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Takeaway – The erythrocyte sedimentation rate (ESR) test or “sed rate test” is a blood test that mainly checks for chronic inflammation. High levels may be used to diagnose or screen for specific conditions. However, this test is not sensitive or specific.

It is often ordered along with other labs. A high sed rate may point to various inflammatory disorders like polymyalgia rheumatica, temporal arteritis, and others. Factors that may help lower inflammation and ESR include engaging in regular exercise, living a healthy and hygienic lifestyle, losing weight if overweight, and eating nutritious foods.

A low sedimentation rate is often normal. In some cases, it may point to blood cell disorders. The most important step is to see your doctor to get adequate diagnosis and treatment.

What can decrease ESR?

Pathophysiology – The ESR test measures the rate at which the red blood cells (RBCs), or erythrocytes, in a sample of whole blood, fall to the bottom of the Westergren tube. This process of “falling” is called sedimentation. RBCs typically fall at a faster rate in people with inflammatory conditions such as infections, cancer, or autoimmune conditions.

• These conditions lead to an increase in the number of proteins in the blood.
• This increase causes red blood cells to stick together (clump) and settle at a faster rate.
• A group of RBCs that are clumped together will form a stack (similar to a stack of coins) called a rouleau (pleural is rouleaux).
• Rouleaux formation is possible because of the particular discoid shape of RBCs.

The flat surfaces of the RBCs allow them to make contact with other RBCs and stick together. Normally, RBCs have negative charges on the outside of the cells, which cause them to repel each other. Many plasma proteins have positive charges and can effectively neutralize the negative surface charges of the RBCs, which allows for the formation of the rouleaux.

Therefore, an increase in plasma proteins (present in inflammatory conditions) will propagate an increase in rouleaux formations, which settle more readily than single red blood cells The settling of the rouleaux aggregates in the Westergren tube occurs at a constant rate. The formation of rouleaux allows the RBCs to settle at a faster rate, thus increasing the ESR.

Therefore, the ESR is not the measure of a single marker but a physical process. Rouleaux formation (and thus the ESR) is affected by the amounts of immunoglobulins and acute phase proteins (prothrombin, plasminogen, fibrinogen, C-reactive protein, alpha-1 antitrypsin, haptoglobin, complement proteins) that are present in several inflammatory conditions.

Acute-phase proteins” (APP) is the name given to a class of approximately 30 distinct, chemically unrelated plasma proteins that are innately regulated in response to infection and inflammation. APP’s are produced by the liver and are functionally controlled by the body in response to several forms of tissue damage or insult.

These proteins act as inhibitors or mediators of the inflammatory response. The detection of the first acute phase protein in the 1930s, the C-reactive protein (CRP), occurred during the analysis of the plasma of patients diagnosed with acute pneumococcal pneumonia.

The CRP and many other acute-phase proteins may increase during ongoing tissue damage, either acutely or chronically. “Acute phase” is still used to label these proteins that change in concentration during certain disease processes, regardless of chronicity. The fluctuating nature of the acute phase proteins in inflammation leads to the increased “stickiness” of RBC’s, the formation of RBC “stacks” (rouleaux formation), and an increase in ESR.

Although many inflammatory illnesses will increase the ESR, other conditions exist that can lower the ESR. These “lowering factors” can exist either as isolated disease processes or in conjunction with other pathologic conditions that raise the ESR, thus giving a “lower than expected” ESR results in light of a serious underlying inflammatory process.

1. Polycythemia (an increased number of red blood cells) will increase blood viscosity and can cause a reduced ESR (reduces the rate at which RBC rouleaux will settle to the bottom of the Westergren tube).
2. Some hemoglobinopathies such as sickle cell disease can lower ESR due to the abnormal shape of red blood cells that impairs rouleaux formation.

Spherocytosis (the presence of sphere-shaped rather than disc-shaped RBCs) also inhibits rouleaux formation and can decrease the ESR.

What happens if ESR count is high?

What do the results mean? – Your provider will use the results of your ESR test along with your medical history, symptoms, and other test results to make a diagnosis. An ESR test alone cannot diagnose conditions that cause inflammation. A high ESR test result may be from a condition that causes inflammation, such as:

• Arteritis
• Arthritis
• Systemic vasculitis
• Polymyalgia rheumatica
• Inflammatory bowel disease
• Kidney disease
• Infection
• Rheumatoid arthritis and other autoimmune diseases
• Heart disease
• Certain cancers

A low ESR test result means your red blood cells sank more slowly than normal. This may be caused by conditions such as:

• A blood disorder, such as:
  • Polycythemia
  • Sickle cell disease (SCD)
  • Leukocytosis, a very high white blood cell count (WBC)
• Heart failure
• Certain kidney and liver problems

If your ESR results are not normal, it doesn’t always mean you have a medical condition that needs treatment. Pregnancy, a menstrual cycle, aging, obesity, drinking alcohol regularly, and exercise can affect ESR results. Certain medicines and supplements may also affect your results, so be sure to tell your provider about any medicines or supplements you are taking.

What is the reason for high ESR in blood?

What Abnormal Results Mean – An abnormal ESR may help with a diagnosis, but it does not prove that you have a certain condition. Other tests are almost always needed. An increased ESR rate may occur in people with:

Anemia Cancers such as lymphoma or multiple myeloma Kidney diseasePregnancyThyroid disease

The immune system helps protect the body against harmful substances. An autoimmune disorder is when the immune system mistakenly attacks and destroys healthy body tissue. ESR is often higher than normal in people with an autoimmune disorder. Common autoimmune disorders include:

Lupus Polymyalgia rheumatica Rheumatoid arthritis in adults or children

Very high ESR levels occur with less common autoimmune or other disorders, including:

Allergic vasculitis Giant cell arteritis Hyperfibrinogenemia (increased fibrinogen levels in the blood) Macroglobulinemia – primary Necrotizing vasculitis

An increased ESR rate may be due to some infections, including:

Bodywide (systemic) infection Bone infections Infection of the heart or heart valves Rheumatic fever Severe skin infections, such as erysipelas Tuberculosis

Lower-than-normal levels occur with:

Congestive heart failure Hyperviscosity Hypofibrinogenemia (decreased fibrinogen levels)Leukemia Low plasma protein (due to liver or kidney disease) Polycythemia Sickle cell anemia

How long does it take for ESR to return to normal?

ESR is an indirect measure of inflammation. ESR levels increase at a slow rate in response to inflammation and can take weeks to return to normal levels.

Is lemon good for high ESR?

ESR levels decreased significantly in arthritis mice after treatment with lemon fruit peel, lemon leaf, hot pepper leaf, and hot pepper fruit by −79.09%, −77.00%, −77.53% and −77.53% respectively (P ⩽ 0.05).

When should I worry about my ESR?

4) Serious Conditions – ESR levels higher than 100 mm/hr could suggest a serious disease, such as infection, heart disease, or cancer, ESR levels higher than normal may predict cancer or cancer progression, like metastasis, Your doctor may order an ESR test to check for specific inflammatory or chronic conditions, along with other tests.

How fast does ESR decrease?

Table 1. – Acute Phase Reactants

ESR	Extremely elevated ESR (>100 mm/hour)-high specificity for infection, malignancy, or arteritis. Rises within 24–48 hours of the onset of inflammation and falls back slowly with resolution.
CRP	Begins to rise after 12–24 hours and peaks within 2–3 days. Low levels of CRP elevation with values between 2 and 10 mg/L measured by a “high sensitivity CRP” assay seen in noninfectious “metabolic inflammatory” states such as cardiac ischemia, uremia, or smoking.
PCT	Detectable within 3–4 hours and peaks within 6–24 hours. Elevated levels not seen in other noninfectious inflammatory conditions such as polymyalgia, inflammatory bowel disease, polyarteritis nodosa, systemic lupus erythematosus, gout, and temporal arteritis. More sensitive and specific than CRP for distinguishing bacterial from noninfectious causes of inflammation
Others	Apolipoproteins: SAA proteins Coagulation Pathway: Fibrinogen, Protein S, Plasminogen Complement System: C3, C4, C9, Factor B, C1 inhibitor Antiproteases: Alpha-1 antitrypsin, Alpha-1 acid glycoprotein Proteins: Haptoglobin, Hemopexin, Hepcidin, Ferritin, Ceruloplasmin Cytokines: IL-1, IL-6, tumor necrosis factor-alpha

Cellulitis In skin and soft tissue infections, ESR and CPR levels on admission may predict the severity of the infection and the duration of hospitalization. In a retrospective study at a tertiary hospital, patients who required longer hospitalization had significantly higher levels of ESR and CRP on admission but similar white blood cell (WBC) counts. The mean CRP and ESR values for the group with more severe disease requiring longer hospitalization was 100 mg/L and 70 mm/hour compared with a mean CRP and ESR of 40 mg/L and 50 mm/hour for the group with less severe disease requiring shorter hospitalization, Another retrospective study reported a statistically significant association between longer hospitalization and a high ESR on admission. The cutoff for ESR in this study was 50 mm/hour, and the mean CRP level was 78 mg/L, Necrotizing Skin and Soft Tissue Infections It is often clinically challenging to differentiate between early necrotizing fasciitis versus more superficial skin and soft tissue involvement. The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) is a laboratory-based scoring method that, in its original validation study, reported a PPV of 92% and a negative predictive of 96% for necrotizing skin and soft tissue infection for a LRINEC score of equal to or more than 6, A CRP level of more than 150 mg/L was assigned a score of 4 in this scoring system. Some subsequent reports on attempts at validating LRINEC score have failed to show reliable sensitivity, Another study reported that a PCT ratio of 1.14 or more between the postoperative day 1 and day 2 after surgery for necrotizing fasciitis indicated successful surgical treatment with a sensitivity of 0.83 and a specificity of 0.71. The PPV was 75.8%, and the negative predictive value (NPV) was 80.0%, Osteoarticular Infections The likelihood of diabetic foot osteomyelitis increases with ESR value of more than 70 mm/h, In another prospective study, the sensitivity and specificity of CRP for the diagnosis of osteomyelitis at a level of more than 14 mg/L was 0.85 and 0.83; the sensitivity and specificity of ESR at a level more than 67 mm/hour was 0.84 and 0.75; and the sensitivity and specificity of PCT at a level more than 0.30 ng/mL was 0.81 and 0.71. All values declined after initiation of treatment with antibiotics. The CRP and PCT values returned to near-normal levels by day 7, whereas the values of ESR remained high for up to 3 months only in patients with osteomyelitis. The authors recommended that ESR be used for the follow-up of patients with osteomyelitis, A meta-analysis on the diagnostic value of PCT in osteoarticular infections indicated that PCT may be more suitable as a marker for rule-in diagnosis rather than for exclusion of septic arthritis or osteomyelitis, and that use of a lower cutoff value at 0.2–0.3 ng/mL may improve its diagnostic performance, In spondylodiscitis, ESR is elevated in over 90% of cases, with mean values ranging from 43 mm/hour to 87 mm/hour, In the same review, no correlation in the value of ESR was found to the severity of infection or patient’s age. The authors also noted that a fall in ESR to more than 25% of its presenting value was a good prognostic marker, but an unchanged or rising ESR was more difficult to interpret. C-reactive protein has a good sensitivity and was noted to be elevated in patients with acute spondylodiscitis in a number of studies. In these patients, CRP returned to normal within 3 months after the successful treatment of infection, In septic arthritis, both CRP and ESR have a high sensitivity at a cutoff value of 20 mg/L and 15 mm/hour, respectively, Measurement of CRP in the synovial fluid does not offer a better diagnostic advantage, Procalcitonin can be useful in the diagnosis of bacterial joint infections in patients with inflammatory rheumatic diseases, Prosthetic Joint Infections In a meta-analysis involving more than 30 studies and 300 patients, the authors concluded that the diagnostic accuracy for prosthetic joint infection was best for serum IL-6 level, followed by serum CRP level and ESR, The pooled sensitivity and specificity were noted to be 0.97 and 0.91 for IL-6, 0.88 and 0.74 for CRP, and 0.75 and 0.70 for ESR, respectively. C-reactive protein may remain elevated for up to 6 weeks and ESR may remain elevated up to 26 weeks after prosthetic joint surgery. Another study on the diagnosis of early prosthetic joint infection reported a high sensitivity of CRP, with optimal cutoff value of 93 mg/L, and high specificity of synovial WBC count, with optimal cutoff value of 12 800 cells/mL. The combination of a normal ESR and CRP level is reliable for predicting the absence of prosthetic joint infection, Sepsis and Septic Shock In a meta-analysis involving 30 studies and 3244 critically ill patients, the authors concluded that PCT is a helpful biomarker for early diagnosis of sepsis in critically ill patients. The cutoff for PCT concentrations differed between 0.5 ng/mL and 2.0 ng/mL, with a median of 1.1 ng/mL. The pooled sensitivity and specificity of serum PCT levels in the early diagnosis of sepsis was noted to be 0.77 (95% CI, 0.72–0.81) and 0.79 (95% CI, 0.74–0.84), respectively, In another systematic review, the authors concluded that PCT levels in early stages of sepsis are significantly lower among the survivors compared with nonsurvivors of sepsis. A maximum PCT level of 1–5 ng/mL correlated with a 90-day mortality of 11%; a maximum PCT level of 51–100 ng/mL correlated with a 90-day mortality of 42%, In a meta-analysis comparing PCT with CRP as a diagnostic test for sepsis after surgery or trauma, the authors concluded that PCT was superior to CRP, Another meta-analysis examining patients with bacteremia concluded that low PCT levels can be used to rule out the presence of bacteremia, Procalcitonin level elevations of 0.5 ng/mL occur very early during sepsis with levels increasing from systemic inflammatory response syndrome (0.6 −2.0 ng/mL) to severe sepsis (2–10 ng/mL) and septic shock (10 ng/mL). Most importantly, viral infections, recent surgery, and chronic inflammatory states are not associated with an increment in PCT levels, A meta-analysis of 16 studies examining serum PCT as a diagnostic marker in neonatal sepsis reported a pooled sensitivity and specificity of 0.81 and 0.91, respectively, The diagnostic accuracy of PCT seemed higher for neonates with late-onset sepsis (>72 hours of life) than for those with early onset sepsis. A persistently negative CRP or a CRP that decreases to < 10 mg/L in 24 hours has a good NPV in neonatal bacterial sepsis, Respiratory Infections There is increasing evidence on the usefulness of PCT as a biomarker in lower respiratory tract infections. Procalcitonin levels can be useful in early identification of bacterial pneumonia, guide antibiotic management, and help stratify patients with a higher risk of developing complications. In a randomized trial involving 302 consecutive patients, PCT guidance substantially reduced antibiotic use in lower respiratory tract infections without compromising outcomes from withholding antibiotics. In the PCT group, antibiotic treatment was based on serum PCT concentrations as follows: strongly discouraged, 0.25 µg/L; strongly encouraged, >0.5 µg/L, A Cochrane database review of more than 14 trials also concluded that the use of PCT to guide initiation and duration of antibiotic treatment in patients with pneumonia was not associated with higher mortality rates or treatment failure, Two other studies reported on the usefulness of a higher PCT level as a measure of severity in patients with bacteremia or a higher Pneumonia Severity Index score, The serum PCT levels do not correlate well with culture-proven empyema with a sensitivity and specificity of 0.76 and 0.81 at a cutoff value of 0.19 µg/L, Two systematic reviews on the usefulness of CRP in the diagnosis and management of lower respiratory tract infections did not report any significant benefit in its role as a diagnostic or management modality, Another study reported extremely high CRP levels (mean levels >166 mg/L) in patients with pneumococcal and legionella pneumonia, There is good quality evidence to suggest that PCT guidance to discontinue antibiotic therapy in pneumonia reduces antibiotic usage in intensive care units (ICUs) and reduces duration of antibiotic use and prescription rates with a reduction in total antibiotic exposure in ambulatory care or inpatient setting in patients with pneumonia. There is also at least moderate evidence that PCT guidance to discontinue antibiotic therapy does not increase morbidity, as indicated by ICU length of stay, and that PCT guidance does not increase mortality, hospital length of stay, or ICU admission rates in patients diagnosed with pneumonia in an inpatient or ambulatory care setting (Table ​ 2 ).

What ESR level is alarming?

When should I worry about my ESR? – To get an ESR rate over 100 mm/hr should already cause an alarm. While going beyond the normal range suggests health issues related to inflammation, an extremely high ESR rate entails severe medical conditions such as cancer, heart disease, and untreated infections. Consult your doctor to secure other diagnostic procedures.

Can stress cause high ESR levels?

Abstract – The effect of a 75-hour vigil on the erythrocyte sedimentation rate (ESR), i.a., was studied in two experiments with 63 healthy male volunteers. The ESR was increased at the end of the vigil compared with pre-exposure values. The increases did not correlate significantly with concomitant changes in serum triglycerides, free fatty acids, cholesterol or gammaglobulins, except for a significant, negative correlation with cholesterol changes in one of the two studies.

Is ESR 40 high treatment?

Is ESR 40 high? Yes, it is high. ESR levels of 40 mm/hr clearly indicate a state of systemic inflammation among people who already have an inflammatory disease.

What are the stages of ESR?

Abstract – Erythrocyte Sedimentation Rate (ESR) is a simple, non-specific clinical test. Most models of erythrocyte sedimentation (ES) are formulated as a sigmoid function but consider the ES process to consist of three distinct phases: single-cell fall; fall of rouleaux and aggregates; cell packing.

Recently, a piecewise (three-phase) continuous model has been developed. Our study applies ES data from 29 haematologically normal subjects to this model and re-evaluates the mechanism of ES using the derived model parameters. Using the Westergren technique, ES readings were taken every 10 minutes for 300 minutes.

Three subjects remained in the first phase, while 26 displayed three discrete phases. For the 26 subjects, the average rate of fall of the sedimenting particles in the first phase 87 microns/min, while that of the second phase was 176 microns/min. The ratio of these two values suggests an alternative nature of sedimenting particles in the first phase.

What is the fastest way to reduce ESR?

Takeaway – The erythrocyte sedimentation rate (ESR) test or “sed rate test” is a blood test that mainly checks for chronic inflammation. High levels may be used to diagnose or screen for specific conditions. However, this test is not sensitive or specific.

1. It is often ordered along with other labs.
2. A high sed rate may point to various inflammatory disorders like polymyalgia rheumatica, temporal arteritis, and others.
3. Factors that may help lower inflammation and ESR include engaging in regular exercise, living a healthy and hygienic lifestyle, losing weight if overweight, and eating nutritious foods.

A low sedimentation rate is often normal. In some cases, it may point to blood cell disorders. The most important step is to see your doctor to get adequate diagnosis and treatment.

How can I lower my ESR and CRP naturally?

C-Reactive Protein, Inflammation, and Cardiovascular Disease: Clinical Update Two-and-a-half years ago, we presented C-reactive protein (CRP) data from the Women’s Health Study, a large prospective study of 30,000 healthy middle-aged women followed over 10 years for the occurrence of first-ever cardiovascular events (the final results of the Women’s Health Study regarding the effects of aspirin and of vitamin E randomization have just been published ).

• We showed that high-sensitivity CRP is a very good predictor of vascular events in this population.
• Moreover, CRP provides prognostic information beyond low-density lipids (LDL).
• We identified a unique population—low-LDL, high-CRP individuals —that otherwise might have been missed.
• This was the impetus for the JUPITER trial, which I’ll mention later.

At all levels of LDL, at all levels of metabolic syndrome, and at all levels of Framingham risk, CRP provides additive information on vascular risk. In conjunction with Peter Wilson and Scott Grundy, we are developing a CRP-modified Framingham Risk Score.

• There are now 34 large-scale prospective studies that have all come to the same conclusion: CRP is one of the most consistent risk stratifiers that we have.
• But it is important to think beyond CRP as a simple marker for high risk of disease.
• It also tells us something about the underlying biology.
• Metabolic Syndrome and CRP There is a component of the metabolic syndrome that’s proinflammatory and hypofibrolytic, which conveys additional risk.

Two years ago, we were able to show that CRP provided further discriminatory value to the presence or absence of metabolic syndrome. Patients without metabolic syndrome and with low CRP have very low risk; patients with metabolic syndrome and high CRP have very high risk.

1. Clearly, when the inflammatory mechanisms are engaged, metabolic syndrome patients do much worse.
2. There is tremendous enthusiasm among endocrine investigators for tying together the endocrine dysfunction of metabolic syndrome and the development of both diabetes and vascular events.
3. It might even be possible to redefine metabolic syndrome to include this added risk.

One way to do this would be to leave the obesity component alone, and to change the triglyceride and HDL components to one (since they are so often linked): triglycerides greater than 150 or an HDL less than 40. Keep the blood pressure and glucose components, but add a new qualifier: a CRP greater than 3.

This modified definition seems to predict both diabetes and vascular events better than the old one does, at least in our cohorts, where we’ve tested it. Unfortunately, the big picture is a little more complicated. For high sensitivity assays of CRP or “hsCRP,” we say that less than 1 mg/L is low risk, 1 to 3 mg/L is moderate risk, and greater than 3 mg/L is high risk—that’s simple enough.

But the continuum extends beyond that. The patients with the very highest levels of hsCRP —5 to 10, 10 to 20, or even greater than 20 mg/L—are, in fact, at the very highest risk. These are not false positives. These data help to explain why those with periodontal disease, arthritis, and other systemic inflammatory disorders all have higher vascular risk.

Perhaps inflammation from any cause has an adverse effect on the vascular endothelium. What about lowering CRP? Does that reduce risk? There’s no doubt that the very best way to lower CRP is through exercise, weight loss, and dietary control; of course, those are all proven already to lower vascular risk.

There is a paper that came out in February comparing the Atkins diet, the Zone diet, the Weight Watchers diet, and the Ornish diet. All these diets did basically the same thing: they got weight down a little bit, the lipid ratios came down, the CRPs came down, and insulin levels came down.

These processes are all intimately interrelated. Dieting works. Even gastric bypass surgery works. CRP, interleukin-6 (IL-6), and tumor necrosis factor (TNF) all come down in gastric surgery patients. But just removing the fat isn’t good enough. Our patients have to do the hard work. As published in the New England Journal of Medicine last year, liposuction does not alter insulin sensitivity; does not reduce CRP, IL-6, or TNF; and does not affect other risk factors for coronary heart disease.

I believe that the true impact of exercise has been underestimated in the general community. There are over 50 papers about the impact of exercise on inflammatory markers and event reduction. Here is an example: Milani and coworkers noted that cardiac rehab did a nice job of lowering CRPs, regardless of whether the patients were or were not on statins.

Moreover, CRPs fell whether or not the patients actually lost weight. The exercise benefit was independent of weight loss. Recent Data Pertaining to Statins Do we as cardiologists need to think about monitoring CRP in secondary prevention? These are already high-risk patients; is there incremental benefit to measuring CRP? In January of this year, 2 new papers came out that have really added important new perspective to this question.

We performed a prespecified analysis in PROVE IT/TIMI 22 to determine how much of the benefit of statin therapy was attributable to LDL reduction and how much was attributable to CRP reduction. We examined the achieved LDL and the achieved CRP at 30 days, to allow resolution of the acute-phase CRP and provide time for the statins to have a stabilizing effect on LDL.

From 30 days onward, how well did we predict events? Those who got their LDLs below 70 mg/dL, and about 50% of the patients did, had a lower event rate. But there is another side to the story. Fifty percent of the patients got their CRPs below 2 mg/L and 50% were above 2 mg/L at 30 days, and those levels were equally predictive of subsequent events.

Are these the same patients or are they different patients? We were pretty confident that they were going to be different patients, because in all the prior work, there was virtually no relationship between LDL and CRP, and no relationship in the change in LDL and the change in CRP.

• That’s exactly what we found.
• Only 3% of the variance in your patients’ CRP can be predicted on the basis of their LDL.
• So what happens if CRP comes down, but LDL doesn’t? What we found was about a 50% reduction in events in this population.
• What if the LDL does come down? Does lowering the CRP more provide more benefit? The simple answer to that question is yes.

Roughly 25% not only got the LDL below 70 mg/dL, they also got the CRP below 2 mg/L, and as a group these patients did substantially better in terms of long-term event-free survival. Moreover, if the CRP went down even further, to less than 1 mg/L, the event rates were lower still.

The predictive value of hsCRP stands up even after adjusting for age, sex, smoking status, diabetes, hypertension, obesity, peak creatine kinase, Killip class, early revascularization, and HDL; nothing changes. Even with these adjustments, CRP remains a strong predictor of outcome. But a major question remains.

Is it the drug, or is it the levels? The more potent a statin, on average, the greater the CRP reduction; but for the individual patient, this is a highly variable response. In PROVE IT/TIMI 22, what is particularly interesting is that if the LDL was below 70 mg/dL and the CRP was below 2 mg/L, the survival was the same regardless of the drug used.

The same was true for people with an LDL below 70 and high CRPs, and in people with LDLs above 70 and either high or low CRPs. In other words, what mattered was not so much the drug; what mattered was whether or not the patients achieved the “dual goals” of both LDL and CRP reduction. Achieving these dual goals appears to be more important than how you get there.

When we adjusted for only these 2 factors—the LDL and the CRP that were achieved—and re-examined the over-all benefit in the PROVE IT trial of atorvastatin 80 mg versus pravastatin 40 mg, the odds ratio went to 1.00; there was no difference. The REVERSAL data appeared simultaneously; the same drugs were used, in the same doses, in stable patients, looking at intravascular ultrasound measurements of plaque volume.

• Those results also showed no relationship between the change in LDL and the change in CRP, either with pravastatin or atorvastatin.
• As LDL comes down, we look for a slowing of the progression of the disease.
• As the CRP comes down, there is also a slowing of the progression with a little twist—namely that when the CRPs come down a lot, the atheroma volume actually starts to fall below the zero line.

The REVERSAL investigators did a similar stratified analysis, like the one we did in PROVE IT/TIMI 22, looking at whether patients ended up above or below the median LDL and CRP levels. When the LDL and the CRP did not come below their medians, there was an 8-mm 3 progression.

1. When only the LDL came down below median, there was less progression.
2. When only the CRP came down, there was some regression.
3. And when they both came down, there was more regression.
4. What we’ve learned from these 2 studies is that patients on statin therapy who achieve low levels of CRP have better clinical outcomes at all levels of achieved LDL.

The best clinical outcomes are obtained among statin-treated patients who achieve the dual goals of an LDL below 70 mg/dL and a CRP below 2 mg/L. This is true for statin-treated patients; we don’t know if this is true for patients on other classes of drugs.

The relationship between achieved LDL and achieved CRP is highly variable for individual patients and cannot be predicted on a clinical basis. Therefore, strategies to optimally and effectively prescribe statins to reduce risk may need to measure and monitor CRP in exactly the same way we measure and monitor LDL.

The JUPITER trial goes farther, to look at primary prevention patients who don’t normally qualify for statins: apparently healthy people with LDLs of less than 130 and CRPs above 2. We’re randomizing these patients to either rosuvastatin or placebo and looking at hard clinical endpoints at 3 to 4 years in 15,000 patients.

Genetics I want to say a few final words about genetics. A number of polymorphisms in the CRP gene have been identified by our group, as well as by other investigators around the world. Led by David Miller and David Kwiatkowski, we did a sequencing project across 3 different large populations—the Women’s Health Study, our PRINCE cohort, and the Physicians’ Health Study—and showed consistent effects across all 3 cohorts.

We also would suggest that about half of the population variance in CRP is attributable to lifestyle: smoking, diet, exercise all things that are modifiable. Because the other half is primarily inherited, the question arises: Can we identify any pharmacogenetic issues that will help us to design future trials to figure out what patients to target for this inflammatory response? We hope to have the opportunity to answer that question in the not-too-distant future.

What causes high ESR but normal CRP?

Patients with high CRP but normal ESR typically have infection, ischemia, or thromboembolism. Patients with high ESR but normal CRP may have systemic inflammatory or autoimmune processes, including those associated with malignancy.

Can garlic reduce ESR in blood?

Conclusion – The results imply that administrating 400 mg of standardized garlic extract twice a day for 8 weeks resulted in a significant reduction in IL-6, CRP and ESR. Since inflammatory state can be a serious life threatening condition in PD patients, we suggest prescribing this safe and well-tolerated natural substance to attenuate the inflammatory state in these patients.

What is the fastest way to reduce ESR?

Takeaway – The erythrocyte sedimentation rate (ESR) test or “sed rate test” is a blood test that mainly checks for chronic inflammation. High levels may be used to diagnose or screen for specific conditions. However, this test is not sensitive or specific.

It is often ordered along with other labs. A high sed rate may point to various inflammatory disorders like polymyalgia rheumatica, temporal arteritis, and others. Factors that may help lower inflammation and ESR include engaging in regular exercise, living a healthy and hygienic lifestyle, losing weight if overweight, and eating nutritious foods.

A low sedimentation rate is often normal. In some cases, it may point to blood cell disorders. The most important step is to see your doctor to get adequate diagnosis and treatment.

When should I worry about my ESR?

4) Serious Conditions – ESR levels higher than 100 mm/hr could suggest a serious disease, such as infection, heart disease, or cancer, ESR levels higher than normal may predict cancer or cancer progression, like metastasis, Your doctor may order an ESR test to check for specific inflammatory or chronic conditions, along with other tests.

What ESR level is alarming?

When should I worry about my ESR? – To get an ESR rate over 100 mm/hr should already cause an alarm. While going beyond the normal range suggests health issues related to inflammation, an extremely high ESR rate entails severe medical conditions such as cancer, heart disease, and untreated infections. Consult your doctor to secure other diagnostic procedures.

Can a healthy person have high ESR?

Why do I need this test? – You may need this test if you have symptoms of one of the diseases that may cause ESR to go up. You may also need this test if you have already been diagnosed with a disease that causes a high ESR. The test can allow your healthcare provider to see how well you are responding to treatment.

Temporal arteritis Rheumatoid arthritis Polymyalgia rheumatica

ESR is not used as a screening test in people who do not have symptoms or to diagnose disease because many conditions can cause it to increase. It might also go up in many normal cases. ESR doesn’t tell your healthcare provider whether you have a specific disease. It only suggests that you may have an active disease process in your body.