Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disorder that has multiorgan involvement. The continuation of inflammation in lupus could be attributed to failure of the resolution process because of deficiency of potent endogenous proresolution-inducing molecules such as lipoxin A4 (LXA4), leading to progression and flares of lupus and lupus nephritis. The aim of this study was to assess the levels of urinary LXA4 in SLE patients and in healthy controls, and to correlate them with various clinical and laboratory data as well as renal biopsy and disease activity indices (DAIs). A total of 40 adult female SLE patients were included in this study. Forty healthy women age-matched with SLE patients served as the control group. All patients were subjected to a full assessment of history, clinical examination, assessment of DAIs (SLEDAI and renal SLEDAI), and laboratory investigations including the urinary LXA4/creatinine ratio assessed by enzyme linked immunosorbent assay. Urinary LXA4/creatinine ratio levels were found to be significantly higher in all SLE patients compared with the healthy controls (P = 0.037). The median level of the urinary LXA4/creatinine ratio was lower in SLE patients with nephritis than in patients without nephritis (0.1 and 0.3 ng/ml, respectively), but with no statistical significance (P = 0.11). The urinary LXA4/creatinine ratio levels were found to be significantly lower in SLE patients with cardiovascular manifestations as well as those with neuropsychiatric manifestations (P = 0.009, 0.04 respectively). This was a novel study that was carried out to assess the levels of urinary LXA4 in SLE patients. It showed that the urinary LXA4/creatinine ratio levels were significantly lower in SLE patients with cardiovascular and neuropsychiatric manifestations and nonsignificantly lower in patients with nephritis, suggesting that insufficiency of LXA4 in the human body may be responsible for major organ involvement in SLE patients. Accordingly, LXA4 is suggested to be an inflammatory biomarker not only for lupus nephritis but also for other systemic manifestations in SLE.
Highlights
Systemic lupus erythematosus (SLE) is an autoimmune disorder that has multiorgan involvement
It is noteworthy that Wu et al [15], who studied the temporal changes in blood and urinary lipoxin A4 (LXA4), LTB4, and urinary LTE4 in 49 children with Henoch– Schönlein purpura, showed that blood and urinary LXA4 in the active phase were higher than those of the controls and further increased in early resolution, and this was in contrast to the blood LTB4 and urinary LTB4 and LTE4, which showed an early peak in the active phase and a subsequent decrease during early resolution
Our results showed that the median level of the urinary LXA4/creatinine ratio was lower in SLE patients with nephritis than in patients without nephritis (0.1, 0.3 ng/ml, respectively), but with no statistical significance (P = 0.113)
Summary
Systemic lupus erythematosus (SLE) is an autoimmune disorder that has multiorgan involvement. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by diverse multisystem involvement and the production of an array of autoantibodies. Clinical features in individual patients can be quite variable, ranging from mild joint and skin involvement to severe life-threatening internal organ disease [1]. Renal involvement is common in SLE and is a significant cause of morbidity and mortality. Up to 25% of these patients still develop end-stage renal disease 10 years after the onset of renal compromise. The 5- and 10-year renal survival rates of lupus nephritis in the 1990s ranged between 83–93 and 74–84%, respectively [3]
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