The Pathogenesis of Henoch-Schönlein Purpura by Malaria

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Sir, We read with great interest the recent contribution by Thapa et al. They reported a 9-year-old boy with Henoch–Schonlein purpura (HSP) triggered by falciparum cerebral malaria and speculated that HSP may be associated with increased IgA levels and reduced factor XIII levels. However, we would like to add some possible mechanisms to the development of HSP by cerebral malarial infection. Davin et al suggested that a significant increase in IgA plasma levels might be related to an impairment of the reticuloendothelial system (RES) function during the acute phase of HSP. Similarly, Mibei et al reported that a reduction of the clearance of immunoglobulins by downregulation of Fc receptors might explain the association of both increased immunoglobulin levels and circulating immune complexes with cerebral malaria. Troye-Blomberg et al also showed that elevated levels of serum antibodies to activating malaria antigens are associated with the production of interleukin-4 (IL-4) by activated human T cells, which can upregulate Fc receptors for IgE (FceRII) on macrophages that could lead to the release of tumor necrosis factor (TNF)-a, a potent proinflammatory cytokine elevated in children with cerebral malaria. Because TNF-a is regarded as one of the contributing factors to the development of HSP, and Kawasaki et al described that serum IL-4 concentrations were significantly elevated at the acute phase in HSP patients, there is a possibility that the dominance of Th-2 cytokines in malarial infection might affect the development of HSP, which is often associated with elevated IgE. Therefore, we speculate that not only increased IgA levels due to reduced Fc-receptor function in RES system but also elevated IL-4, TNF-a, and IgE levels might contribute to the development of HSP triggered by falciparum cerebral malaria. However, further studies are necessary to elucidate whether decreased factor XIII levels themselves during malarial infection could contribute to the development of HSP, because they are often considered to be a secondary process by inflammatory reaction due to vasculitis rather than a primary process.