Neutrophil-to-Lymphocyte Ratio Is a Prognostic Marker in

Acute Ischemic Stroke

Jie Xue, MD, Wensi Huang, MD, Xiaoli Chen, MD, Qian Li, MD, Zhengyi Cai, MD,
Tieer Yu, MD, and Bei Shao, MD

Background: Neutrophil-to-lymphocyte ratio is an independent predictor of mor-

tality in patients with acute ischemic stroke. However, it is uncertain whether
neutrophil-to-lymphocyte ratio is related with functional outcome and recurrent
ischemic stroke. In this study, we aimed to investigate the relationship of neutrophil-
to-lymphocyte ratio with stroke severity, functional outcome, and recurrent ischemic
stroke after acute ischemic stroke. Methods: A total of 280 patients with acute isch-
emic stroke were included in the study. Patients were divided into 3 groups according
to the neutrophil-to-lymphocyte ratio value (<2, 2-3, >3). Demographic, clinical,
and laboratory data were collected for all patients. We evaluated the association
between neutrophil-to-lymphocyte ratio and (1) stroke severity on admission, (2)
functional outcome at 3 months, and (3) recurrent ischemic stroke. Regression anal-
yses were performed, adjusting for confounders. Results: After adjustment for potential
confounders, neutrophil-to-lymphocyte ratio was associated with an increased risk
of stroke severity on admission (odds ratio [OR] 1.364, 95% confidence interval
[CI] 1.101-1.690, P = .005) and primary unfavorable outcome (OR 1.455, 95% CI
1.083-1.956, P = .013). After a median of 1.13 years (interquartile range.91-1.42) of
follow-up, neutrophil-to-lymphocyte ratio was associated with recurrent isch-
emic stroke after adjustment (hazard ratio 1.499, 95% CI 1.161-1.935, P = .002).
Conclusions: Our study suggests that neutrophil-to-lymphocyte ratio is associ-
ated with stroke severity on admission, primary unfavorable functional outcome,
and recurrent ischemic stroke in patients with acute ischemic stroke. Key Words:
Neutrophil-to-lymphocyte ratio—acute ischemic stroke—prognosis—inflammation.
© 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.

Introduction
Stroke is classically defined as a neurological deficit at-
tributed to an acute focal injury of the central nervous
system by a vascular cause and is the major cause of dis-
ability and mortality in the world.1 In China, it superseded
From the Department of Neurology, The First Affiliated Hospital
of Wenzhou Medical University, Wenzhou 325000, China.
Received July 11, 2016; revision received October 10, 2016; accepted
November 13, 2016.
Address correspondence to Bei Shao, MD, Department of Neurology,
The First Affiliated Hospital of Wenzhou Medical University, Shangcai
Road, Wenzhou 325000, China. E-mails: shaobei56@126.com.
1052-3057/$ - see front matter
© 2017 National Stroke Association. Published by Elsevier Inc. All
rights reserved.
http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2016.11.010
heart disease and became the first leading cause of death
and adult disability, with an annual stroke mortality rate
of approximately 157 per 100,000 people.2 Ischemic stroke
accounts for 80%-85% of all cases and is characterized
by the cutting off of cerebral blood flow that results in
damaged brain tissues.3 Therefore, it is important to un-
derstand the whole process of the development of this
disease and do what is possible to control the risk factors
at an earlier stage.
It has been demonstrated that inflammatory response
participates in all pathophysiological processes of acute
ischemic stroke (AIS).4 Inflammation mediators are ex-
pressed at low levels in normal brain tissue. An ischemic
brain could induce the release of proinflammatory cytokines
and recruitment of immune cells, which represent an im-
portant mechanism of secondary progression of brain
lesion.5 A large body of evidence has confirmed that the

650 Journal of Stroke and Cerebrovascular Diseases, Vol. 26, No. 3 (March), 2017: pp 650–657
NEUTROPHIL-TO-LYMPHOCYTE RATIO IN AIS
inflammatory response exacerbates ischemic brain injury
and neurological dysfunction.4,6,7 As main immune cells,
neutrophils and lymphocytes play important roles in me-
diating the response to cerebrovascular disease. In patients
with AIS, early higher white blood cell (WBC) and neu-
trophil counts were found to be correlated with larger
infarct volumes and increased stroke severity. 8 In-
creased peripheral WBCs and neutrophil counts were also
observed to be associated with recurrent ischemic stroke,9
whereas low lymphocyte counts were seen to be asso-
ciated with a poor functional outcome at 3 months after
AIS.10
Recently, it was reported that WBC is an independent
predictor of stroke severity, greater degree of disability,
and 30-day mortality in patients with AIS.11 Neutrophil-
to-lymphocyte ratio (NLR) is a simple marker that can
be easily calculated from the differential WBC count. It
has been newly reported that NLR is an indicator of overall
systemic inflammatory status in the Asian population.12
As a marker of systemic inflammation, NLR was related
to poor prognosis in patients with cancer and coronary
artery disease.13-15 This ratio has been thought as a better
predictive factor than total WBC count or neutrophil count
in cardiovascular disease.16 In recent studies, NLR was
shown to correlate with mortality in patients with AIS.17,18
However, the effects of NLR on functional outcome and
recurrent ischemic stroke in AIS are still uncertain.
In this study, we aimed to evaluate the relationship
between stroke severity, functional outcome, recurrent isch-
emic stroke, and NLR in patients with AIS.
Materials and Methods
Study Population
This study was performed beginning February 2014 to
May 2015. Patients with AIS were recruited from the First
Affiliated Hospital of Wenzhou Medical University as in-
patients admitted to the neurology department. We enrolled
only patients who were admitted to the hospital with a
diagnosis of AIS within 6 days of presentation of symp-
toms. Stroke was defined as the first symptomatic
occurrence of ischemic stroke according to the recom-
mendations from the World Health Organization.19 The
exclusion criteria for patients were the following: (1) those
diagnosed with infection within 1 week before stroke onset
or within 72 hours after admission; (2) patients with he-
matologic disorders, coronary heart disease, or a history
of cancer; (3) use of steroids or immunosuppressants; (4)
stroke history within 6 month; and (5) patients de-
ceased during hospital admission. One patient died from
acute respiratory failure and circulatory failure caused
by stroke. Ischemic stroke etiologic subtypes were clas-
sified according to the Trial of Org 10172 in Acute Stroke
Treatment criteria.20
The study was approved by the ethics committee of
the First Affiliated Hospital of Wenzhou Medical Uni-
651
versity. All patients or their legal representations signed
the informed consent before inclusion in this study.
Clinical Data
Baseline clinical data were collected for all patients, in-
cluding demographic information (age, gender, body mass
index) and risk factors (hypertension, diabetes mellitus,
hyperlipidemia, atrial fibrillation [AF], smoking, and alcohol
drinking). Hypertension was defined as systolic blood pres-
sure (BP) of 140 mm Hg, a diastolic BP of 90 mm Hg,
the reported use of antihypertensive medications, or a
history of diagnosed hypertension. Diabetes mellitus was
defined as fasting serum glucose of ≥126 mg/dL (7 mmol/
L), a non-fasting glucose of ≥200 mg/dL (11.1 mmol/L),
use of diabetic medications, or a previously established
diagnosis. Hyperlipidemia was diagnosed if low-
density lipoproteins (LDL)-cholesterol level is ≥4.1 mmol/
L, total cholesterol level is ≥6.2 mmol/L, or use of lipid-
lowering agents after being diagnosed with hyperlipidemia.
A history of AF was defined as AF recorded at the time
of the electrocardiography or any previously known
episode of AF. All patients were examined with cranial
magnetic resonance imaging. The infract volume was cal-
culated on diffusion-weighted imaging using the formula
.5 × a × b × c.21 Treatments were managed for the en-
rolled patients according to previously described
guidelines.22
Blood samples of all patients were collected and ana-
lyzed within 24 hours after admission. Laboratory
parameters such as WBC count, total cholesterol, triglyc-
erides, high-density lipoproteins, LDL, high-sensitivity
c-reactive protein (Hs-CRP), serum creatinine, fasting blood
glucose, and glycated hemoglobin were tested in the hos-
pital’s biochemistry department. NLR was calculated as
the ratio of neutrophil count to lymphocyte count.
Stroke Severity and Short-Term Functional Outcome
Stroke severity was assessed based on the National In-
stitutes of Health Stroke Scale (NIHSS).23 According to
a previous study, we defined moderate to severe stroke
with NIHSS ≥ 6, whereas mild stroke had NIHSS scores
of 0-5.24 The primary functional outcome was measured
at 3 months after stroke onset using the modified Rankin
scale (mRS, scores range from 0 to 6).25 An unfavorable
functional outcome was defined as mRS of 3-6 points.10
Barthel index (BI)26 was collected at the same time as sec-
ondary functional outcome, and a score below 85 on the
BI was defined as a poor outcome.
Recurrent Ischemic Stroke
Patients were followed-up by electronic medical records
or telephone interviews to confirm whether recurrent isch-
emic stroke had occurred. The follow-up period was
defined as the time from the date of admission to the
652
date of the recurrent ischemic stroke or to November 12,
2015, if no ischemic stroke event was reported.
Statistical Analysis
All statistical analyses were performed with the SPSS
Statistics 22.0 software (SPSS Inc., Chicago, IL). Contin-
uous data were presented as the mean value ± standard
deviation or median with interquartile range. Distribu-
tion normality was analyzed with the Kolmogorov–
Smirnov test. Differences between mean values were
assessed using the unpaired t-test or by analysis of vari-
ance. Kruskal–Wallis and Mann–Whitney U tests were used
for the comparison of non-normally distributed vari-
ables. Categorical data were expressed as frequency and
percentage, and were assessed using the chi-square test.
The study population were divided into group 1 (NLR
<2), group 2 (NLR 2-3), and group 3 (NLR >3) based on
a previous study.15 Spearman’s rank correlation was per-
formed for bivariate correlation. Multivariate logistic
regression analysis was used to test whether higher NLR
predicted worse stroke severity and functional outcome
in AIS. Cox proportional hazard models were per-
formed to evaluate the relationship between NLR and
recurrent ischemic stroke. The backward elimination
method was applied, and removal criteria for steps were
accepted as ≥.10. All data analyses were adjusted for po-
tential confounders. Receiver operating characteristic curve
analysis was used to determine the predictive values of
NLR for stroke severity (NIHSS ≥ 6), primary unfavor-
able functional outcome (mRS >2), and secondary poor
outcome (BI <85). A 2-sided P value <.05 was defined
as statistically significant.
Results
Baseline Characteristics
A total of 292 patients with AIS fulfilled the criteria;
280 patients finished the 3-month follow-up, whereas 12
patients could not be contacted. Baseline characteristics
of participants in the AIS group are shown in Table 1.
The mean age of patients with AIS was 61.8 ± 10.2 years
old and 107 (38.2%) were women. Patients with AIS were
divided into 3 groups according to the NLR value: 121
patients (43.2%) were in group 1 (NLR < 2), 102 patients
(36.4%) were in group 2 (NLR 2-3), and 57 patients (20.4%)
were in group 3 (NLR >3). The patients in group 3 were
more likely to be male and had a significantly higher level
of WBC and Hs-CRP. The infarct volume of group 3 was
also found to be larger than the other 2 groups.
Stroke Severity and Functional Outcome
Moderate to severe strokes on admission were found
in 77 patients (27.5%). After 3 months of follow-up, a
primary unfavorable outcome was found in 50 patients
(17.9%), whereas 35 patients (12.5%) had a secondary un-
J. XUE ET AL.
favorable outcome. There were significant differences
among the 3 subgroups; the patients in group 3 had more
moderate to severe stroke and worse functional outcome
(Table 2). There was a positive correlation between NLR
and NIHSS score (r = .247, P < .001; Fig 1). In the mul-
tivariable model adjusting for age, gender, the time from
stroke onset to admission, systolic BP, diastolic BP, hy-
pertension, diabetes mellitus, hyperlipidemia, AF, smoking,
alcohol drinking, infarct volume, WBC, Hs-CRP, fasting
blood glucose, glycated hemoglobin, LDL, serum creati-
nine, and medications, higher NLR was associated with
an increased risk of moderate to severe stroke on ad-
mission (odds ratio [OR] 1.364, 95% confidence interval
[CI] 1.101-1.690, P = .005). NLR was associated with primary
unfavorable outcome in the multivariable model with
further adjustment for NIHSS score (OR 1.455, 95% CI
1.083-1.956, P = .013). However, NLR was not associ-
ated with secondary unfavorable outcome (OR 1.271, 95%
CI .928-1.739, P = .135) (Table 3).
In the receiver operating characteristic curve analysis,
the optimal cutoff value of NLR for prediction of stroke
severity on admission was found to be 1.87 with a sen-
sitivity of 81.8% and a specificity of 42.9% (area under
the curve: .646, 95% CI .575-.717). The optimal cutoff value
of NLR for prediction of primary unfavorable outcome
was 2.39 with a sensitivity of 72.0% and a specificity of
70.9% (area under the curve: .717, 95% CI .638-.796), and
for prediction of secondary unfavorable outcome was 2.39
with a sensitivity of 71.4% and a specificity of 68.2% (area
under the curve: .696, 95% CI .607-.785) (Fig 2).
Recurrent Ischemic Stroke
In our study, over a median of 1.13 years (interquartile
range .91-1.42) of follow-up, 12 recurrent ischemic events
occurred: 6 were atherosclerotic, 1 was cardioembolic, 1
was lacunar, and 4 were cryptogenic. The patients in group
3 had a higher risk of recurrent ischemic stroke than the
patients in the other 2 groups, but the difference was not
statistically significant (Table 2). In the Cox regression anal-
ysis, NLR was considered as a continuous variable and
was associated with recurrent ischemic stroke after ad-
justment for potential confounders (hazard ratio 1.499,
95% CI 1.161-1.935, P = .002) (Table 3).
Discussion
This is the first study evaluating the value of NLR in
predicting poor prognosis in patients with AIS system-
atically. The results indicate that a higher NLR is associated
with stroke severity on admission, short-term unfavor-
able outcome, and recurrent ischemic stroke after AIS.
Moreover, the best estimated cutoff values of NLR for
prediction of stroke severity and unfavorable outcome
were presented in our study.
Inflammatory response plays an important role in the
process of ischemic stroke,4 and systemic inflammation
 NEUTROPHIL-TO-LYMPHOCYTE RATIO IN AIS
Table 1. Comparisons among the 3 subgroups according to NLR with regard to clinical and laboratory data

NLR on admission

Total NLR < 2 (121, 43.2%) NLR 2-3 (102, 36.4%) NLR > 3 (57, 20.4%) P value

Age (y) 61.8 ± 10.2 60.3 ± 11.2 63.3 ± 8.8 62.0 ± 10.0 .092
Gender (female) 107 (38.2) 59 (48.8) 31 (30.4) 17 (29.8) .007
BMI (kg/m2) 24.0 (21.8-25.9) 24.2 (22.0-25.9) 23.5 (21.5-25.8) 24.2 (22.0-26.1) .489
Systolic BP, mm Hg 160.6 ± 23.6 157.1 ± 23.5 162.7 ± 23.7 164.5 ± 22.7 .067
Diastolic BP, mm Hg 85.1 ± 13.7 84.1 ± 12.3 84.2 ± 13.4 88.9 ± 16.3 .078
Admission to hospital (d) 2.0 (1.0-3.0) 2.0 (1.0-4.0) 2.0 (1.0-3.0) 2.0 (2.0-3.0) .885
Hypertension(n) 223 (79.6) 88 (72.7) 90 (88.2) 45 (78.9) .016
Diabetes (n) 97 (34.6) 43 (35.5) 37 (36.3) 17 (29.8) .688
Hyperlipidemia (n) 84 (30.0) 40 (33.1) 28 (27.5) 16 (28.1) .620
AF (n) 24 (8.6) 14 (11.6) 4 (3.9) 6 (10.5) .106
Smoking (n) 110 (39.3) 38 (31.4) 49 (48.0) 23 (40.4) .040
Alcohol drinking (n) 82 (29.3) 29 (24.0) 35 (34.3) 18 (31.6) .218
Infract volume (cm3) 1.9 (.6-5.8) 1.4 (.5-3.6) 1.4 (.6-5.8) 3.0 (.7-7.6) .037
Stroke etiologic subtypes .848
Atherosclerotic 186 (66.4) 81 (66.9) 66 (64.7) 39 (68.4)
Cardioembolic 28 (10.0) 14 (11.6) 8 (7.8) 6 (10.5)
Lacunar 48 (17.2) 18 (14.9) 20 (19.6) 10 (17.6)
Cryptogenic 18 (6.4) 8 (6.6) 8 (7.9) 2 (3.5)
Laboratory tests
WBC (109/L) 6.6 (5.5-7.9) 6.1 (5.2-6.9) 7.1 (5.8-8.1) 7.5 (6.3-9.0) <.001
Neutrophils (109/L) 3.9 (3.2-4.9) 3.3 (2.8-3.8) 4.3 (3.6-5.0) 5.3 (4.5-6.7) <.001
Lymphocytes (109/L) 1.9 (1.5-2.3) 2.2 (1.8-2.5) 1.8 (1.5-2.2) 1.4 (1.2-1.6) <.001
NLR 2.1 (1.6-2.7) 1.7 (1.3-1.8) 2.4 (2.2-2.6) 3.9 (3.2-4.8) <.001
Hs-CRP (mg/L) 2.0 (.8-4.7) 1.5 (.6-3.8) 2.1 (.9-4.1) 4.7 (1.3-9.2) <.001
FBG (mmol/L) 5.0 (4.5-6.5) 5.0 (4.6-6.6) 5.0 (4.6-6.7) 5.1 (4.2-6.1) .329
HbA1c (%) 5.9 (5.5-7.0) 5.9 (5.5-6.6) 5.9 (5.5-6.9) 6.0 (5.6-7.3) .605
TC (mmol/L) 4.9 ± 1.1 5.1 ± 1.1 4.8 ± 1.0 4.9 ± 1.1 .057
TG (mmol/L) 1.6 (1.2-2.2) 1.7 (1.3-2.5) 1.5 (1.2-2.0) 1.6 (1.3-2.0) .257
HDL (mmol/L) 1.1 (.9-1.2) 1.1 (.9-1.2) 1.1 (.9-1.2) 1.1 (1.0-1.3) .689
LDL (mmol/L) 3.0 ± .9 3.1 ± 1.0 2.8 ± .8 2.9 ± .9 .039
SCr (μmol/L) 69.0 (59.0-82.0) 65.0 (56.5-81.0) 75.0 (63.0-86.3) 68.0 (58.5-78.5) .008
Medications
Antiplatelet agents (n) 258 (92.1) 108 (89.3) 98 (96.1) 52 (91.2) .162
Anticoagulation agents (n) 19 (6.8) 13 (10.7) 2 (2.0) 4 (7.0) .034
Statin (n) 277 (98.9) 118 (97.5) 102 (100.0) 57 (100.0) .233

Abbreviations: AF, atrial fibrillation; BMI, body mass index; BP, blood pressure; FBG, fasting blood glucose; HbA1c, glycated hemoglobin; HDL, high-density lipoproteins; Hs-CRP, high-
sensitivity c-reactive protein; LDL, low-density lipoproteins; NLR, neutrophil-to-lymphocyte ratio; SCr, serum creatinine; TC, total cholesterol; TG, triglycerides; WBC, white blood cell.

653
Data are presented as means (±SD) and medians (IQR) or as number (percentage).
654 J. XUE ET AL.
was suggested to increase susceptibility to stroke.6 As a

P value
system inflammatory marker, WBCs increase signifi-

<.001
<.001
<.001
.171
cantly from admission to 3 months after stroke when
compared with control cases,27 and elevated WBC count
is related to poor outcome in patients with AIS.11,28 Dif-
ferent subtypes of WBC may have different roles in

NLR > 3 (n = 57, 20.4%)

response to cerebrovascular disease. Neutrophils first ac-
cumulate in cerebral vessels within hours and may

27 (47.4%)
20 (35.1%)
15 (26.3%)
contribute to the extension of infarctions for impeding

5 (8.8%)
microvascular perfusion.29 A previous study has con-
firmed that early leukocytosis and neutrophilia were

Abbreviations: BI, Barthel index; mRS, modified Rankin scale; NIHSS, National Institutes of Health Stroke Scale; NLR, neutrophil-to-lymphocyte ratio.
associated with infarct volumes assessed by diffusion-
weighted magnetic resonance imaging in the early stage
of ischemic stroke.8 Neutrophils are recruited to the isch-
emic brain and may cause the release of some
inflammatory mediators such as proteolysis enzymes or
NLR 2-3 (n = 102, 36.4%)

free oxygen radicals to the damaged areas.30,31 Higher total

NLR on admission

WBC and neutrophil counts were recently reported to be

Table 2. Comparison of outcomes between subgroups based on NLR

27 (26.5%)
19 (18.6%)
11 (10.8%)

associated with more severe stroke at admission in pa-

3 (2.9%)

tients with acute cerebral infarction.10

Lymphocytes are elevated in the ischemic brain later than
neutrophils (3-6 days post stroke).32 Lymphocytes are a prog-
nostic marker for cardiovascular disease. However, the role
of lymphocytes in the pathogenesis of ischemic stroke is
still controversial. Several studies reported that lympho-
cytes have an important role in healing and repair effects
on inflammation.31,33 On the contrary, lymphocytes are sug-
NLR < 2 (n = 121, 43.2%)

gested to be sources of proinflammatory cytokines and

cytotoxic substances, and have a main negative contribu-
23 (19.0%)
11 (9.1%)
9 (7.4%)
4 (3.3%)

tion to ischemic brain.34 Clinical evidence has shown that

lower lymphocyte counts are associated with poor neu-
rological improvement in the early phase and worse long-
term functional outcome.10
NLR is a simple marker connected with both neutro-
phils and lymphocytes. Recently, NLR has been proposed
as an independent predictor of severity and mortality of
coronary artery syndromes.14,15,35 Celikbilek et al18 found
77 (27.5%)
50 (17.9%)
35 (12.5%)
12 (4.3%)

that NLR is higher in patients with atherothrombotic AIS

Total

than in patients with transient ischemic attack and in

control subjects. A number of studies have supported that
NLR is an independent factor for prediction of short-
term mortality in patients with AIS.17,18,36 Furthermore, NLR
was reported to be a predictor of mortality indepen-
Secondary unfavorable outcome (BI <85)
Primary unfavorable outcome (mRS ≥ 3)

dent from infarct volume in patients with AIS.37 The

Moderate to severe stroke (NIHSS ≥ 6)

correlation between NLR and carotid artery stenosis has

been mentioned in recent publications.38,39
High NLR on admission is a marker of stroke sever-
ity and short-term unfavorable outcome after AIS. This
Recurrent ischemic stroke
Outcomes

relationship remains significant even after adjustment for

a number of potential confounders. The injury of the isch-
emic brain caused by neutrophil infiltration and the release
of inflammatory mediators may be the explanation for
our findings that elevated NLR is correlated with stroke
severity and short-term unfavorable outcome. Mean-
while, we determined the optimal cutoff value of NLR
for prediction of prognosis. The optimal value of NLR
NEUTROPHIL-TO-LYMPHOCYTE RATIO IN AIS 655

Figure 1. Correlation between neutrophil-to-lymphocyte

ratio (NLR) and NIHSS score; r[spearman] = .247,
P < .001.

for prediction of stroke severity on admission was 1.87.
In addition, an NLR of 2.39 was the best cutoff value
for predicting both primary and secondary unfavorable
outcomes. Leukocyte counts and mainly neutrophil counts
were reportedly associated with recurrent ischemic stroke
in a large population study.9 However, the relationship
between NLR and recurrent ischemic stroke remains
unclear. We evaluated the association between NLR and
recurrent ischemic stroke for the first time and found that
NLR was an independent predictor for recurrent isch-
emic stroke in patients with AIS.
Traditional viewpoints propose that inhibiting neutro-
phils has shown to improve clinical outcomes in some
experimental stroke models.40,41 Our results also support
that anti-inflammatory therapy may be a potential treat-
ment for AIS. However, anti-neutrophil treatment was
suggested to be ineffective in a clinical study.42 It was
reported that some chemical mediators in inflammatory
responses might be beneficial for brain recovery after
stroke.43 A better understanding of immunomodulation
therapy may be the balance of anti-inflammatory and
proinflammatory therapies to improve outcomes in pa-
tients with AIS.
Several limitations should be considered. First, the
median time from stroke onset to admission was 2 days,
whereas the median time was within 24 hours in pre-
vious studies for determining the correlation between NLR
and poor prognosis. Second, the study design was ret-
rospective and the data were collected from 1 hospital,
both of which might cause selection bias. Third, the limited
number of our study population and low recurrent stroke
incidence might lead to insufficient power for the eval-
uation of the relationship between NLR and recurrent
ischemic stroke. Finally, many diseases and factors that
might affect inflammatory markers were not taken into
consideration.
In conclusion, our study found that NLR is a simple
marker for predicting stroke severity on admission, primary
unfavorable functional outcome, and recurrent ischemic
stroke after AIS. Further investigation is needed for
dynamic monitoring of NLR to better understand the value
of this marker in larger cohorts.

Table 3. Relationship between stroke severity, functional outcome, recurrent ischemic stroke, and NLR

Outcomes Results 95% CI P value Multivariable model

Moderate to severe stroke (NIHSS ≥ 6) OR = 1.364 (1.101-1.690) .005 Model (1)

primary unfavorable outcome (mRS ≥ 3) OR = 1.455 (1.083-1.956) .013 Model (2)
secondary unfavorable outcome (BI <85) OR = 1.271 (.928-1.739) .135 Model (2)
Recurrent ischemic stroke HR = 1.499 (1.161-1.935) .002 Model (2)

Abbreviations: BI, Barthel index; CI: confidence interval; HR, hazard ratio; mRS, modified Rankin scale; NIHSS, National Institutes of
Health Stroke Scale; NLR, neutrophil-to-lymphocyte ratio; OR, odds ratio.
The results (OR, HR) are reported per 1 increase in NLR.
Multivariable model (1): adjusts for age, gender, the time from stroke onset to admission, systolic blood pressure, diastolic blood pres-
sure, hypertension, diabetes mellitus, hyperlipidemia, atrial fibrillation, smoking, alcohol drinking, infarct volume, WBC, Hs-CRP, FBG, HbA1c,
LDL, serum creatinine, and medications.
Multivariable model (2): model (1) + NIHSS score.
656
Figure 2. The receiver operating characteristic (ROC) curve of neutrophil-
to-lymphocyte ratio (NLR) to determine the optimal cutoff values of (A)
severe stroke on admission, (B) primary unfavorable outcome, and (C) sec-
ondary unfavorable outcome; Abbreviations: AUC, area under the curve;
CI, confidence interval.
J. XUE ET AL.
Acknowledgment: This research was supported by the
Healthcare Clinic of the First Affiliated Hospital of Wenzhou
Medical University.
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