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Lu et al. Microbleeds and inflammatory marker levels

Table 4: OR (95% CI) for CMB status per 1SD increase in inflammation factors (values were log transformed for
analysis)
CMB Deep or infratentorial CMB Lobar CMB
Variable Model 1 Model 2 Model 1 Model 2 Model 1 Model 2
OR (95% CI) OR (95% CI) OR (95% CI) OR (95% CI) OR (95% CI) OR (95% CI)
hs-CRP 1.852 (1.435-2.391) ‡ 1.745 (1.342-2.270) ‡ 2.372 (1.680-3.262) ‡ 2.302 (1.520-3.482) ‡ 1.578 (1.043-2.337) ‡ 1.534 (1.009-2.259) ‡
IL-6 1.469 (1.204-1.792) † 1.223 (1.018-1.533) ‡ 1.480 (1.102-2.492) ‡ 1.334 (1.008-3.660) † 1.422 (1.001-2.678) ‡ 1.508 (1.097-3.428) †
MMP-9 1.397 (1.196-1.632) ‡ 1.284 (1.082-1.423) ‡ 1.420 (1.241-1.799) ‡ 1.287 (1.145-1.599) ‡ 1.293 (1.142-2.423) ‡ 1.242 (1.178-1.409) ‡
† ‡
P < 0.05, P < 0.01, compared with the no CMB group. Model 1: adjusted for age and sex; Model 2: adjusted for age, sex, body mass
index, smoking, alcohol intake, hypertension, diabetes, hyperlipidemia, coronary heart disease, the presence of silent lacunar infarction and
white matter lesion and antithrombotic drugs. CMB: cerebral microbleeds; SD: standard deviation; CI: confidence interval; OR: odd ratios;
hs-CRP: high-sensitivity C-reactive protein; IL: interleukin; MMP: matrix metalloproteinase
were 1.745 (1.342-2.270), 1.223 (1.018-1.533) and result of amyloid angiopathy. [18] Several studies have
1.284 (1.082-1.423), respectively. Furthermore, the demonstrated strictly that lobar CMB was associated
associations between inflammatory marker level and with the apolipoprotein E4 allele and diastolic blood
deep or infratentorial CMB or lobar CMB remained pressure. On the other hand, systolic blood pressure,
significant after adjustment for age and sex (Model 1) pulse pressure, silent lacunar infarction, white matter
and after additional adjustment for the traditional risk hyperintensities and smoking were associated with
factors (Model 2). The adjusted ORs of hs-CRP, IL-6 CMB in the deep or infratentorial regions. [19] In our
and MMP-9 for the presence of deep or infratentorial study, hypertension, SLI, WML were associated with
CMB were 2.302 (1.520-3.482), 1.334 (1.008-3.660) higher incidence of CMB, and thus were strong risk
and 1.287 (1.145-1.599), respectively. For the factors of CMB. The associations between traditional
presence of lobar CMB, the adjusted ORs of hs-CRP, risk factors and deep or infratentorial CMB remained
IL-6 and MMP-9 were 1.534 (1.009-2.259), 1.508 significant. Our results were consistent with previous
(1.097-3.428) and 1.242 (1.178-1.409), respectively. studies. Shams et al. [16] observed that patients with
CMB were significantly aged, had hypertension, and
DISCUSSION had lower cognitive function. A number of studies
have shown that age is an independent risk factor
[11]
The prevalence of CMBs varies from different of CMB. Vernooij et al. found that the incidence
population. A meta-analyze found that incidence of CMB increased with age from 17.8% in persons
of CMBs was 44% in ischemic stroke, 83% in aged 60-69 years to 38.3% in those over 80 years.
There were significant differences in MoCA Scores
intracerebral hemorrhage, and 5-6% in healthy and using antithrombotic drugs between the CMB
adults. [15] In this study, the incidence of CMBs group and no CMB group. Several studies reported
was 24.38%, 30 patients (61.22%) had deep or an association between the presence of CMB and
infratentorial CMB, 19 patients (38.78%) had lobar impaired cognitive function. [20,21] Small vessel disease
CMB. The prevalence of CMB in our study was can be visualized as white matter hyperintensities
higher than that in healthy adults, but, lower than that and SLI but also as CMB on brain MRI. [21] A number
in ischemic stroke. The first possible reason was the of studies found that almost all the CMB patients
patients who participated without acute infarction had various degrees of WML and different numbers
or transient ischemic attack. The second possible of SLI. Gregoire et al. found that CMB were more
[6]
reason was the use of SWI, it may increase the numerous and prevalent in antiplatelet users who
prevalence and number of CMB detected, compared developed symptomatic ICH compared with matched
with T2 GRE. antiplatelet-users who did not develop ICH. This data
suggested a potential role for CMB as a risk factor
On assessment, CMB are often categorized for antiplatelet-associated ICH. The relationship
according to location, separating strictly lobar between alcohol intake and CMB needed to be
CMB from deep or infratentorial CMB. Lobar CMB further studied.
represents cerebral amyloid angiopathy, but, deep
and infratentorial CMB is attributed to hypertensive Our study showed that the levels of hs-CRP, IL-6, MMP-
arteriopathy. [16] Poels et al. [17] found an association 9 in CMB group were significantly higher than those in
between atherosclerosis and deep or infratentorial no CMB group. The regression analysis showed that
CMB in individuals with uncontrolled hypertension. inflammatory factors such as hs-CRP, IL-6 and MMP-
This may explain the theoretical assumption 9 were the independent risk factors of CMB. Also,
that deep or infratentorial CMB are attributed to they were also the independent risk factors of deep or
hypertensive vasculopathy, whereas lobar CMB are a infratentorial CMB and lobar CMB. This suggested that
Neuroimmunology and Neuroinflammation ¦ Volume 4 ¦ August 08, 2017 149