Hematopathology / ESR Determinants
Determinants of the Erythrocyte Sedimentation Rate
in the Era of Microinflammation
Excluding Subjects With Elevated C-Reactive Protein Levels
Arie Steinvil, MD, Itzhak Shapira, MD, Yaron Arbel, MD, Dan Justo, MD, Shlomo Berliner, MD, PhD,
and Ori Rogowski, MD
Key Words: Erythrocyte sedimentation rate; High-sensitivity C-reactive protein; Microinflammation
DOI: 10.1309/U04E2YFJRR6JQQTK
Abstract
The erythrocyte sedimentation rate (ESR) can
be used to identify low-grade inflammation that
contributes to future vascular events. ESR determinants,
however, have not been explored in the absence of a
subclinical or microinflammatory response.
The ESR was determined in a large cohort of
apparently healthy participants, excluding subjects
with high-sensitivity C-reactive protein (hs-CRP)
concentrations more than 5 mg/L (47.62 nmol/L).
Linear regression models were used to identify the
determinants of the ESR.
The study population comprised 6,237 subjects.
The main laboratory variables found to affect ESR
were levels of fibrinogen, hemoglobin, globulin, and
triglycerides (all P < .001; R2 = 0.34 and 0.44 for men
and women, respectively). Sex was found to affect ESR
alone and in combined interactions with most other
variables. Age did not affect ESR.
The main determinants of ESR in an inflammation-
free cohort are sex and levels of fibrinogen,
hemoglobin, globulins, and triglycerides.
486 Am J Clin Pathol 2008;129:486-491
486 DOI: 10.1309/U04E2YFJRR6JQQTK
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Atherothrombotic disease is a leading cause of morbidity
and mortality in the Western world and is associated with low-
grade, subclinical inflammation (so-called microinflamma-
tion). In this regard, the Westergren erythrocyte sedimentation
rate (ESR) has been shown to be an established inflammation-
sensitive biomarker with proven prognostic value.1-3 Yet,
previous studies that explored the normal values and determi-
nants of ESR in apparently healthy subjects and subjects with
atherothrombotic risk factors did not use accepted biomarkers
to exclude the presence of a significant acute phase response
in the subjects.2,4-6 This limitation has been repeatedly noted
in the literature.3,7 We analyzed the determinants of ESR
in a cohort of apparently healthy subjects and subjects with
atherothrombotic risk factors in whom the eventual presence
of a significant acute phase response was excluded by using a
high-sensitivity C-reactive protein (hs-CRP) assay.
Materials and Methods
Population
We analyzed the data collected as part of the Tel-Aviv
Medical Center Inflammation Survey (TAMCIS), a registered
data bank of the Israeli Ministry of Justice.8-11 This is a rela-
tively large survey of apparently healthy subjects attending a
center for periodic health examinations.
In our study, patients attending the Tel-Aviv Sourasky
Medical Center, Tel-Aviv, Israel, for a routine health exami-
nation between September 2002 and May 2007 were invited
to participate in the TAMCIS. All subjects enrolled were
recruited during their routine annual health checkup and
© American Society for Clinical Pathology

gave written consent in accordance with the guidelines of
the institutional ethics committee. A total of 11,274 subjects
gave informed consent (7,095 men and 4,179 women). A
systematic examination ruled out enrollment bias owing to
sociodemographic and biomedical variables.
We initially excluded 2,627 subjects owing to known
inflammatory diseases (eg, arthritis, inflammatory bowel
disease, or psoriasis), pregnancy, steroidal or nonsteroidal
treatment (except for aspirin at a dose of ≤325 mg/d), acute
infection, or invasive procedures (eg, surgery or catheteriza-
tion) during the last 6 months. We later excluded 584 subjects
from the analysis owing to a history of proven atherothrom-
botic event (myocardial infarction, cerebrovascular disease,
or peripheral artery occlusion disease) or known diabetes
mellitus. We further excluded 210 subjects with missing
ESR measurements or with relatively high ESR values (>50
mm/h), as done in previous similar studies,1 and an addi-
tional 692 with anemia, defined as hemoglobin concentrations
below the lower limit of normal in our local laboratory (13.5
g/dL [135 g/L] and 11.7 g/dL [117 g/L] for men and women,
respectively). Finally, to exclude hidden inflammation and/or
infections, we excluded 924 subjects with hs-CRP concentra-
tions of more than 5 mg/L (47.62 nmol/L). Following these
exclusions, the study group comprised 6,237 subjects (4,187
men and 2,050 women).
Laboratory Methods
The ESR was determined by using the method of
Westergren.12,13 In brief, 4.5 mL of venous blood was sam-
pled in a BD Vacutainer (Becton Dickinson, Franklin Lakes,
NJ) containing a 0.5-mL, 3.8% solution of sodium citrate.
The test tube was mixed gently immediately following blood
sampling and again just before measuring, which took place
within 2 hours after the blood was drawn. A standard 200-
mm, Westergren method glass tube was filled to the zero mark
at the top, set in a vertical position, and left for 1 hour. The
distance from the bottom of the surface of the meniscus to
the top of the column was then measured, and the result was
expressed as millimeters in the first hour.
Analysis of the CBC count was performed using the
Coulter STKS electronic cell analyzer (Beckman Coulter, Nyon,
Switzerland). Fibrinogen was quantified by the method of
Clauss14 and using a Sysmex 6000 autoanalyzer (Sysmex,
Hyaga, Japan), and the hs-CRP was measured by using a Behring
BN II Nephelometer (DADE Behring, Marburg, Germany).15
Definition of Atherothrombotic Risk Factors
Results of the routine health checkup were assessed
by using certain definitions to recognize atherothrombotic
risk factors. These included diabetes mellitus, which was
defined as a fasting blood glucose level of 126 mg/dL (7.0
mmol/L) or more or the intake of insulin or oral hypoglycemic
© American Society for Clinical Pathology
Hematopathology / Original Article
medications. Hypertension was defined as a blood pressure
of 140/90 mm Hg or more in 2 separate measurements or the
intake of antihypertensive medications. Dyslipidemia was
defined as low-density lipoprotein or non–high-density lipo-
protein cholesterol concentrations (for subjects with elevated
triglyceride concentrations of 200 mg/dL [2.26 mmol/L] or
more) higher than the recommended levels according to the
risk profile defined by the updated Adult Treatment Panel III
recommendations16 or the intake of lipid-lowering medica-
tions. Smokers were defined as subjects who smoked at least
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5 cigarettes per day and past smokers as subjects who had quit
smoking for at least 30 days before examination.
Statistical Analysis
All data were summarized and displayed as mean (SE) for
continuous variables and as number (percentage) of patients in
each group for categorical variables. For all categorical variables
the χ2 statistic was used for assessing the statistical significance
between the 2 sexes, and the independent Student t test was used
for continuous variables. The age-adjusted comparison of con-
tinuous variables between the 2 sexes was done by using analysis
of covariance under a general linear model.
To assess which variables contribute to the variability
of ESR, we performed linear regression using the stepwise
method with ESR as the dependent variable and many known
and possible confounding parameters as the independent
variables, which included sex; age; waist measurement;
body mass index; alcohol consumption and sports activity;
use of medication, including aspirin, α-blockers, β-blockers,
calcium channel blockers, angiotensin converting enzyme
inhibitors, angiotensin II receptor blockers, statins, fibrates,
oral contraceptives, and hormone replacement therapy; car-
diovascular risk factors, including systolic and diastolic blood
pressure measurements, smoking status, family history of
coronary heart disease, lipid profile including high-density
lipoprotein, low-density lipoprotein, and triglyceride concen-
trations; and glucose, serum albumin and globulin, hemoglo-
bin, and fibrinogen concentrations.
In addition to the linear regression models and to evalu-
ate the importance of age, we divided our cohort into age
groups, excluded the small groups of subjects younger than
20 years and older than 70 years, and calculated the mean
ESR and fibrinogen concentration in each age group plus the
overall significance between the age groups and the linear
trend between groups, using 1-way analysis of variance. The
comparison of ESR in the age groups following adjustment
for the differences in fibrinogen concentration between the
groups was done using analysis of covariance under a gen-
eral linear model. Finally, to test the prediction capability of
ESR, we randomly chose approximately 70% of the cohort
and calculated the simple linear regression equation with the
3 variables that demonstrated the highest partial correlations
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487 DOI: 10.1309/U04E2YFJRR6JQQTK 487
Hematopathology / ESR Determinants

in the previous linear regression models and compared the
estimated ESR based on this equation with the measured ESR
in the remaining 30% of the cohort by using the paired t test.
All of the analyses were considered significant at a 2-tailed P
value of less than .05. The SPSS statistical package was used
to perform all statistical evaluation (SPSS, Chicago, IL).
Results
We analyzed the data for 6,237 apparently healthy
measurements, relevant laboratory values, inflammation-
sensitive biomarkers including the ESR, sports activity, and
alcohol consumption in the 2 sexes are described in zTable 1z.
We noted significant differences between sexes in all param-
eters. The respective cardiovascular risk factors and frequency
of medication used in the 2 sexes are described in zTable 2z.
To assess which variables explain best the variabil-
ity in ESR, we performed linear regressions. In the first
regression, we included data for all subjects together and
included sex as a factor in the analysis and the interaction

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subjects (4,187 men and 2,050 women) at a mean (SD) age between sex and other parameters. The results (not shown)
of 44 (11) years. The anthropometric values, blood pressure demonstrated that sex has an important effect on the ESR

zTable 1z
Baseline Population Characteristics by Sex*

Men (n = 4,187) Women (n = 2,050) P

Age (y) 43 (0.2) 45 (0.2) <.001

BMI (kg/m2) 27 (0.1) 24 (0.1) <.001
Waist measurement (cm) 95 (0.1) 80 (0.2) <.001
Blood pressure (mm Hg)
Systolic 124 (0.2) 115 (0.3) <.001
Diastolic 78 (0.1) 73 (0.2) <.001
Glucose (mg/dL) 93 (0.2) 88 (0.2) <.001
(mmol/L) 5.16 (0.01) 4.89 (0.01)
Cholesterol
LDL (mg/dL) 124 (0.5) 119 (0.7) <.001
(mmol/L) 3.21 (0.01) 3.08 (0.02)
HDL (mg/dL) 51 (0.2) 66 (0.3) <.001
(mmol/L) 1.32 (0.01) 1.7 (0.01)
Triglycerides (mg/dL) 130 (1.1) 93 (1.6) <.001
(mmol/L) 1.46 (0.01) 1.05 (0.02)
Fibrinogen (mg/dL) 272 (0.8) 294 (1.1) <.001
(µmol/L) 7.99 (0.02) 8.64 (0.03)
hs-CRP (mg/L) 1.13 (1.0)
1.06 (1.0) .003
(nmol/L) 10.76 (9.52) 10.10 (9.52)
ESR (mm/h) 8.9 (0.1) 16.3 (0.1) <.001
Sports activity (h/wk) 2.5 (0.05)
2.1 (0.07) <.001
Alcohol consumption (glasses per wk) 1.4 (0.03)
0.6 (0.05) <.001

BMI, body mass index; ESR, erythrocyte sedimentation rate; HDL, high-density lipoprotein; hs-CRP, high-sensitivity C-reactive protein; LDL, low-density lipoprotein.
* Data are given as mean (SE). All means (besides age) are adjusted for age.

zTable 2z
Baseline Frequencies of Medication and Cardiovascular Risk Factors by Sex*

Men (n = 4,187) Women (n = 2,050) P

Hypertension 866 (20.7) 255 (12.4) <.001

Dyslipidemia 1,250 (29.9) 417 (20.3) <.001
Current smoker 690 (16.5) 407 (19.9) <.001
Past smoker 1,069 (25.5) 414 (20.2)
Family history of CHD 601 (14.4) 380 (18.5) <.001
Aspirin 203 (4.8) 43 (2.1) <.001
β-Blockers 123 (2.9) 55 (2.7) .570
Calcium channel blockers 64 (1.5) 23 (1.1) .198
ACE inhibitors 97 (2.3) 36 (1.8) .150
ARBs 30 (0.7) 6 (0.3) .038
Statins 282 (6.7) 120 (5.9) .183
Fibrates 33 (0.8) 10 (0.5) .178
Oral contraceptives — 221 (10.8) —
Hormone replacement therapy — 201 (9.8) —

ACE, angiotensin converting enzyme; ARB, angiotensin II receptor blocker; CHD, coronary heart disease.
* Data are given as number (percentage).

488 Am J Clin Pathol 2008;129:486-491 © American Society for Clinical Pathology

488 DOI: 10.1309/U04E2YFJRR6JQQTK
 Hematopathology / Original Article

with significant interaction between sex and most other vari-
ables that influenced the ESR (such as levels of fibrinogen,
hemoglobin, globulins, and triglycerides). Owing to this find-
ing and to simplify the results, we decided to analyze the sexes
separately. zTable 3z gives the results of the linear regression
performed for each sex separately. Fibrinogen, hemoglobin,
and serum globulin levels are the most important variables
that explain most of the variability in the results of ESR (R2
= 0.34 and 0.44 for men and women, respectively), without
significant differences between the sexes.
cohort into 5 age groups of 10 years and calculated the mean
ESR and fibrinogen concentration zTable 4z. As in previously
published data, we found significant increases in ESR and
fibrinogen with increasing age (P for linear trend < .001 for
both variables in the 2 sexes), which was nonsignificant or
marginally significant for ESR when we adjusted for fibrino-
gen differences (Table 4).
Finally, to evaluate the magnitude of ESR prediction
error, based on the 3 most important determinants we
found, we reanalyzed the linear regression equation based

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Surprisingly, age did not enter the model for men and
entered the model for women with very low partial correla-
tion. To solve this discrepancy with previous studies that did
not include fibrinogen levels in the analyses, we divided our
on a randomly selected 70% of the cohort zTable 5z and
calculated the estimated ESR for the remaining 30% of the
cohort. The mean differences (95% confidence interval)
between the measured and estimated ESR in this group
were 0.18 (–0.11 to 0.47; P = .22) and –0.37 (–0.83 to 0.10;
P = .13) for men and women, respectively.

zTable 3z
Linear Regression Results for Erythrocyte Sedimentation Rate
in Men and Women

Partial
β P Correlation

Men (R2 = 0.34)

zTable 5z
Fibrinogen
.053 <.001 0.475
Hemoglobin –2.130
<.001 –0.328 Concise Linear Regression Results for a Randomly Selected
Globulins
.344 <.001 0.219 70% of the Cohort
Triglycerides
.008 <.001 0.108
BMI
.076 .002 0.050 Partial
Women (R2 = 0.44) β P Correlation
Fibrinogen
.074 <.001 0.526
Hemoglobin –3.768
<.001 –0.441 Men (R2 = 0.33)
Globulins
.504 <.001 0.256 Fibrinogen .055 <.001 0.505
LDL
.015 .001 0.073 Hemoglobin –1.968 <.001 –0.309
Waist
.045 .004 0.065 Globulins .377 <.001 0.240
Triglycerides
.008 .008 0.060 Women (R2 = 0.41)
Fibrate use 6.041 .008 0.060 Fibrinogen .081 <.001 0.555
Age
.037 .017 0.054 Hemoglobin –3.650 <.001 –0.424
Past smoker –0.744
.030 –0.049 Globulins .545 <.001 0.273

BMI, body mass index; LDL, low-density lipoprotein.

zTable 4z
Mean ESR, Fibrinogen Level, and Fibrinogen-Adjusted ESR According to 10-year Age Groups in Men and Women*

Age Group ANOVA

P for
21-30 31-40 41-50 51-60 61-70 P Trend

Men (n = 609) (n = 1,105) (n = 1,297) (n = 952) (n = 208)

ESR 6.9 (6.5-7.3) 8.4 (8.1-8.7) 9.1 (8.8-9.4) 9.6 (9.2-10.0) 11.3 (10.4-12.3) <.001 <.001
Fibrinogen 240 (236-244) 260 (257-263) 278 (275-280) 287 (283-290) 300 (293-306) <.001 <.001
(mg/dL)
ESR†
8.5 (8.1-9.0) 8.9 (8.6-9.2) 8.7 (8.4-9.0) 8.7 (8.4-9.0) 9.8 (9.1-10.5) .038
Women (n = 215) (n = 396) (n = 736) (n = 610) (n = 73)
ESR 13.6 (12.6-14.6) 15.3 (14.6-16.1) 16.5 (15.9-17.0) 17.8 (17.1-18.4) 18.0 (16.1-19.9) <.001 <.001
Fibrinogen 269 (262-276) 285 (280-290) 296 (292-299) 312 (308-316) 303 (291-314) <.001 <.001
(mg/dL)
ESR†
15.6 (14.6-16.5) 16.1 (15.4-16.8) 16.5 (16.0-17.0) 16.6 (16.1-17.2) 17.4 (15.8-19.0) .222

ANOVA, analysis of variance; ESR, erythrocyte sedimentation rate.

* Fibrinogen levels are given in conventional units; to convert to Système International units (µmol/L), multiply by 0.0294. Parenthetical values represent the 95% confidence

interval for the mean.

† Fibrinogen-adjusted estimated marginal mean of ESR.

© American Society for Clinical Pathology Am J Clin Pathol 2008;129:486-491 489

489 DOI: 10.1309/U04E2YFJRR6JQQTK 489
Hematopathology / ESR Determinants
Discussion
The present study is the first to document the determi-
nants of ESR in a relatively large group of apparently healthy
subjects and subjects with atherothrombotic risk factors
in whom significant underlying acute phase response was
excluded by using an hs-CRP assay and a conservative cutoff
level of 5 mg/L (47.62 nmol/L). Our main finding is that the
determinants of ESR in these carefully selected subjects are
similar to what has been shown in the past and include the lev-
els of fibrinogen, hemoglobin, globulins, and triglycerides.2,4-6
These findings are relevant for the use of ESR as a cheap and
readily available screening tool for the presence of low-grade
inflammation in apparently healthy people and people with
atherothrombotic risk factors. This low-grade inflammation
on the one hand and the ESR on the other have been shown
to be of help in the process of singling out people at risk. In
addition, the present study helps to define normal values for
people who indeed have a relatively low inflammatory burden
and atherothrombotic risk.
Sex differences were significant for all population char-
acteristics, including acute phase response proteins. Sex has
an important role in defining normal values for the ESR. In
our analysis, sex had significant statistical interactions with
all of the major determinants of the ESR, demonstrating an
additive effect on the ESR and on its components.
Age did not correlate strongly with ESR. Previous large
population studies2,4,6 demonstrated an age-related increase in
the normal values of ESR. This finding was also noted in our
primary analysis. However, when we adjusted our results for
the fibrinogen concentration, the main laboratory determinant
of the ESR, we found that age had no consistent linearity with
ESR. Furthermore, when we compared age groups, we first
found an age-related difference and trend as noted in previous
studies. However, when we again adjusted our results to the
mean fibrinogen level in each age group, there was no dif-
ference in the ESR between groups. The fibrinogen effect on
ESR is well described in the literature,17,18 which makes it a
variable that cannot be ignored in any study investigating the
ESR. The limitation of the previous studies that did not con-
sider fibrinogen levels as a possible confounder in their ESR
analysis was also noted in the literature.3,7
The finding that ESR might be age independent is further
supported by the previous work of Feher and colleagues19,20
on hemorheological parameters and aging. Feher and col-
leagues studied the differences in fibrinogen, hematocrit, RBC
aggregation, and plasma and whole blood viscosity in 3 age
groups (<45, 45-65, >60 years) in 6,236 cardiovascular and
cerebrovascular patients and in a selected smaller group with
matching parameters to exclude the effect of risk profile. In
the whole population, the correlation of these hemorheologi-
cal parameters and advancing age was inconsistent, and in the
490 Am J Clin Pathol 2008;129:486-491
490 DOI: 10.1309/U04E2YFJRR6JQQTK
selected population, these parameters did not correlate with
advancing age at all. Our results add to these data, suggesting
that ESR as well is independent of aging and that increased
values are probably associated with higher prevalence of dis-
eases such as atherosclerosis. In that context, ESR may have
a potential role in early detection of hyperfibrinogenemia and
low-grade inflammation21 and as a marker of the atheroscle-
rotic burden in apparently healthy people.22
We finally validated our results by constructing a linear
equation23 based on the main 3 contributors of ESR for each
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sex in a randomly selected 70% of the study population.
When we applied this equation to data for the remaining 30%
of the study population, we found no statistically significant
difference between the measured and predicted ESR. Such
an equation might be useful for an indirect measure of the
fibrinogen level.
The ESR is an easy-to-use and inexpensive method that
can aid in early detection of microinflammation and eventual
atherosclerotic burden. Its main determinants are sex and lev-
els of fibrinogen, hemoglobin, globulins, and triglycerides.
The ESR is not strongly related to age.
From the Department of Internal Medicine “D,” Tel-Aviv
Sourasky Medical Center and Sackler Faculty of Medicine, Tel-
Aviv University, Tel-Aviv, Israel.
Address reprint requests to Dr Rogowski: Internal Medicine
“D,” Tel-Aviv Sourasky Medical Center, 6 Weizman St, Tel-Aviv,
64239 Israel.
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