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Clinical and pathological implications of IgG antibody responses to Helicobacter pylori and its virulence factors in non-ulcer dyspepsia

Xia, H.H.-X. (författare)
Department of Medicine, University of Sydney, Nepean Hospital, Penrith, NSW, Australia
Talley, N.J. (författare)
Department of Medicine, University of Sydney, Nepean Hospital, Penrith, NSW, Australia, Department of Medicine, University of Sydney, Nepean Hospital, PO Box 63, Penrith, NSW 2751, Australia
Blum, A.L. (författare)
Division of Gastroenterology, Ctr. Hosp. Universitaire Vaudois, Lausanne, Switzerland
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O'Morain, C.A. (författare)
Department of Gastroenterology, Meath Hospital, Trinity College, Dublin, Ireland
Stolte, M. (författare)
Institute for Pathology, Klinikum Bayreuth, Bayreuth, Germany
Bolling-Sternevald, E. (författare)
Linköpings universitet,Institutionen för biomedicin och kirurgi,Hälsouniversitetet
Mitchell, H.M. (författare)
Sch. of Biotech./Biomol. Sciences, University of New South Wales, Sydney, NSW, Australia
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 (creator_code:org_t)
2003-03-26
2003
Engelska.
Ingår i: Alimentary Pharmacology and Therapeutics. - : Wiley. - 0269-2813 .- 1365-2036. ; 17:7, s. 935-943
  • Tidskriftsartikel (refereegranskat)
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  • Aim: To determine whether pre-treatment antibody response to Helicobacter pylori virulence factors predicts eradication success and symptom relief 12 months after triple therapy in non-ulcer dyspepsia. Methods: H. pylori-positive patients with non-ulcer dyspepsia received 1-week omeprazole-based triple therapy, or omeprazole plus placebos. Symptoms were assessed using a validated Likert scale. Gastric biopsies taken before and 12 months after treatment were used for histological examination. Pre-treatment blood samples were used for the detection of anti-H. pylori immunoglobulin G (IgG) antibodies, and specific IgG antibodies to 19.5-, 26.5-, 30-, 35-, 89- (VacA) and 116-KDa (CagA) antigens of H. pylori. Results: IgG antibodies to the six antigens were detected in 62%, 96%, 88%, 47%, 54% and 78% of patients, respectively. The presence of antibody to 19.5-, 26.5- or 30-kDa antigen was associated with an increased anti-H. pylori IgG absorbance index. IgG absorbance indices were greater in those with H. pylori eradication (vs. persistent infection). The prevalence of antibodies to the six antigens was not significantly different between those with symptom relief vs. those without. The 19.5kDa antigen (P = 0.018) and VacA (P = 0.001) were independent risk factors for body gastritis. Conclusions: An increased pre-treatment anti-H. pylori IgG absorbance index may be a useful predictor of the success of eradication therapy. Although the 19.5-kDa antigen and VacA were associated with body gastritis, none of the six antigens tested predicted symptom relief after triple therapy.

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