Am. Drewes et al., Sensitivity and distensibility of the rectum and sigmoid colon in patientswith irritable bowel syndrome, SC J GASTR, 36(8), 2001, pp. 827-832
Background: Hyperalgesia to visceral stimuli is a biological marker of the
irritable bowel syndrome (IBS). Abnormal pain processing is probably of mos
t importance, but biomechanical abnormalities of the gut wall may also cont
ribute to the findings. In the current study, we investigated the sensation
of the gut to electrical stimuli as well as the distensibility of the rect
um and sigmoid colon in IBS patients and a control group. Methods: Nine pat
ients with IBS and 11 controls entered the study. The pain threshold to ele
ctrical stimuli at the rectosigmoid junction was determined with bipolar el
ectrodes integrated on the biopsy forceps for the endoscope. Subsequently,
controlled distensions of the sigmoid colon and rectum were performed with
a balloon integrated on a probe for impedance planimetry, providing the pos
sibility to measure the cross-sectional area (CSA), wall tension and strain
to different pressures together with the sensation ratings. Results: The p
ain detection thresholds to electrical stimuli at the rectosigmoid junction
were 12.5 (range 7-39) mA in controls and 7.5 (range 0.75-12) mA in IBS pa
tients (P = 0.03). The calculated pressures at the pain detection threshold
in the sigmoid colon were lower in the IBS patients (31.5 (range 5-58) ver
sus 5 cm (range 5-25) water; P = 0.03), otherwise no differences were seen
in sensation rating to the: different distension pressures. The CSA was sli
ghtly higher in controls to the different pressures, whereas no differences
between the groups were seen in strain and tension of the rectum and sigmo
id colon. Conclusion: The visceral hypersensitivity in IBS seems to be rela
ted to alterations in the nervous system rather than biomechanical paramete
rs such as the tension and strain of the gut wall. Treatment of pain in IBS
should therefore be based on drugs with documented action on the nocicepti
ve pathways in the central nervous system.