Autonomic dysfunctions in patients with inflammatory bowel disease in clinical remission
Purnima Sharma1, Govind K Makharia, Vineet Ahuja
1Department of Physiology, All India Institute of Medical Sciences, Room No: 2007, Ansari Nagar, New Delhi, 110608, India.
Introduction And Objective:
The autonomic nervous system, especially the parasympathetic system, has been reported to modulate the immune response in chronic inflammatory disorders. Autonomic dysfunctions have been reported earlier in patients with inflammatory bowel disease; however, the results have been conflicting. We therefore evaluated autonomic functions in patients with inflammatory bowel disease (IBD) in clinical remission.
Patients And Methods:
Heart rate variability, a marker of autonomic functions, which included time-domain, frequency-domain, and nonlinear indices (Poincaré plot) was assessed using Nevrokard, version 6.4.0 Slovenia, in 118 patients with IBD (ulcerative colitis [UC] 62, and Crohn's disease [CD] 56) and 58 healthy controls.
Results:
There was no difference in mean of R-R intervals in patients with UC, CD, and healthy controls. Frequency domain indices (absolute values of total power, high-frequency power, and low-frequency power) were lower in patients with UC and CD vs. healthy controls. High-frequency (HFnu) (expressed in normalized units) was significantly lower in UC compared to healthy controls. There was no significant difference in the low-frequency (LFnu) and LF/HF ratio in UC, CD, and healthy controls. Amongst the Poincaré plot indices, while standard deviation of the instantaneous R-R interval variability (SD1nu) was lower in UC and CD vs. healthy controls, there was no significant difference in the long-term R-R interval variability (SD2nu).
Conclusions:
Patients with inflammatory bowel disease have lower autonomic functions. Patients with UC have significantly lower parasympathetic function in comparison to those with CD and healthy controls. These autonomic dysfunctions in patients with IBD may have a bearing on the pathogenesis of IBD.
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