title: Neural alterations in surgical stage chronic pancreatitis are independent of the underlying aetiology.
abstract: OBJECTIVE
  Among various causes, nerve alterations and neuroimmune interactions have been suggested to participate in the generation of pain in chronic pancreatitis (CP). In this study, we compared neural changes and the pattern of perineural inflammatory cell infiltrates in three different aetiological forms of CP (alcoholic, idiopathic, and tropical) and evaluated whether differences exist between these groups.
  
  
  METHODS
  A total of 35 patients with CP (12 tropical, 12 idiopathic, and 11 alcoholic) were included. Ten normal pancreatic tissues obtained from healthy organ donors served as controls. In all samples, the number of nerves, area of neural tissue, nerve size, and percentage of neural tissue and perineural inflammatory cell infiltrates were analysed histologically.
  
  
  RESULTS
  The median number of nerves per 10 mm2 tissue area was 2.3, 4.3, 4.4, and 2.6 in the normal pancreas, alcoholic CP, idiopathic CP, and tropical CP, respectively. Median area of neural tissue per 10 mm2 was 2550, 21 803, 18 595, and 24 666 microm2 in the normal pancreas, alcoholic CP, idiopathic CP, and tropical CP, respectively. Median nerve diameter was 36.85 microm in the normal pancreas, 80.6 microm in alcoholic CP, 68.95 microm in idiopathic CP, and 93.05 microm in tropical CP. In comparison with normal controls, all of these parameters were significantly increased except the number of nerves in tropical CP. For all parameters there were no significant differences between alcoholic, idiopathic, and tropical CP. When the degree of perineural inflammation was evaluated, no differences were observed among the three CP groups.
  
  
  CONCLUSIONS
  Independent of the underlying aetiology, CP is associated with an increase in neural tissue, and neural alterations occur in a similar fashion irrespective of the type of initiating event.
authors.affiliation: Department of Visceral and Transplantation Surgery, University of Bern, Inselspital, Bern, Switzerland. Helmut_Friess@med.uni-heidelberg.de
authors.forename: H
authors.initials: H
authors.lastname: Friess
authors.forename: S
authors.initials: S
authors.lastname: Shrikhande
authors.forename: M
authors.initials: M
authors.lastname: Shrikhande
authors.forename: M
authors.initials: M
authors.lastname: Martignoni
authors.forename: C
authors.initials: C
authors.lastname: Kulli
authors.forename: A
authors.initials: A
authors.lastname: Zimmermann
authors.forename: A
authors.initials: A
authors.lastname: Kappeler
authors.forename: H
authors.initials: H
authors.lastname: Ramesh
authors.forename: M
authors.initials: M
authors.lastname: Büchler
mesh_terms: D000328:Adult; D002908:Chronic Disease; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009419:Nerve Tissue Proteins / Q000032:analysis; D010179:Pancreas / Q000294:innervation*; D010195:Pancreatitis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D019512:Pancreatitis, Alcoholic / Q000378:metabolism / Q000473:pathology; D017933:Peripheral Nervous System / Q000473:pathology; D013869:Thiolester Hydrolases / Q000032:analysis; D043222:Ubiquitin Thiolesterase
chemical_list: D009419:Nerve Tissue Proteins; D013869:Thiolester Hydrolases; D043222:Ubiquitin Thiolesterase