CRP & hs-CRP
The body's fastest inflammation alarm — and a hidden heart risk predictor
C-reactive protein rises within 6 hours of infection, injury, or autoimmune flare — and falls just as fast when the trigger resolves. At ultra-low concentrations measured by hs-CRP, it independently predicts heart attack risk years before symptoms appear.
CRP is produced by the liver in response to interleukin-6 (IL-6), released at sites of injury or infection. It activates complement and marks pathogens and damaged cells for phagocytosis. Its rapid kinetics — rising within 6–12 hours, doubling every 8 hours at peak — make it the most responsive marker of acute inflammation. At picomolar concentrations measured by hs-CRP, it also independently predicts cardiovascular events in otherwise healthy individuals.
Reference Ranges
How clinicians interpret CRP / hs-CRP results — from optimal to concerning.
⚠ Reference ranges vary by laboratory and assay. Always interpret your result in context of your laboratory's own reference intervals and your clinical presentation.
What raises CRP / hs-CRP
Typically rises to 100–500 mg/L in serious bacterial infection — the most potent CRP driver.
Peaks 48–72h post-op. Failure to fall after day 3 suggests wound infection or anastomotic leak.
RA, vasculitis, IBD — CRP tracks disease activity. SLE is an exception: often low CRP despite high ESR.
Visceral adipose tissue releases IL-6, chronically raising hs-CRP. Independent CVD risk factor in metabolic syndrome.
Cigarette smoke triggers vascular inflammation, raising hs-CRP 0.5–1 mg/L above non-smokers chronically.
Rises 4–6h after MI, peaks at 72h. Elevated hs-CRP post-MI independently predicts re-infarction risk.
What lowers CRP / hs-CRP
Reduce hs-CRP by 30–40% independent of LDL lowering. JUPITER trial showed statin benefit in those with low LDL but elevated hs-CRP.
Regular aerobic exercise lowers hs-CRP by improving insulin sensitivity and reducing adipose inflammation.
Each 1 kg reduction lowers hs-CRP by ~0.13 mg/L — reducing chronic low-grade inflammation of obesity.
CRP halves every 19 hours once the infectious stimulus is cleared — serial daily CRP is a reliable treatment response tool.
Conditions this biomarker signals
When CRP / hs-CRP is outside normal range, these are the most clinically significant possibilities.
CRP > 100 strongly associated with bacterial (not viral) sepsis. Serial rises on antibiotics = treatment failure.
hs-CRP 1–3 mg/L doubles CVD risk independently of LDL. Used in ASCVD risk reclassification.
CRP tracks RA disease activity (DAS28-CRP composite score). Guides treatment escalation.
In active SLE, CRP is often normal despite high ESR and disease activity. High CRP in SLE suggests bacterial co-infection.
Which tests measure this biomarker
CRP / hs-CRP may be included in or ordered alongside these panels.
Acute infection, autoimmune disease monitoring, post-operative surveillance. Detection limit ~3–5 mg/L.
Cardiovascular risk stratification. Same molecule, high-sensitivity assay detecting < 0.5 mg/L.
How CRP activates innate immunity
CRP is not merely a passive marker — it actively participates in innate immunity. Its pentameric ring structure binds phosphocholine on damaged cell membranes and bacterial surfaces, then activates the classical complement pathway (C1q), promoting opsonisation and phagocytosis. The JUPITER trial (17,802 patients) demonstrated statin-mediated 37% CRP reduction and 44% fewer cardiovascular events in patients with elevated hs-CRP but normal LDL — establishing hs-CRP as an independent therapeutic target.
Rises within 6 hours of stimulus
CRP rises within 6–12 hours, doubles every 8 hours at peak, and returns to baseline within days of resolution. This makes CRP the best kinetic inflammation marker — ESR lags by 24–48h and stays elevated for weeks after resolution.
IL-6 is the master CRP switch
IL-6 from macrophages and adipocytes is the primary stimulus for hepatic CRP synthesis. This explains why tocilizumab (anti-IL-6 receptor) dramatically suppresses CRP in rheumatoid arthritis and cytokine release syndrome.
Statins treat inflammation, not just LDL
The JUPITER RCT randomised 17,802 healthy adults with LDL < 130 but hs-CRP ≥ 2 mg/L. Rosuvastatin reduced hs-CRP by 37% and major CV events by 44% — establishing anti-inflammatory benefit independent of LDL lowering.
Clinical use — when and why this is ordered
How clinicians use CRP / hs-CRP in practice — the real-world scenarios where it changes decisions.
Bacterial vs viral distinction
CRP > 50 mg/L strongly favours bacterial infection. Viral illness rarely exceeds 20–30 mg/L. Guides antibiotic stewardship in primary care and ED.
CV risk stratification (hs-CRP)
Added to ASCVD risk calculators when 10-year risk is 7.5–20% (intermediate risk) — hs-CRP ≥ 2 mg/L supports statin initiation.
Post-operative complication detection
CRP > 190 mg/L on day 3 after colorectal surgery has > 90% sensitivity for anastomotic leak.
IBD and autoimmune disease monitoring
CRP tracks mucosal inflammation in Crohn's disease. Component of DAS28 composite disease activity score in RA.