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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Abdominal aortic calcification in patients with inflammatory bowel disease: does anti-tumor necrosis factor α use
Aikaterini Mantaka1,2, Nikolaos Galanakis3, Dimitrios Tsetis1,3
1Faculty of Medicine, University of Crete, Heraklion, Greece.
Insights
Over a third of inflammatory bowel disease (IBD) patients show moderate-severe abdominal aortic calcium (AAC) deposition. Anti-tumor necrosis factor-alpha (TNF-α) therapy may protect against atherosclerosis in IBD patients.
Area of Science:
- Cardiovascular Medicine
- Gastroenterology
- Radiology
Background:
- Abdominal aortic calcium (AAC) is a marker for early atherosclerosis.
- No prior studies evaluated AAC in inflammatory bowel disease (IBD).
Purpose of the Study:
- To evaluate AAC deposition in IBD patients.
- To correlate AAC with IBD characteristics and cardiovascular disease (CVD) risk factors.
Main Methods:
- AAC quantified via CT or enterography in 98 IBD patients and matched controls.
- Correlations assessed with IBD features, disease activity, labs, and CVD risk factors.
Main Results:
- Moderate-severe AAC found in 35.7% of IBD patients vs. 30.6% of controls.
- IBD with CVD and ulcerative colitis showed higher severe atherosclerotic lesions.
- Extensive disease and lifetime steroid use were independent AAC risk factors in non-CVD IBD patients.
- Anti-TNF-α use was negatively associated with AAC in non-CVD IBD patients.
Conclusions:
- Over one-third of IBD patients exhibit moderate-severe AAC.
- Anti-TNF-α agents may offer protection against AAC deposition and atherosclerosis in IBD.
Background/Aims:
Abdominal aortic calcium (AAC) deposition has been suggested as a marker of early atherosclerosis. There is no published data on the evaluation of AAC in inflammatory bowel disease (IBD).
Methods:
AAC was quantified by computed tomography or enterography scans performed in 98 IBD patients and 1:1 age and sex matched controls. AAC deposition was correlated with IBD characteristics, disease activity or severity parameters, laboratory tests and cardiovascular disease (CVD) risk factors.
Results:
Moderate-severe grade of AAC was found in 35.7% of IBD patients compared to 30.6% of controls (P= 0.544). IBD with CVD and ulcerative colitis patients had significantly higher rates of more severe atherosclerotic lesions (P= 0.001 and P= 0.01, respectively). AAC deposition was similarly distributed in age groups ( < 45, 45-64, and ≥ 65 years) among patients and controls. Multivariate analysis after excluding CVD risk confounders for non-CVD patients found extensive disease (P= 0.019) and lifetime steroids (P= 0.04) as independent risk factors for AAC. Anti-tumor necrosis factor α (TNF-α) use was negatively associated with AAC deposition in non-CVD IBD patients (odds ratio, 0.023; 95% confidence interval, 0.001-0.594; P= 0.023).
Conclusions:
More than one-third of IBD patients have moderate to severe AAC. Better control of inflammation with anti-TNF-α agents seems to protect IBD patients from ACC deposition and subsequent atherosclerosis.
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