C-reactive protein

CRP is a pentameric protein produced by hepatocytes as part of the acute-phase response, primarily driven by IL-6 (also IL-1 and TNF-alpha). It functions in innate immunity by binding to phosphocholine on damaged cells and microbial surfaces, activating the classical complement pathway and promoting opsonization for phagocytosis.

Clinically, CRP is a nonspecific but sensitive marker of inflammation. It rises rapidly (within hours) and falls quickly once the inciting cause resolves, making it useful for monitoring disease activity and response to treatment—more dynamic than ESR, which rises and falls more slowly. Elevated CRP is seen in bacterial infections (often markedly elevated, e.g., >100 mg/L), autoimmune/inflammatory conditions (rheumatoid arthritis, IBD, vasculitis), tissue necrosis (MI, malignancy), and postoperative states.

A high-sensitivity CRP (hs-CRP) assay is used to assess cardiovascular risk, as low-grade vascular inflammation contributes to atherosclerosis; hs-CRP >3 mg/L is associated with increased risk of cardiovascular events and is sometimes used to guide statin therapy (e.g., JUPITER trial).

CRP is less useful in distinguishing bacterial vs. viral infection compared to procalcitonin, and it does not indicate the source or cause of inflammation—it must be interpreted alongside clinical context and other markers (ESR, procalcitonin, WBC count). Notably, CRP may remain normal in certain conditions like SLE flares (unless serositis or infection is present), a classic board-relevant pearl distinguishing it from other autoimmune conditions like RA where CRP/ESR are typically elevated.