Serum Amyloid A Levels Associated with Gastrointestinal Manifestations in Henoch-Schönlein Purpura
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Henoch-Schönlein purpura (HSP) is considered as an immune-mediated inflammatory disease. Serum amyloid A (SAA) is an acute-phase protein with proinflammatory effects. We investigated the levels of SAA in HSP patients and examined whether SAA levels are associated with organ involvement and disease severity. Seventy patients with HSP, including 35 with nephritis (HSPN) and 35 without HSPN, and 20 controls were recruited in our study. SAA levels were measured and other clinical laboratory parameters, including C-reactive protein, erythrocyte sedimentation rate, complement 3 (C3), C4, and immunoglobulin (Ig) A, were recorded. SAA levels were not found to be independently associated with renal, joint involvement, and disease severity. However, higher SAA levels were observed in HSP patients with gastrointestinal (GI) manifestations (p = 0.006, p c = 0.048). Moreover, the levels of SAA were significantly associated with duration of disease (p < 0.005, p c < 0.04). Our findings suggested that SAA was significantly associated with disease duration and GI manifestations in HSP patients.
KEY WORDSHenoch-Schönlein purpura acute-phase protein serum amyloid A disease severity
This study was funded by the supporting program of the Ministry of Human Resource of China Oversea Returned scholars.
- 6.Lin, S.J., J.L. Huang, and K.H. Hsieh. 1998. Clinical and laboratory correlation of acute Henoch-Schönlein purpura in children. Zhonghua Minguo Guo Xiao Er Ke Yi Xue Hui Za Zhi 39: 94–98.Google Scholar
- 13.Visvanathan, S., C. Wagner, J. Rojas, et al. 2009. E-selectin, interleukin 18, serum amyloid A, and matrix metalloproteinase 9 are associated with clinical response to golimumab plus methotrexate in patients with active rheumatoid arthritis despite methotrexate therapy. Journal of Rheumatology 36: 1371–1379.PubMedCrossRefGoogle Scholar
- 22.Cai, H., C. Song, I. Endoh, et al. 2007. Serum amyloid A induces monocyte tissue factor. Journal of Immunology 178: 1852–1860.Google Scholar