A case of lethal enteroviral haemolytic uraemic syndrome?

IgG, Epstein-Barr virus, measles and rubella were positive but within the normal range, we suspected that the AHS may have been induced by influenza virus infection. Her symptoms diminished following withdrawal of allopurinol and administration of predonisolone. Current hypotheses for mechanisms of the AHS onset include two pathways Fig. 1. First, storage of allopurinol and its metabolite, oxypurinol, may directly inflict cell damage, especially in patients with renal dysfunction. A second possible pathway suggests that a type III allergic reaction caused by allopurinol may induce the re-activation of HHV-6, or activation of other opportunistic viruses, such as cytomegalovirus [2] and Epstein-Barr virus [3], through the activation of Tlymphocytes. Recently, CD46 was identified as a receptor for HHV-6, and it was therefore suggested that this reactivated virus damages cells, including epidermal cells and lymphocytes, via CD46 binding [4]. In the present case, the influenza virus titre was elevated in parallel with the clinical symptoms of AHS, and it is possible that this virus exacerbated the cascade reaction in the same way as do other viruses. We suggest that such community-acquired bacterial and viral infections may also accelerate these cascade reactions and that genetic factors may interact with these events.