Sedimentation Rate (ESR) Test
The erythrocyte sedimentation rate measures how far red cells fall through a column of anticoagulated whole blood in one hour, an indirect reflection of fibrinogen and immunoglobulin levels raised by inflammation. C-reactive protein has largely superseded it for acute inflammation, but ESR remains embedded in the classification criteria for giant cell arteritis and polymyalgia rheumatica.
1
Biomarkers
Blood (whole blood)
Sample
1–2 business days
Turnaround
No
Fasting
What is the ESR test?
The Sedimentation Rate Test measures how far red cells settle through a column of anticoagulated whole blood in one hour. Sedimentation is driven by rouleaux formation, which is promoted by fibrinogen and immunoglobulins, so the ESR rises indirectly when the acute-phase response increases these plasma proteins. It is ordered as a non-specific marker of inflammation, most importantly in suspected giant cell arteritis and polymyalgia rheumatica, and in monitoring established inflammatory disease. Within inflammatory assessment, ESR is an old and indirect test that C-reactive protein has largely displaced for general purposes. CRP is a direct measure, rises within hours rather than over one to two days, falls promptly once inflammation resolves, and is unaffected by anaemia, red cell morphology, age, or sex — all of which confound ESR. Where the question is simply whether acute inflammation is present, CRP is the better test. ESR retains specific value nonetheless. It is written into the classification criteria for giant cell arteritis and polymyalgia rheumatica and is customarily ordered alongside CRP in those presentations, it features in rheumatoid arthritis disease activity scores such as DAS28, its slow decline suits the monitoring of chronic conditions where CRP fluctuates, and a very high ESR with a disproportionately normal CRP is a recognised pointer to paraproteinaemia. The critical caution is that a normal ESR does not exclude giant cell arteritis — a proportion of biopsy-proven cases have a normal ESR — so a normal result must never override strong clinical suspicion in a patient with visual symptoms or jaw claudication. ESR is best used as a supporting measure alongside CRP and the clinical picture, not as a standalone screening test.
What does the ESR test measure?
The erythrocyte sedimentation rate measures how far red cells fall through a column of anticoagulated whole blood in one hour. Sedimentation depends on rouleaux formation — the stacking of red cells — which is promoted by asymmetric plasma proteins, principally fibrinogen and to a lesser extent immunoglobulins. Inflammation raises fibrinogen through the acute-phase response, increasing rouleaux and accelerating the fall. Because it depends on hepatic fibrinogen synthesis, ESR rises slowly over 24 to 48 hours and falls slowly over days to weeks, and because it depends on red cell mass and morphology it is directly influenced by haematocrit and red cell shape.
ESR is an indirect, non-specific marker of inflammation whose value lies in specific clinical contexts rather than general screening. C-reactive protein has largely superseded it for detecting and monitoring acute inflammation, responding within hours rather than days and being unaffected by anaemia or red cell morphology. ESR nonetheless retains established roles: it is embedded in the classification criteria for giant cell arteritis and polymyalgia rheumatica, is used in disease activity scoring in rheumatoid arthritis, and remains useful in monitoring chronic inflammatory conditions and in investigating suspected osteomyelitis. It is markedly elevated by paraproteinaemia, which is itself a diagnostic clue.
Why is the ESR test ordered?
- Suspected giant cell arteritis, where ESR forms part of the classification criteria and is ordered together with CRP — noting that a normal ESR does not exclude the diagnosis
- Suspected polymyalgia rheumatica, presenting with proximal girdle pain and stiffness, as part of the diagnostic assessment alongside CRP
- Monitoring disease activity in rheumatoid arthritis, where ESR contributes to composite activity scores such as DAS28
- Monitoring of established chronic inflammatory conditions, where the slower decline of ESR can better reflect sustained activity than fluctuating CRP
- Investigation of suspected osteomyelitis or deep infection, where ESR supports the assessment alongside imaging and CRP
- Evaluation of unexplained constitutional symptoms — persistent fatigue, weight loss, fever of unknown origin — as a supporting non-specific inflammatory marker
- Investigation of a markedly elevated ESR disproportionate to CRP, which raises the possibility of paraproteinaemia and warrants protein electrophoresis
Sample collection and turnaround
Sample type
Blood (whole blood)
Fasting required
No
Collection method
Venipuncture at patient service centre
Turnaround
1–2 business days
Collection notes
Requires a correctly and completely filled anticoagulated whole blood tube — underfilling alters the anticoagulant ratio and distorts the result. The specimen must be run within the laboratory's permitted window after collection, typically within four hours at room temperature, and kept vertical and free of vibration. Order alongside CRP in suspected giant cell arteritis or polymyalgia rheumatica, and document anaemia, pregnancy, corticosteroid or NSAID therapy, and any known haemoglobinopathy.
Specimen requirements
Completely filled anticoagulated whole blood tube per LabCorp protocol. Do not use a clotted, underfilled, or haemolysed specimen. Must be analysed within the laboratory's specified time window; follow LabCorp transport and storage guidelines.
What can affect ESR results?
Sedimentation depends on red cell mass, so anaemia accelerates the fall and raises ESR independent of inflammation, while polycythaemia slows it and can mask a genuine inflammatory elevation. This is a fundamental limitation not shared by CRP.
ESR rises with age and is higher in women, and increases substantially through pregnancy and the postpartum period through physiological changes in fibrinogen and haematocrit. Results must be interpreted against age- and sex-appropriate expectations rather than a single adult limit.
Monoclonal or markedly increased polyclonal immunoglobulins strongly promote rouleaux formation and can raise ESR to very high values. A markedly elevated ESR with a disproportionately normal CRP should prompt consideration of myeloma or Waldenström macroglobulinaemia.
Sickle cells, spherocytes, and marked poikilocytosis impair rouleaux formation and lower ESR, so patients with sickle cell disease or hereditary spherocytosis may have a falsely low result despite active inflammation.
ESR must be run within a defined window after collection — typically within four hours at room temperature — and requires a correctly filled EDTA or citrate tube kept vertical and free of vibration. Delay, underfilling, clotting, or elevated ambient temperature all distort the result.
Obesity is associated with modestly higher ESR through raised fibrinogen, while corticosteroids and non-steroidal anti-inflammatory drugs suppress the acute-phase response and can lower ESR, potentially masking active disease. Medication history should be documented, particularly in patients already started on steroids for suspected giant cell arteritis.
What do ESR results mean?
Elevated
A raised ESR indicates an increase in fibrinogen or immunoglobulins and is non-specific — infection, autoimmune and connective tissue disease, malignancy, tissue injury, and chronic kidney disease all elevate it, as do anaemia, older age, and pregnancy independent of inflammation. Moderate elevation requires clinical correlation rather than a specific diagnostic conclusion. A markedly elevated ESR, conventionally above 100 mm/hr, narrows the differential towards giant cell arteritis, active connective tissue disease, serious infection including osteomyelitis and endocarditis, malignancy, and paraproteinaemia, and warrants prompt and directed investigation. An ESR disproportionately high relative to CRP specifically suggests a paraprotein.
Normal
A normal ESR does not exclude significant inflammatory disease. This matters most in giant cell arteritis, where a proportion of biopsy-proven cases have a normal ESR, so a normal result must not override strong clinical suspicion in a patient with visual symptoms, jaw claudication, or new temporal headache — such patients require urgent specialist assessment regardless. A normal ESR is also expected early in acute inflammation, since the rise lags by 24 to 48 hours, and may be spuriously normal in polycythaemia or where red cell morphology impairs rouleaux.
Reduced
A low ESR is rarely clinically meaningful but can reflect polycythaemia, marked leucocytosis, red cell morphological abnormalities such as sickle cells or spherocytes, hypofibrinogenaemia, or severe hepatic disease with impaired fibrinogen synthesis. Its principal significance is that it may mask genuine inflammation in these patients.
Note: ESR is an indirect, non-specific measure that is slower to rise and fall than CRP and is confounded by anaemia, red cell morphology, age, sex, pregnancy, and paraproteins. It is not a screening test for occult disease in asymptomatic patients, where a mildly raised result generates investigation without benefit. It is customarily ordered alongside CRP rather than instead of it, and the two are complementary — discordance between them is itself informative. Results depend heavily on correct tube fill, prompt running within the permitted window, and stable temperature.
Frequently asked questions
It measures how far red cells settle through a column of anticoagulated whole blood in one hour. Sedimentation is driven by rouleaux formation, which is promoted by fibrinogen and immunoglobulins, so ESR rises indirectly with inflammation.
How to access the ESR test
The ESR reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.
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Published: July 16, 2026
Last reviewed: July 16, 2026
- Hunder GG, et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum. (1990)
- Dasgupta B, et al. 2012 provisional classification criteria for polymyalgia rheumatica: a European League Against Rheumatism/American College of Rheumatology collaborative initiative. Ann Rheum Dis. (2012)
- Brigden ML. Clinical utility of the erythrocyte sedimentation rate. Am Fam Physician. (1999)
- Kermani TA, et al. Utility of erythrocyte sedimentation rate and C-reactive protein for the diagnosis of giant cell arteritis. Semin Arthritis Rheum. (2012)
This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.
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