TITLE

INCREASED EXPRESSION OF GALANIN IN MUCOSAL NERVES OF PATIENTS WITH PAINFUL DIVERTICULAR DISEASE

AUTHOR(S)
Simpson, J.; Sundler, F.; Jenkins, D.; Spiller, R.C.
PUB. DATE
April 2003
SOURCE
Gut;Apr2003 Supplement 1, Vol. 52, pA87
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: Galanin is a neuropeptide distributed widely throughout the central and peripheral nervous system. In particular, its presence has been demonstrated in dorsal root ganglia, spinal dorsal horn neurones and enteric nerves. It is known to have a modulatory function on nociception and peripheral nerve injury has been shown to upregulate its synthesis. We have previously shown that resection sections for complicated diverticular disease shown evidence of neural damage and regeneration within the enteric nervous system (ENS). Aim: To quantify the level of galanin expressed by mucosal nerves in patients with symptomatic and asymptomatic diverticular disease. Method: Ten symptomatic and ten asymptomatic patients underwent flexible sigmoidoscopy and multiple peridiverticula biopsies were obtained. Standard fluorescent immuno-histochemical methods were used. Mucosal nerves were identified using PGP9.5 and peripherin. Using digitised image analysis, the level of galanin immunoreactivity within mucosal nerves was expressed as percentage area of lamina propia. Results: Median age was 68.5 years (range 49-70) with no difference between groups. Symptomatic patients experienced recurrent abdominal pain on a median of 6 (range 3-12) days/month. Duration of the pain was 4 (0.75-12) hours. No pain was experienced by the asymptomatic group. The percentage area of galanin immunoreactivity within the lamina propia was 0.155% in symptomatic patients compared with 0.004% in controls (p < 0.0001 Mann-Whitney). Conclusion: There is an increased expression of galanin within colonic mucosal nerves in patients with painful diverticular disease. Although the direct effect of this change in the development of abdominal pain is as yet unclear, the increased expression implies previous or ongoing injury to the ENS in symptomatic patients, possibly due to inflammation.
ACCESSION #
9747864

 

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