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Moreover, nonsteroidal anti-inflammatory drugs (NSAIDs), prototypic inhibitors of cyclooxygenase (COX) activity and PGE2 production, can trigger or worsen the disease (51, 52)

This state is marked by more pronounced systemic-inflammatory-response features than in canonical and low-grade inflammation, including cytokine elevations by orders of magnitude, coagulopathy with systemic microthrombosis, systemic tissue injury, and activation of the hypothalamicpituitaryadrenal distress axis, and therefore requires integrated criteria for differential diagnosis [926]

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