What is the Origin of High-Sensitivity C-Reactive Protein (hs-CRP)?

C-Reactive Protein was first identified in the 1930s, named for its ability to bind to the C-polysaccharide of Streptococcus pneumoniae. The subsequent development of the high-sensitivity assay allowed for the precise measurement of the lower, chronic levels of inflammation relevant to cardiovascular risk, distinguishing it from the massive elevations seen in acute infections. This technological refinement transformed CRP from an acute infection marker into a prognostic indicator of chronic disease.

What is the Mechanism of High-Sensitivity C-Reactive Protein (hs-CRP)?

In response to inflammatory signals, primarily Interleukin-6 (IL-6), hepatocytes in the liver rapidly increase the synthesis and secretion of CRP into the bloodstream. Once circulating, CRP functions as an opsonin, binding to damaged cells and pathogens to facilitate their clearance by the immune system. Elevated hs-CRP, even at low levels, reflects a persistent activation of this inflammatory cascade, often driven by visceral adiposity or hormonal imbalances, which contributes to the initiation and progression of atherosclerotic plaque formation.

High-Sensitivity C-Reactive Protein (hs-CRP)

Meaning

A clinically valuable, non-specific biomarker of systemic low-grade inflammation, measured using a high-sensitivity assay capable of detecting subtle elevations in circulating C-Reactive Protein (CRP) levels. CRP is an acute-phase reactant protein synthesized primarily by the liver in response to inflammatory cytokines. Elevated hs-CRP levels are clinically utilized not only to detect chronic inflammatory states but also as an independent risk factor for cardiovascular disease and metabolic syndrome, often reflecting underlying hormonal and endothelial dysfunction. Monitoring this marker is an integral part of proactive health and longevity assessments.

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