There was no significant statistical correlation between the level of serum LXA4 and urinary LXA4/creatinine ratio and activity scores (SLEDAI and renal SLEDAI) in all SLE patients. Also, there was no significant difference between WHO classes of Lupus nephritis in SLE patients as regards serum LXA4 and urinary LXA4/creatinine ratio.

Conclusion

This is a novel study that showed that the urinary LXA4/creatinine ratio levels were significantly lower in SLE patients with cardiovascular and those with neuropsychiatric manifestations, however, it was non significantly lower in patients with nephritis. This may suggest that insufficiency of LXA4 may be responsible for some of the systemic manifestations of SLE, making the disease progressive and more serious. Accordingly, LXA4 could be an inflammatory biomarker for systemic manifestations in SLE patients.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/is-liopxin-a4-a-biomarker-for-systemic-lupus-erythematosus/