Reading inflammatory markers: CRP, hs-CRP, ESR and ferritin
CRP, hs-CRP, ESR and ferritin all flag inflammation, but they answer different questions. CRP and ESR show whether inflammation is present and roughly how much; high-sensitivity CRP (hs-CRP) measures the same protein at much lower levels to gauge long-term cardiovascular risk; and ferritin, mainly an iron-storage protein, doubles as an acute-phase reactant that rises with inflammation and can mask iron deficiency. None of them tells you the cause. This guide explains what each measures, how they differ, what raises them benignly versus concerningly, and how to read them together using UK reference ranges.
Key facts
- CRP is fast and fairly specific: it rises 6 to 12 hours after a trigger, peaks around 48 hours, with a half-life of about 19 hours. Most UK labs flag it above about 5 mg/L.12
- Standard CRP cannot reliably read below about 3 to 5 mg/L; high-sensitivity CRP reads down to roughly 0.3 mg/L, which is what makes it useful for cardiovascular risk.3
- ESR is slower and less specific: it reflects plasma proteins indirectly, takes days to move, and rises with age and in women.4
- Ferritin is an acute-phase reactant as well as an iron store, so a normal or high value can hide genuine iron deficiency when inflammation is present.7
What each marker actually measures
C-reactive protein (CRP) is made by the liver in response to interleukin-6, a signal released during infection, injury and inflammation. The liver ramps it up and down fast, so CRP works almost like a real-time gauge: it climbs within hours, peaks around 48 hours, and falls with a half-life of roughly 19 hours once the stimulus settles.1 That speed is its main advantage over ESR.
High-sensitivity CRP (hs-CRP) is the same protein measured with a more sensitive method. An ordinary CRP assay is built for the large rises of infection, with a floor around 3 to 5 mg/L; the high-sensitivity assay reads down to about 0.3 mg/L, letting it tell a CRP of 0.6 from one of 2.4: meaningless for infection, meaningful for vascular risk.3
Erythrocyte sedimentation rate (ESR) is indirect: it measures how fast red cells settle in a thin tube over one hour. When inflammatory proteins such as fibrinogen and immunoglobulins rise, red cells clump and sink faster, so ESR is a sluggish, downstream reflection that lags CRP and is swayed by non-inflammatory factors.4
Ferritin mainly stores iron, but the liver also raises it during inflammation, making it a positive acute-phase reactant that cannot be read as pure iron status when CRP is up.7 We cover iron interpretation in depth in our guide to reading ferritin and iron status.
Standard CRP versus hs-CRP: why the distinction matters
A standard CRP answers whether there is active inflammation now: a suspected chest or urine infection, an arthritis flare, post-operative monitoring. NICE uses it this way in suspected lower respiratory tract infection: broadly, do not routinely offer antibiotics below 20 mg/L, consider a delayed prescription between 20 and 100 mg/L, and offer antibiotics above 100 mg/L.5
hs-CRP answers a different question: future cardiovascular risk in someone currently well, where chronic low-grade inflammation sits below what a standard assay can resolve. The widely used bands, from the American Heart Association and US Centers for Disease Control (2003), are below 1 mg/L lower risk, 1 to 3 average, above 3 higher.3
Evidence strength: hs-CRP as a cardiovascular marker rests on large trials. JUPITER (Ridker and colleagues, New England Journal of Medicine, 2008) randomised 17,802 apparently healthy adults with LDL below 130 mg/dL but hs-CRP of 2 mg/L or above to rosuvastatin 20 mg or placebo, and found roughly a 44 percent reduction in major cardiovascular events.6 CANTOS (same group, 2017) went further: in 10,061 people after a heart attack with raised hs-CRP, the anti-inflammatory drug canakinumab cut recurrent events without lowering cholesterol at all, the first clear proof that targeting inflammation itself reduces risk.9
In UK practice hs-CRP is one risk-enhancing factor among many, not a routine screen. Our insights articles cover how single results gain meaning only in context.
Why ESR is slower and less specific
ESR predates CRP by decades but its weaknesses are real. Because it depends on red cell behaviour and slow-turnover proteins, it can take a day or more to rise and several days to fall, long after CRP has normalised. It is also swayed by factors unrelated to inflammation: anaemia and pregnancy raise it, abnormal red cell counts distort it, and it climbs naturally with age and runs higher in women.4 The Miller formula (BMJ, 1983) sets the upper limit of normal at age divided by 2 for men, and age plus 10 divided by 2 for women.4 So an ESR of 25 mm/h is firmly abnormal in a 30-year-old man but unremarkable in an 80-year-old woman.
ESR still earns its place in conditions driven by the slower proteins it reflects, such as polymyalgia rheumatica and giant cell arteritis. Even so, a normal ESR and CRP do not rule out giant cell arteritis, so a strong clinical suspicion warrants urgent action regardless of the numbers.8
Ferritin: an iron store that doubles as an inflammation marker
Ferritin is the marker most likely to be misread, because it wears two hats. Usually it reports iron stores, and a low ferritin is the single most useful test for iron deficiency. But inflammation, infection, liver disease, alcohol, metabolic syndrome and some cancers all raise it independently of iron, producing two classic traps.
The first is a falsely reassuring ferritin: someone is genuinely iron deficient, but inflammation lifts the reading into the normal range. This is why the World Health Organization sets the deficiency cut-off at 15 micrograms per litre in healthy people but raises it to 70 when inflammation is present, and why ferritin should be read alongside CRP and transferrin saturation, not alone.7 The second trap is assuming a high ferritin means iron overload, when most raised ferritins are acute-phase responses or reflect fatty liver or alcohol. True overload such as haemochromatosis is confirmed by a raised transferrin saturation, typically investigated when ferritin exceeds about 300 micrograms per litre in men and postmenopausal women, or 200 in premenopausal women.
Reading them together: benign versus concerning
No single inflammatory marker is a diagnosis; the skill is reading them as a pattern. The table summarises typical adult UK reference ranges and common benign versus concerning causes.
| Marker | What it measures | Typical UK range | Raised benignly by | Raised concerningly by |
|---|---|---|---|---|
| CRP | Liver protein, current inflammation | Below ~5 mg/L2 | Recent viral illness, exercise, minor injury, obesity, pregnancy | Bacterial infection (often >50 to 100), active autoimmune flare, abscess5 |
| hs-CRP | Same protein, low-level chronic inflammation | <1 low, 1 to 3 average, >3 higher CV risk3 | Obesity, smoking, recent infection (recheck when well) | Persistent elevation: higher cardiovascular risk6 |
| ESR | Red-cell settling, indirect protein marker | Age-adjusted (Miller formula)4 | Older age, female sex, anaemia, pregnancy | Polymyalgia rheumatica, giant cell arteritis, chronic infection, myeloma8 |
| Ferritin | Iron stores, plus acute-phase reactant | Female ~11 to 310; male ~24 to 340 ug/L2 | Inflammation, infection, alcohol, fatty liver, exercise | Iron overload (with high transferrin saturation), liver disease, malignancy7 |
A few combinations recur. A raised CRP with a normal ESR often means a recent trigger ESR has not caught up with. A raised ESR with a normal or falling CRP can mean resolving inflammation, or a non-inflammatory cause such as age or anaemia. A high ferritin with a raised CRP usually reflects the acute-phase response, not iron overload. A mildly raised marker in someone well, with an obvious benign explanation, is usually best handled by a repeat once any acute illness has passed. If you are organising several results to discuss, our stack builder can help.
Inflammatory markers are non-specific. A normal CRP or ESR does not exclude serious disease (notably giant cell arteritis or early infection), and a raised one does not identify a cause. Persistent, unexplained or markedly high results, or any marker paired with red-flag symptoms such as unexplained weight loss, night sweats, new severe headache or fever, need clinical assessment rather than self-interpretation.
What to ask your GP
- Was my CRP the standard test or high-sensitivity, and were we asking about current infection or long-term heart risk?
- My ESR is raised: have we accounted for my age and sex before treating it as abnormal?
- My ferritin looks normal but I have iron-deficiency symptoms: was my CRP up at the same time, and should we check transferrin saturation?
- My ferritin is high: is this an acute-phase response, or do we need transferrin saturation to rule out iron overload?
- Should we simply repeat these markers once any recent illness has cleared, to see the trend?
References
- North Bristol NHS Trust, Severn Pathology. C-reactive protein (CRP): kinetics and clinical use. nbt.nhs.uk, accessed 2026.
- North Bristol NHS Trust, Severn Pathology. CRP and Ferritin test information and adult reference ranges. nbt.nhs.uk, accessed 2026.
- Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice. A statement for healthcare professionals from the CDC and the AHA. Circulation. 2003;107(3):499-511. ahajournals.org.
- Miller A, Green M, Robinson D. Simple rule for calculating normal erythrocyte sedimentation rate. Br Med J (Clin Res Ed). 1983;286(6361):266. PMC1546487.
- National Institute for Health and Care Excellence. Pneumonia in adults: diagnosis and management (CG191), CRP testing recommendations. nice.org.uk, accessed 2026.
- Ridker PM, Danielson E, Fonseca FAH, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein (JUPITER). N Engl J Med. 2008;359(21):2195-2207. nejm.org.
- World Health Organization. WHO guideline on use of ferritin concentrations to assess iron status in individuals and populations. 2020. who.int.
- van der Geest KSM, Sandovici M, Brouwer E, Mackie SL. Diagnostic accuracy of symptoms, physical signs and laboratory tests for giant cell arteritis: a systematic review and meta-analysis. JAMA Intern Med. 2020;180(10):1295-1304. PMID 32804186.
- Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease (CANTOS). N Engl J Med. 2017;377(12):1119-1131. nejm.org.
This article is educational and does not constitute medical advice, diagnosis, or a treatment recommendation. Medication uses described as “off-label” are not licensed for that purpose in the UK and should only be considered under qualified clinical supervision. Always speak to your GP, pharmacist, or a registered specialist before starting, stopping, or changing any treatment. If you have severe or alarm symptoms - unintentional weight loss, blood in your stool, difficulty swallowing, persistent vomiting, a fever, or severe pain - seek urgent medical care.