Pulmonary edema in pediatric patients with EV71 brainstem encephalitis was associated with a 64.3% mortality rate, elevated inflammatory cytokines, and lymphocyte depletion.
Observational (n=73)
What are the immune mechanisms and cytokine profiles associated with pulmonary edema in pediatric patients with EV71 brainstem encephalitis?
EV71-associated pulmonary edema in pediatric brainstem encephalitis is characterized by an extensive inflammatory response with elevated IL-10, IL-13, and IFN-gamma, alongside lymphocyte depletion.
Taiwan experienced several epidemics of enterovirus 71 (EV71) infections, which were associated with brainstem encephalitis (BE) and pulmonary edema (PE). To elucidate the role of immune mechanisms in the pathogenesis of BE caused by EV71 and its fatal complication, PE, we analyzed the laboratory findings, cytokine, and immunophenotypes of 73 EV71-infected patients with BE. Patients were stratified by disease: PE (n=14), autonomic nervous system (ANS) dysregulation (n=25), and isolated BE (n=34). The mortality rate for PE was 64.3%. Leukocytosis and thrombocytosis were significantly more frequent among patients with PE. A significant elevation of plasma interleukin (IL)-10, IL-13, and interferon (IFN)-gamma levels observed in patients with PE. Patients with PE also had lower circulating CD4(+) T cells, CD8(+) T cells, and natural killer (NK) cells. An extensive peripheral and central nervous system inflammatory response with abnormal IL-10, IL-13, and IFN-gamma cytokine production and lymphocyte depletion appears to be responsible for the pathogenesis of EV71-associated PE.
Wang et al. (Fri,) conducted a observational in Enterovirus 71 brainstem encephalitis (n=73). Pulmonary edema vs. Autonomic nervous system dysregulation or isolated brainstem encephalitis was evaluated on Mortality rate. Pulmonary edema in pediatric patients with EV71 brainstem encephalitis was associated with a 64.3% mortality rate, elevated inflammatory cytokines, and lymphocyte depletion.