Analysis of seasonal tendencies in pediatric Henoch–Schönlein purpura and comparison with outbreak of infectious diseases

Hwang, Hyun Ho; Lim, In Seok; Choi, Byung-Sun; Yi, Dae Yong

and we confirmed similar result. [22] [23] [24] On the other hand, we also confirmed a possibility of rotavirus that it has not been previously reported as predisposing cause of HSP. However, we cannot conclude that the incidence of HSP is triggered by only 1 causative virus. Interestingly, unlike the other age groups, the adolescence group showed more HSP patients in summer (August) than during autumn (September to November). Due to the number of patients in this group, it is expected that the overall outbreak of HSP among patients in August was more, though a clear cause for this increase in incidence could not be determined. However, our finding with bocavirus, which appeared to be most active during relatively warm weather, is clearly interesting. Although not investigated in this study, additional studies are needed to determine the association with enteroviruses that occur in summer. Comparison of the virus epidemics based on the age groups of the patients also produced interesting results. Depending on the age group, there were various types of viruses that were temporally associated with HSP. RSV showed a similar temporal pattern in the early childhood group but was not confirmed in all patients and other age groups. While norovirus was associated with HSP in early childhood and middle childhood group, rotavirus that rarely occurred in early adolescence also showed an association with HSP. Even if it occurs after a viral infection, it is difficult to confirm that a single virus is a causative agent. Nevertheless, our study is significant because it suggests the possibility of a causative disease by confirming the coincidence of HSP and some viruses that were not previously linked to HSP such as rotavirus, norovirus, or bocavirus. Further studies are needed to confirm our findings. Because existing predisposing factors are often not directly evidenced by causal relationships, but rather through anecdotal cases, the results of this study about relationship to seasonal variation may raise the possibility of a novel pathogen associated with HSP. However, our study has some limitations. First, we compared the timings when a particular virus was positively identified and the incidence of HSP. The results were confirmed using statistical methods by experts specializing in preventive medicine and statistics. But it was not possible to confirm whether the virus caused HSP. It is known that IgA-containing immune complexes triggered by infectious diseases are deposited on organs such as skin, kidneys, and gastrointestinal tract and can cause HSP, and we can only assume that the viruses suspected of causing HSP have similar mechanisms. [2, 27, 28] However, studies on whether only specific viruses or bacteria cause HSP should be continued. Second, there is a limitation in the extent of virus detection. While the data included HSP outbreaks for all patients <18 years of age in South Korea, virus detection tests were given to only patients with severe respiratory symptoms. Therefore, the patients who were not tested but have symptoms were not included in the study. Also, if the causative virus itself is not as severe as rhinovirus, its detection rate would have been much lower than actual incidence. On the contrary, if there was, for example, an influenza virus epidemic which caused severe symptoms, and relatively more tests were conducted, its actual detection rate would have been higher than that of other viruses. Finally, there is a limita