Does canakinumab reverse overexpression of inflammatory response genes in tumour necrosis factor receptor-associated periodic syndrome?
These gene expression data support a model in which canakinumab produces clinical benefit in TRAPS by increasing neutrophil apoptosis and reducing pro-inflammatory signals resulting from the inhibition of IL-1β. Notably, treatment normalised the overexpression of TNFRSF1A, suggesting that canakinumab has a direct impact on the main pathogenic mechanism in TRAPS.
Based on the low frequency of illness, the absence of stage II disease, and the inability to establish the efficacy of early antibiotic treatment, we suggest that physicians not routinely use prophylactic antibiotics for deer tick bites.