The problem with ESR as discussed by others is a lack of specificity. While selected uses can be defended as a disease marker in selected patients with autoimmune disorders followed by one assay platform type, most of the reported clinical uses of ESR as a disease screening tool are better performed by other assays, such as CRP and more recently biomarkers in infection/sepsis such as procalcitonin, neutrophil CD64, soluble CD163, cell free DNA plasma levels, TREM-1, IL-6, and others.
I have attached the International Council for Standardization in Haematology (ICSH) guideline publication for ESR, which some may find useful.
Since nobody answered I will try it - but I am not such an expert in this field. First, I assume you mean "erythrocyte sedimentation rate" (ESR), which should have many different abbreviations and expressions in all other languages than english (and many here in researchgate are not trained in english speaking countries). As you suggested yourself it may be elevated for no obvious cause and in many different scenarios - I personally know quite healthy people with such a constant elevation over decades and with no real symptoms of any related disease. It may not be that valuable as just one single test since it can be elevated in so many different scenarios. It all depends on the clinical symptoms, other diagnostics, therapies. It may just indicate to look closer, if no other parameters are evident. It may serve as an indicator of how a treatment works or a disease may come back. Since it is such an old test, there should be many more specific tests around with better differentiating potential.
Thank you Robert Eibl for being the first and only one "until now" to answer my query. I asked this question because I get puzzled each time one of my patients gets a high ESR and they don't get a reasonable answer "if any" from their supposedly physicians. Although I am an oral medicine specialist "I treat patients with oral problems", some times I get stuck with cases that have a local oral inflammatory condition and an elevated ESR at the same time. This time it was an Arab lady in her forties who recently developed recurrent oral ulceration seemingly not associated with any systemic problem. I could confirm that apart from obesity and mild hypertension, she is healthy. She did all tests in Germany to check all systems and she was reassured that there is nothing wrong with her. Does a local inflammatory condition in the mouth cause an elevation in ESR? And if a patient shows an elevation in ESR, what other tests should be done?
Take-home message: ESR + clinical findings + other side tests will give you a more complete picture and guide your treatment. Most of the time ESR should not be used alone.
Many thanks to Ahed, Martin and Rafael for your contributions. I always thought of ESR as an indication of Ag-Ab reaction on the RBCs, which makes them aggregate (agglutinate?), and this usually happens when abs are increased due to autoimmune or inflammatory disorder. Does anybody have a reference that can guide me in understanding the basics of ESR?
ESR measures sedimentations rate of erythrocytes in time. The main contributor to ESR is the physical feature of plasma, mainly so called acute phase proteins - which are produced due to acute or chronic inflammation, mainly by liver. The protein content in plasma is the main factor influencing the ESR. This is very unspecific marker, but as a screening tool is good.
Just a small addition; as a rule of thumb if you find a very high ESR like more then 100 think of malignancy, as extreme high ESR is not so common in other disease. I have found many patient of having cancer and the only clue in the beginning was very high ESR.
Thank you Ewa and Abdul qayoum for your informative addition. What value of ESR you consider significant and may require further investigation? For example, a value of 40?
Dear Najla Dar-Odeh, I think it is ideal how you care about your patients. Thank you for adding more information, but I think it is rather difficult to really add any more suggestions relevant to the case. It may be straightforward if you could contact the original physicians who may have checked and excluded any serious conditions by further tests. Such tests may have included other (similarly) unspecific (CRP), but also many highly specific parameters to exclude any disease. Usually, physicians may recommend specific time intervals/schedules for monitoring such questionable or elevated parameters.
I agree with Robert, however the reference value for control group exists also for ESR. Depending to methods the values can be different. You have to ask the laboratory about their reference value and method they use, and of course to contact doctor to find out the diagnosis. The value of ESR will not tell You the diagnosis, except values above 100, which are really alarming and most often met in cancer patients.
Giant cell arteritis (temporal arteritis) and polymylagia rheumatica are often associated with very high ESR. Of course, these are rare diseases and the ESR elevation is not specific for them, so the test is not diagnostic. A low ESR does not completely rule them out but makes them much less likely. I do not consider ESR to be a diagnostic test, but as a nonspecific indicator of inflammation which, in combination with the clinical presentation, can rule disease in (higher probability) or out (not possible or lower probability).
Acute phase reactants are products or cells that increase as a response to inflammation, infection or malignancy. They are non-specific. Their elevation is not diagnostic for a specific disease. They help to interpret the symptoms within a wide context: for instance swollen joints in osteoarthritis (degenerative disease) versus in rheumatoid arthritis (chronic inflammatory disease). Acute phase reactants include CRP, platelet counts, haptoglobins, ceruloplasmin, Serum amyloid A, fibrinogen and many others.
Acute phase reactants fluctuate with disease activity. Their sensitivity differs. ESR & CRP are the most commonly used for diagnosis and follow-up. ESR is slow to rise, slow to fall (weeks or months). CRP rises and falls quickly (hours or days). The magnitude of elevation of ESR and CRP is very different: CRP can rise thousands-fold.
One must remember that ESR normal values are higher in females, and rise with age. ESR of 40 mm Westergren for instance is normal at age 70.
It is important to know that the level of plasmatic fibrinogen has a strong influence on ESR. Case of hypofibrinogenemia and afibrinogenemia does not have sedimentation rate; it is 0-1mm even presenting inflammation, infection. more information, see Dacie&Lewis ( Practical haematology, Churchill Livingstone) Miscellaneous test.
Traditionally, Estimated Sedimentation Rate was done with Westergren Method. Thus physical constituents of the plasma, the number of the RBC's affects the reading tremendously. In countries like in Malaysia and India, once the reading more than 100mm/hr we would have to screen for Tuberculosis and Neoplasm especially if the patient give history of having B symptoms.
Thank you Tee for your addition. I know of a case of GCA who died because his physicians considered that this is a normal type of headache and did not request ESR
Thank you Majda, your comments are informative and enjoyable as always. Why did you refer to ESR as an acute phase reactant since it reflects chronic conditions like inflammation?
Thank you Ida, I will try to get that reference you mentioned.
your comments Bahariah are appreciated. Tuberculosis may not be a wide-spread problem in my country, but we sure do have a substantial prevalence of malignancy.
ESR is usually elevated in inflammatory process but is not specific. In my speciality - orthopedic surgery- there are others important signs : radiograph abnormality of the bone , clinical status of the patient, etc. It is important assess with the clinical presentation and others laboratories studies (C-reactive protein, for example )
ESR rises with acute as well as chronic inflammation. With two provisions:
1. It is slower than CRP in rising but not very slow ( days not weeks to increase).
2. The magnitude of its rising is lower, quantitatively. It could very well remain normal in a significant percentage of RA patients, despite a chronic inflammation. While it is almost always high in acute inflammation, especially infection. This makes it an insensitive marker for follow-up in that chronic condition (RA).
ESR does not increase during viral infection. if it increases during the course of a viral disease, it usually indicates a superimposed bacterial infection. This is important because it warrants amendment of the treatment program. A common example is common cold, where superimposed bacterial infection calls for antibiotic treatment.
In some established centres we use Serum Procalcitoniin levels that can help to differentiate clearly between viral and bacterial infection. You have to develop your own cut levels in your centre ideally. I have used it and it helps to prognosticate sepsis with multiorgan function as well. I agree with everybody that ESR, CRP, Sr. fibrinogen are just acute reactive proteins and supportive only when it is >100 with other significant symptoms.
Additionaly i want to share you that levels of ESR >100mm/h in presence of
new or unusual headache, scalp tenderness, neurologic or ocular synptoms, jaw claudication, it must to think in GCA, ESR > 100 have a positive LR of 1.9 as Smetana report in JAMA 2002; 287: 92-101, and describe in his work some LR for each synptom. In rheumatology ESR > 100mm/h most to think GCA, it is not a rule, but is a red flag that something its bad, its a shame for your patient.
"The eye does not see what the mind does not know"
ESR depends on the formation of aggregates of red blood cells and their sedimentation velocity. This is influenced by the amount of red blood cells (low ESR in polycythemia, high in anemia), their morphology (red blood cells abnormalities) and changes in the concentration of some proteins with high molecular weight. The proteins alter the charges on the surface of red blood cells and promote the formation of aggregates. Fibrinogen, alpha-2- macroglobulin and γ-globulins will change the balance much easier than a small protein such as CRP. This explains why ESR is a bad test in case of acute inflammation and a good test for chronic inflammation (for example, it is important in the diagnosis of Horton arteritis). But don’t forget the false positive results (in pregnancy) and false negative results (some monoclonal compounds change blood viscosity and can dramatically slow the ESR)!
The problem with ESR as discussed by others is a lack of specificity. While selected uses can be defended as a disease marker in selected patients with autoimmune disorders followed by one assay platform type, most of the reported clinical uses of ESR as a disease screening tool are better performed by other assays, such as CRP and more recently biomarkers in infection/sepsis such as procalcitonin, neutrophil CD64, soluble CD163, cell free DNA plasma levels, TREM-1, IL-6, and others.
I have attached the International Council for Standardization in Haematology (ICSH) guideline publication for ESR, which some may find useful.
I'm often asked the same question and I admit to not be able to respond. The hematocrit of women is lower and the influence of hormones is proven (menstrual cycle, pregnancy). The difference in the hematocrit is relatively small compared to the difference in value of ESR. The difference seems to persist after menopause, so the influence of hormones also seems unlikely for such a difference
Підвищені показники ESR вказують на деструктивні процеси в сполучній тканині, які можуть відбуватися при захворюваннях будь-якого генезу. В переважній більшості випадків це тільки показник їхньої активності. Спочатку спробуйте встановити правильний діагноз клінічно. ESR залишиться показником, за яким Ви будете оцінювати ефективність свого лікування.
If ESR is very low, say less than 1 mm in an hour, what can we conclude from it? I have not come across the significance of a low ESR. The sample I tested also had high expression of IL-6 and INF gamma (derived through FACS), which would suggest inflammation of some kind. This is puzzling, because inflammation has been associated with high ESR. I'd appreciate some help understanding this.