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2014 ; 130
(23
): 2031-9
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Assessment of atherosclerosis in chronic granulomatous disease
#MMPMID25239440
Sibley CT
; Estwick T
; Zavodni A
; Huang CY
; Kwan AC
; Soule BP
; Long Priel DA
; Remaley AT
; Rudman Spergel AK
; Turkbey EB
; Kuhns DB
; Holland SM
; Malech HL
; Zarember KA
; Bluemke DA
; Gallin JI
Circulation
2014[Dec]; 130
(23
): 2031-9
PMID25239440
show ga
BACKGROUND: Patients with chronic granulomatous disease (CGD) experience
immunodeficiency because of defects in the phagocyte NADPH oxidase and the
concomitant reduction in reactive oxygen intermediates. This may result in a
reduction in atherosclerotic injury. METHODS AND RESULTS: We prospectively
assessed the prevalence of cardiovascular risk factors, biomarkers of
inflammation and neutrophil activation, and the presence of magnetic resonance
imaging and computed tomography quantified subclinical atherosclerosis in the
carotid and coronary arteries of 41 patients with CGD and 25 healthy controls in
the same age range. Univariable and multivariable associations among risk
factors, inflammatory markers, and atherosclerosis burden were assessed. Patients
with CGD had significant elevations in traditional risk factors and inflammatory
markers compared with control subjects, including hypertension, high-sensitivity
C-reactive protein, oxidized low-density lipoprotein, and low high-density
lipoprotein. Despite this, patients with CGD had a 22% lower internal carotid
artery wall volume compared with control subjects (361.3±76.4 mm(3) versus
463.5±104.7 mm(3); P<0.001). This difference was comparable in p47(phox)- and
gp91(phox)-deficient subtypes of CGD and independent of risk factors in
multivariate regression analysis. In contrast, the prevalence of coronary
arterial calcification was similar between patients with CGD and control subjects
(14.6%, CGD; 6.3%, controls; P=0.39). CONCLUSIONS: The observation by magnetic
resonance imaging and computerized tomography of reduced carotid but not coronary
artery atherosclerosis in patients with CGD despite the high prevalence of
traditional risk factors raises questions about the role of NADPH oxidase in the
pathogenesis of clinically significant atherosclerosis. Additional
high-resolution studies in multiple vascular beds are required to address the
therapeutic potential of NADPH oxidase inhibition in cardiovascular diseases.
CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique
identifier: NCT01063309.
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