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Invasive procedures were reserved exclusively for managing refractory complications, such as infected necrotizing pancreatitis or persistent pseudocyst-related symptoms ( A critical driver of AP pathogenesis was the dysregulated activation of the nucleotide oligomerization domain (NOD)-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, a cytosolic multiprotein complex that orchestrates caspase-1-mediated maturation of pro-inflammatory cytokines interleukin-1 (IL-1) and IL-18, as well as gasdermin D (GSDMD)-dependent pyroptotic cell death (Martinon et al., 2002)

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