title: Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 1: eradication of Helicobacter in the cachexia of idiopathic parkinsonism.
abstract: BACKGROUND
  Neuronal damage in idiopathic parkinsonism may be in response to ubiquitous occult infection. Since peptic ulceration is prodromal, Helicobacter is a prime candidate.
  
  
  OBJECTIVE
  To consider the candidature of Helicobacter in parkinsonism with cachexia.
  
  
  METHODS
  We explore the relationship between being underweight and inflammatory products in 124 subjects with idiopathic parkinsonism and 195 controls, and present the first case-series evidence of efficacy of Helicobacter eradication, in parkinsonism advanced to the stage of cachexia.
  
  
  RESULTS
  Association of a low body mass index with circulating interleukin-6 was specific to parkinsonism (p = .002), unlike that with antibodies against Helicobacter vacuolating-toxin and cytotoxicity-associated gene product (p < .04). Marked reversibility in both cachexia and disability of idiopathic parkinsonism followed Helicobacter heilmannii eradication in one case, Helicobacter pylori eradication in another, follow-up being > or = 3.5 years. The latter presented with postprandial bloating, and persistent nausea: following eradication, radioisotope gastric-emptying returned towards normal, and upper abdominal symptoms regressed. Reversibility of their cachexia/disability contrasts with the outcome of anti-Helicobacter therapy where eradication repeatedly failed (one case), and in non-Helicobacter gastritis (three cases). Anti-parkinsonian medication remained constant. Intestinal absorption and barrier function were normal in all.
  
  
  CONCLUSIONS
  Categorization, according to presence or absence of Helicobacter infection, was a useful therapeutic tool in late idiopathic parkinsonism.
authors.affiliation: Section of Clinical Neuropharmacology, Institute of Psychiatry, London, UK. dobbs@wellers.demon.co.uk
authors.forename: R John
authors.initials: RJ
authors.lastname: Dobbs
authors.forename: Sylvia M
authors.initials: SM
authors.lastname: Dobbs
authors.forename: Clive
authors.initials: C
authors.lastname: Weller
authors.forename: Ingvar T
authors.initials: IT
authors.lastname: Bjarnason
authors.forename: Ingua T
authors.initials: IT
authors.lastname: Bjarnason
authors.forename: Norman L
authors.initials: NL
authors.lastname: Oxlade
authors.forename: André
authors.initials: A
authors.lastname: Charlett
authors.forename: Mazin A
authors.initials: MA
authors.lastname: Al-Janabi
authors.forename: Robert W
authors.initials: RW
authors.lastname: Kerwin
authors.forename: Robert F
authors.initials: RF
authors.lastname: Mahler
authors.forename: Ashley B
authors.initials: AB
authors.lastname: Price
mesh_terms: D000368:Aged; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D002100:Cachexia / Q000188:drug therapy / Q000209:etiology* / Q000382:microbiology* / Q000503:physiopathology; D002908:Chronic Disease; D005260:Female; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy* / Q000276:immunology; D016480:Helicobacter pylori / Q000187:drug effects*; D006801:Humans; D007249:Inflammation / Q000150:complications*; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000188:drug therapy* / Q000209:etiology* / Q000382:microbiology* / Q000503:physiopathology; D016896:Treatment Outcome
chemical_list: D000900:Anti-Bacterial Agents