Abstract
A chronic inflammatory state is a risk factor for accelerated atherogenesis. The aim of our study was to explore whether Crohn's disease (CD), characterized by recurrent inflammatory episodes, is also associated with accelerated atherogenesis. In 60 CD patients and 122 matched controls, carotid intima media thickness (IMT), a validated marker for the burden and progression of atherosclerosis, was assessed ultrasonographically. Additional subgroup analyses, including plasma levels of acute phase reactants and HDL protein profiling, were performed in 11 consecutive patients with CD in remission, 10 patients with active CD, and 15 healthy controls. Carotid IMT in patients with CD was increased compared with healthy volunteers: 0.71 (0.17) versus 0.59 (0.14) mm (P < 0.0001), respectively. In the subgroup analysis, HDL levels in controls and patients in remission were identical [(1.45 (0.48) and 1.40 (0.46) mmol/l; P = 0.797], whereas HDL during exacerbation was profoundly reduced: 1.02 (0.33) (P = 0.022). HDL from patients with active CD and CD patients in remission was characterized by a reduced ability to attenuate oxidation compared with controls (P = 0.008 and P = 0.024 respectively). Patients with CD have increased IMT compared with matched controls, indicative of accelerated atherogenesis. The changes during CD exacerbation in terms of HDL concentration and composition imply a role for impaired HDL protection in these patients.
Highlights
A chronic inflammatory state is a risk factor for accelerated atherogenesis
In the current exploratory analysis, we show that Crohn’s disease (CD) is associated with an acceleration of the atherosclerotic process, as illustrated by an increased carotid intima media thickness (IMT) in CD patients compared with healthy controls
CD patients were characterized during an inflammatory exacerbation by profoundly decreased levels of HDL combined with biochemical changes of the HDL particle
Summary
A chronic inflammatory state is a risk factor for accelerated atherogenesis. The aim of our study was to explore whether Crohn’s disease (CD), characterized by recurrent inflammatory episodes, is associated with accelerated atherogenesis. HDL levels in controls and patients in remission were identical [(1.45 (0.48) and 1.40 (0.46) mmol/l; P 5 0.797], whereas HDL during exacerbation was profoundly reduced: 1.02 (0.33) (P 5 0.022). Patients with CD have increased IMT compared with matched controls, indicative of accelerated atherogenesis. In several chronic inflammatory disorders, such as systemic lupus erythematosus (SLE) [3], rheumatoid arthritis (RA) [4], human immunodeficiency virus [5], and even periodontitis [6], systemic inflammation has been linked to enhanced atherogenesis, illustrated by an increased incidence of cardiovascular disease (CVD). The current exploratory study was designed to evaluate whether Crohn’s disease (CD) is associated with an increased progression of the atherosclerotic process and whether inflammatory exacerbations are associated with alterations in HDL metabolism. Leukocytes can adhere to activated endothelium and transmigrate to the subendothelial space
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