کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3348841 | 1407788 | 2016 | 6 صفحه PDF | دانلود رایگان |

BackgroundSystemic lupus erythematosus (SLE) is characterized by a vicious cycle maintaining systemic inflammation. It starts by autoantibody production, immune complex formation and complement activation that contribute to inflammation, tissue damage and further autoantibody production.Aim of the workTo evaluate the association between the auto-antibodies (abs), circulating immune complexes (CIC), and complement activity in SLE patients.Patients and methodsThis study involved 30 female SLE patients analyzed for autoantibodies, complement profile including complement hemolytic 50 (CH50), alternative pathway 50, factor B, C1q, C2, C3 and C4 as well as C1q-CIC. SLE disease activity was assessed by the SLE Disease Activity Index (SLEDAI).ResultsThe age of patients was 34 ± 12.8 years, disease duration was 5.2 ± 3.2 years and their mean SLEDAI was 9.96 ± 4.2. Anti-SSA, anti-dsDNA, anti-C1q abs, and CIC were detected in 36.7%, 50%, 50% and 30% of patients, respectively. Anti-SSA were higher in patients with lower compared to normal CH50 activity and C3 level (24.7 vs 88.6 U/ml; p = 0.002 and 118.6 ± 25.18 U/ml vs 15.9 ± 7.3; p < 0.0001 respectively) than the other autoantibodies. Increased CIC were higher in patients with lupus nephritis and were associated with anti-SSA, anti-SSB, anti-C1q, anti-Sm and in patients with low CH50 activity. The CIC significantly correlated with anti-C1q (r = 0.69, p < 0.0001), anti-SSA (r = 0.5, p = 0.005) and negatively with CH50 (r = −0.4, p = 0.046).ConclusionsThe current study confirms that the etiopathogenic anti-SSA autoantibodies are the most associated with hypocomplementemia in SLE. This would stimulate future researches for validation of predictive biomarkers earlier than hypocomplementemia which is still the major unmet need in lupus research and patient care.
Journal: The Egyptian Rheumatologist - Volume 38, Issue 3, July 2016, Pages 171–176