Altered rectal perception is a biological marker of patients with irritable bowel syndrome

Mertz, Howard; Naliboff, Bruce D.; Munakata, Julie; Niazi, Negar; Mayer, Emeran A.

doi:10.1016/0016-5085(95)90267-8

Cited by 892 publications

(777 citation statements)

References 19 publications

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“…Compared with "rapid phasic distension", which mainly stimulates the intestinal serosa receptors, the main effect of AML is through the stimulation of the intestinal mucosa and submucosa receptors. These receptors are involved in different nerve conduction pathways while also participating in intestinal perception (Mertz et al, 1995;Dorn et al, 2007). Visceral hypersensitivity is a biological marker in some IBS cases, especially D-IBS patients.…”

Section: Discussionmentioning

confidence: 99%

Visceral and somatic hypersensitivity, autonomic cardiovascular dysfunction and low-grade inflammation in a subset of irritable bowel syndrome patients

Liu

Chen

et al. 2014

J. Zhejiang Univ. Sci. B

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Abstract:The pathophysiology of irritable bowel syndrome (IBS) is complex and not fully understood, so the aim of this study was to evaluate whether visceral and somatic hypersensitivity, autonomic cardiovascular dysfunction, and low-grade inflammation of the gut wall are associated with diarrhea-predominant IBS (D-IBS). Sixty-two patients with D-IBS and 20 control subjects participated in the study. Using the ascending method of limits (AML) protocol, we demonstrated that D-IBS patients had significantly lower sensory thresholds compared with healthy controls (P<0.001). Using diverse methods, especially the ischemic sensitivity test, for the first time in China, we confirmed that D-IBS patients have somatic hypersensitivity. They had a significantly higher systolic blood pressure and heart rate after a cold stimulus, indicative of autonomic cardiovascular dysfunction. Compared with the control group, D-IBS patients had a significantly higher level of calprotectin (P<0.001). We also found significant correlations between visceral and somatic hypersensitivity, visceral hypersensitivity and autonomic cardiovascular dysfunction, and somatic hypersensitivity and autonomic cardiovascular dysfunction. Our findings may provide valuable suggestions for the treatment of D-IBS.

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Section: Discussionmentioning

confidence: 99%

Visceral and somatic hypersensitivity, autonomic cardiovascular dysfunction and low-grade inflammation in a subset of irritable bowel syndrome patients

Liu

Chen

et al. 2014

J. Zhejiang Univ. Sci. B

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“…We have identified that in a subset of patients with UFI, namely those with RH (as defined by ''simple'' balloon distension), 58 abnormalities of rectosigmoid motor physiology (reduced rectal compliance, increased high amplitude contractions, and altered cyclical contractile activity) exist that are not present in patients with UFI and normal rectal sensation. Such findings may underlie the clinical severity observed in the RH group, including more frequent sensations of urgency and increased bowel frequency, which is in agreement with a recent audit study of over 250 patients with this condition.…”

Section: Discussionmentioning

confidence: 99%

Rectal sensorimotor dysfunction in patients with urge faecal incontinence: evidence from prolonged manometric studies

Chan

2005

Gut

100

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Background and aims: Although external anal sphincter dysfunction is the major cause of urge faecal incontinence, approximately 50% of such patients have evidence of rectal hypersensitivity and report exaggerated stool frequency and urgency. The contribution of rectosigmoid contractile activity to the pathophysiology of this condition is unclear, and thus the relations between symptoms, rectal sensation, and rectosigmoid motor function were investigated. Methods: Fifty two consecutive patients with urge faecal incontinence, referred to a tertiary surgical centre, and 24 volunteers, underwent comprehensive anorectal physiological investigation, including prolonged rectosigmoid manometry. Patients were classified on the basis of balloon distension thresholds into those with rectal hypersensitivity (n = 27) and those with normal rectal sensation (n = 25). Automated quantitative analysis of overall rectosigmoid contractile activities and, specifically, high amplitude contractions and rectal motor complex activity was performed. Results: External anal sphincter dysfunction was similar in both patient groups. Overall, phasic activity and high amplitude contraction frequency were greater, and rectal motor complex variables significantly altered, in those with rectal hypersensitivity. Symptoms, more prevalent in the rectal hypersensitivity group, were also more often associated with rectosigmoid contractile events. For individuals, reduced compliance and increased rectal motor complex frequency were only observed in patients with rectal hypersensitivity. Conclusions: We have identified a subset of patients with urge faecal incontinence-namely, those with rectal hypersensitivity-who demonstrated increased symptoms, enhanced perception, reduced compliance, and exaggerated rectosigmoid motor activity. Comprehensive assessment of rectosigmoid sensorimotor function, in addition to evaluation of anal function, should be considered in the investigation of patients with urge faecal incontinence.

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“…19,20 In this review we will discuss the hypothesis that visceral pain disorders result from abnormalities of the brain-gut axis due to "multiple hits" which include external risk factors such as abuse history and chronic psychological stress in adulthood which together are capable of sensitizing the stress response system to cause alterations in no-An important aspect to enhancing our understanding of IBS pathophysiology is the knowledge that IBS patients exhibit visceral hypersensitivity characterized by hyperalgesia and allodynia in a subset of IBS patients ranging from 33-90% of patients with IBS depending on the study. [37][38][39][40][41][42] Although the cause of visceral hypersensitivity is unknown, clinical studies have shown that chronic stress worsens IBS symptomatology and ELS serves as a risk factor for IBS. [43][44][45][46] The sympatho-medullary and the HPA axes are activated by exposure to stress; the sympatho-medullary axis releases epinephrine from the adrenal medulla, to allow the organism to "fight" or "flee" from a threat, whilst activation of the HPA axis releases cortisol (or corticosterone [CORT] in rodents) from the adrenal cortex to mobilize reserves of glucose with the goal of replenishing the expended sympatho-medullary system.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Stress-induced Visceral Pain

Meerveld

Johnson

2018

J Neurogastroenterol Motil

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Evidence suggests that long-term stress facilitates visceral pain through sensitization of pain pathways and promotes chronic visceral pain disorders such as the irritable bowel syndrome (IBS). This review will describe the importance of stress in exacerbating IBS-induced abdominal pain. Additionally, we will briefly review our understanding of the activation of the hypothalamic-pituitary-adrenal axis by both chronic adult stress and following early life stress in the pathogenesis of IBS. The review will focus on the glucocorticoid receptor and corticotropin-releasing hormone-mediated mechanisms in the amygdala involved in stress-induced visceral hypersensitivity. One potential mechanism underlying persistent effects of stress on visceral sensitivity could be epigenetic modulation of gene expression. While there are relatively few studies examining epigenetically mediated mechanisms involved in stress-induced visceral nociception, alterations in DNA methylation and histone acetylation patterns within the brain, have been linked to alterations in nociceptive signaling via increased expression of pro-nociceptive neurotransmitters. This review will discuss the latest studies investigating the long-term effects of stress on visceral sensitivity. Additionally, we will critically review the importance of experimental models of adult stress and early life stress in enhancing our understanding of the basic molecular mechanisms of nociceptive processing. Taken together, the complex clinical phenotype makes recapitulating IBS in rodent models extremely challenging. However, an aim of this review will be to describe how the use of rodent models of adult stress, early life stress (ELS), and a dysregulated HPA axis has improved our understanding of stress in the pathophysiology of IBS. Pathophysiology of Irritable Bowel Syndrome: Activation of the Brain-Gut AxisEvidence from clinical and basic research points to dysregulation of the bidirectional communication between the brain-gut axis in IBS. 21 The brain-gut axis represents a dynamic interplay between central circuits and peripheral mechanisms. The messengers of this complex circuit include neural, endocrine, metabolic, and immune mediators that are activated by central factors such as stress (Fig. 1). Although IBS is not an inflammatory disorder, the immune system plays a role in the pathogenesis of IBS in at least a subset of patients and likely contributes to the etiology of IBS symptoms. 22,23 A subset of IBS patients display a low grade chronic inflammation, and there is also evidence that following an enteric infection and combined with stressful life events, there is an increased risk of developed post-infectious IBS. [24][25][26][27] Clearly, the immune system and inflammatory processes are modulated by the HPA and autonomic nervous systems. In support, IBS patients also show increased number and reactivity of mast cells. 28,29 Data from peripheral blood mononuclear cells, as well as in mucosal biopsies, from IBS patients show that cytokines levels including TNF-α...

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Altered rectal perception is a biological marker of patients with irritable bowel syndrome

Cited by 892 publications

References 19 publications

Visceral and somatic hypersensitivity, autonomic cardiovascular dysfunction and low-grade inflammation in a subset of irritable bowel syndrome patients

Visceral and somatic hypersensitivity, autonomic cardiovascular dysfunction and low-grade inflammation in a subset of irritable bowel syndrome patients

Rectal sensorimotor dysfunction in patients with urge faecal incontinence: evidence from prolonged manometric studies

Mechanisms of Stress-induced Visceral Pain

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