Summary
C-Reactive Protein (CRP) is a protein produced by the liver in response to inflammation, infection, and tissue damage. It rises rapidly within 6–8 hours of an inflammatory trigger and falls equally quickly once the cause resolves. CRP is the most widely used clinical marker for detecting acute infection, monitoring chronic inflammatory disease activity, and assessing cardiovascular risk — where high-sensitivity CRP (hs-CRP) is used.
CRP is an acute phase reactant: interleukin-6 (IL-6) and other cytokines released at sites of inflammation stimulate hepatic CRP production. Levels can rise more than 1,000-fold from a baseline of 100 mg/L within hours of a significant bacterial infection.
At the other end of the scale, high-sensitivity CRP (hs-CRP) measures low-level chronic inflammation at concentrations below 10 mg/L. In this range, CRP is a powerful independent predictor of cardiovascular risk: hs-CRP > 3 mg/L is associated with roughly double the cardiovascular event rate compared with < 1 mg/L, even when LDL cholesterol is normal. CRP is also elevated in obesity, type 2 diabetes, autoimmune disease, and NAFLD — reflecting the chronic low-grade inflammation underlying metabolic disease.
What It Is
CRP is a member of the pentraxin family of pattern-recognition molecules. It was originally identified in the serum of patients with pneumococcal pneumonia as a protein that reacted with the C-polysaccharide of Streptococcus pneumoniae — hence its name. It binds to phosphocholine and other damaged cell debris, activating the complement system and promoting phagocytosis.
CRP is produced exclusively by hepatocytes under the control of IL-6 (primarily), IL-1β, and TNF-α. Its half-life is approximately 19 hours, making it a responsive real-time marker of inflammation. Levels normalise within days of resolution.
Conventional CRP assay detects > 5–10 mg/L; high-sensitivity CRP (hs-CRP) is reliable down to 0.1 mg/L. For cardiovascular risk assessment, hs-CRP is used; for infection and acute disease monitoring, conventional CRP is sufficient.
Functions
Infection and inflammation detector
CRP is the most sensitive routine marker for acute bacterial infection — a high CRP in an unwell patient is a key signal to act.
Chronic disease activity monitor
In conditions like rheumatoid arthritis, IBD, and lupus, serial CRP measurements track disease flares and treatment response.
Cardiovascular risk predictor
hs-CRP > 3 mg/L independently doubles cardiovascular event risk — reflecting the role of chronic vascular inflammation in atherosclerosis.
Antibiotic stewardship tool
CRP helps distinguish bacterial (high CRP) from viral (usually low CRP) infections — supporting appropriate antibiotic decisions.
Reference Ranges
C-Reactive Protein (CRP / hs-CRP)
Measured in mg/L| Status | Range (mg/L) | What it means |
|---|---|---|
| Optimal | < 1 | Low cardiovascular risk; no significant acute or chronic inflammation. |
| Low-grade | 1–3 | Mild chronic inflammation — metabolic syndrome, obesity, or subclinical infection. Moderate cardiovascular risk. |
| Elevated | 3–10 | Significant inflammation — investigate for infection, autoimmune disease, or significant cardiovascular risk. |
| Markedly high | > 10 | Acute infection, major tissue damage, or severe autoimmune flare — clinical review required. |
For cardiovascular risk assessment, hs-CRP thresholds of < 1 (low), 1–3 (intermediate), and > 3 mg/L (high) are used. For infection and inflammation monitoring, conventional CRP and clinical context guide interpretation.
Symptoms of Imbalance
CRP itself causes no symptoms — it is a biomarker of the underlying inflammatory process.
- Low CRP indicates no significant inflammation — this is the normal, desirable state
- Symptoms of the underlying cause — infection: fever, pain; autoimmune: joint swelling
- Fatigue and malaise (from systemic inflammation)
- In chronic low-grade elevation: often no specific symptoms
Causes of Imbalance
- Low CRP is normal and desirable
- Very low CRP associated with anti-inflammatory diets, exercise, and healthy weight
- Acute bacterial infection (CRP rises dramatically — often > 50–100 mg/L)
- Autoimmune disease flares (RA, IBD, lupus, vasculitis)
- Tissue damage (surgery, trauma, myocardial infarction)
- Chronic low-grade: obesity, type 2 diabetes, NAFLD, metabolic syndrome
- Malignancy (particularly haematological)
- Viral infections (usually only moderately elevated)
- Smoking — independent CRP raiser
FAQs
Both measure the same protein, but high-sensitivity CRP (hs-CRP) is a more precise assay that can accurately measure concentrations down to 0.1 mg/L — the range relevant for cardiovascular risk. Standard CRP assays are reliable down to 5–10 mg/L, which is sufficient for detecting infection and acute inflammation. When CRP is used for cardiovascular risk stratification, an hs-CRP assay must be specified.
A mildly elevated CRP (1–10 mg/L) in an otherwise well person most commonly reflects low-grade chronic inflammation from obesity, visceral fat, NAFLD, insulin resistance, or smoking. It can also be transiently elevated after minor illness, dental work, or strenuous exercise. If elevated CRP is persistent without obvious cause, further investigation (autoimmune screening, liver function, full blood count) is warranted.
No. While CRP rises dramatically in bacterial infection (often > 50–100 mg/L), it also rises in autoimmune disease flares, tissue damage (heart attack, surgery, trauma), malignancy, and chronic inflammatory conditions. The degree of elevation is a useful guide: CRP > 100 mg/L strongly suggests bacterial infection; CRP 10–100 mg/L warrants clinical review; CRP 1–10 mg/L may reflect chronic low-grade inflammation.
Yes — effectively. Weight loss (particularly visceral fat reduction) is the most impactful intervention. Other evidence-based CRP-lowering strategies include: regular aerobic exercise (reduces CRP by 20–30%), smoking cessation, a Mediterranean-style diet (rich in omega-3s, polyphenols, and fibre), improved sleep quality, and stress reduction. Statins also reduce hs-CRP independently of LDL reduction — the JUPITER trial showed significant cardiovascular benefit in people with elevated hs-CRP and normal LDL.
For most purposes, CRP is preferred. It rises and falls faster than ESR (6–8 hours vs 24–48 hours), making it more responsive to changes in disease activity. CRP is more specific for inflammation, whereas ESR rises with any condition that increases plasma proteins (pregnancy, paraproteinaemia). However, ESR remains elevated longer after an inflammatory episode — useful for tracking conditions like temporal arteritis and polymyalgia rheumatica, where it is specifically validated.
References
- Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation. 2003;107(3):363–369. View source
- Pepys MB, Hirschfield GM. C-reactive protein: a critical update. J Clin Invest. 2003;111(12):1805–1812. View source
- Ridker PM, et al. JUPITER trial: rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195–2207. View source