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Summary

Background

The long-term prognosis of Henoch–Schönlein purpura (HSP) is determined by the severity of renal involvement, known as HSP nephritis, which varies considerably from patient to patient. There is now increasing evidence that dysregulated cytokine production plays a crucial role in human autoimmune and inflammatory processes.

Aim

To explore the possible contributions of serum antistreptolysin O, C-reactive protein, IgA, interleukin (IL)-6, IL-8, tumour necrosis factor (TNF)-α, anticardiolipin antibody (aCL) and antiphosphatidylserine–prothrombin complex antibody (anti-PSPT) in the pathogenesis of HSP, and to evaluate correlations between those biological parameters and the clinical features.

Methods

Records were reviewed of 58 patients with HSP who presented initially with palpable purpura between 2003 and 2009. Serum IL-6 levels were determined by chemiluminescent enzyme immunoassay, IL-8 levels by ELISA and TNF-α levels by quantitative sandwich enzyme immunoassay. Serum aCL and anti-PSPT levels were measured according to our previously published procedures.

Results

There was a significant correlation between the serum IL-6 and IgA anti-PSPT levels, and also between the serum IL-8 and IgA anti-PSPT levels. Serum IL-8 and IgA aCL levels were both significantly higher in patients with renal involvement than in those without. Serum IL-6 and IgM anti-PSPT levels were also significantly higher in patients with gastrointestinal symptoms than in those without.

Conclusions

We suggest that serum IL-6 and IL-8 associated with antiphospholipid antibodies play a pivotal role in the induction of HSP. Based on our results, IL-8 and IgA aCL levels could be useful as markers to monitor the development of HSP nephritis, and IL-6 and IgM anti-PSPT levels could be used as markers to monitor the development of gastrointestinal involvement.