Abstract
Catestatin (CST) is an important peptide in the pathophysiology of chronic inflammatory disorders. However, clinical studies on inflammatory bowel disease (IBD) patients are lacking. Our goal was to investigate CST concentrations in IBD patients compared to healthy subjects. Additionally, we aimed to determine arterial stiffness parameters in relation to CST. This cross-sectional study compared 80 IBD patients (45 Crohn’s disease (CD) and 35 ulcerative colitis (UC) patients) with 75 control subjects. Serum CST levels were significantly higher in the IBD group compared to control subjects (11.29 ± 9.14 vs. 7.13 ± 6.08 ng/mL, p = 0.001) and in the UC group compared to CD patients (13.50 ± 9.58 vs. 9.03 ± 6.92 ng/mL, p = 0.021), irrespective of age and BMI. IBD patients exhibited significantly higher values of heart rate adjusted central augmentation index (cAIx-75) (14.88 ± 10.59 vs. 6.87 ± 9.50 %, p < 0.001) and pulse wave velocity (PWV) (8.06 ± 3.23 vs. 6.42 ± 1.47 m/s, p < 0.001) compared to control group. Furthermore, PWV was the only significant independent correlate of CST (B = 1.20, t = 4.15, p < 0.001), while CST, PWV, cAIx-75, high-sensitivity C-reactive protein and BMI were significant predictors of positive IBD status (1.089 (1.022–1.161), 1.515 (1.166–1.968), 1.060 (1.024–1.097), 1.458 (1.116–1.906), 0.793 (0.683–0.920), respectively). Serum CST levels were significantly higher in IBD patients compared to controls and an independent positive correlation of CST with PWV existed. Therefore, it is possible that CST could have a role in the complex pathophysiology of IBD and its cardiovascular complications.
Highlights
Inflammatory bowel disease (IBD) is a chronic, relapsing disorder that predominately affects small and large intestine, and its two main manifestations are in the form of ulcerative colitis (UC) and Crohn’s disease (CD) [1]
The adverse inflammatory effect on arteries was further confirmed with a recent systematic review by Zanoli et al, that reported a significant increase in pulse wave velocity (PWV), a golden standard for estimation of arterial stiffness, in patients with IBD
There was no significant difference in anthropometric characteristics between studied groups, except in body weight (75.03 ± 14.10 vs. 80.47 ± 13.28 kg, p = 0.015) and body height (176.41 ± 9.27 vs. 180.03 ± 9.18 cm, p = 0.017) which were lower in IBD patients
Summary
Inflammatory bowel disease (IBD) is a chronic, relapsing disorder that predominately affects small and large intestine, and its two main manifestations are in the form of ulcerative colitis (UC) and Crohn’s disease (CD) [1]. IBD is believed to be caused by a combination of several predisposing conditions, such as genetic structure, abnormal immunological response and exposure to environmental factors [2]. It is considered that its hallmark characteristic, chronic intestinal inflammation, occurs when an abnormal immunological response causes microvascular endothelial cell damage [3]. The probable reason for this paradox lies in chronic inflammation effect on arteries, and the heavily connection of IBD with a number of cardiovascular disorders, including atherosclerosis, endothelial dysfunction and increased arterial stiffness [6,7,8]. The adverse inflammatory effect on arteries was further confirmed with a recent systematic review by Zanoli et al, that reported a significant increase in pulse wave velocity (PWV), a golden standard for estimation of arterial stiffness, in patients with IBD. Increased arterial stiffness likely presents the initiation and/or progression of atherogenesis and arterial hypertension [9]
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