Publication

Antiplatelet therapy, Helicobacter pylori infection and complicated peptic ulcer disease in diabetes: the Fremantle Diabetes Study

Journal Paper/Review - Jan 1, 2009

Units
PubMed
Doi

Citation
Schimke K, Chubb S, Davis W, Phillips P, Davis T. Antiplatelet therapy, Helicobacter pylori infection and complicated peptic ulcer disease in diabetes: the Fremantle Diabetes Study. Diabetic medicine : a journal of the British Diabetic Association 2009; 26:70-5.
Type
Journal Paper/Review (English)
Journal
Diabetic medicine : a journal of the British Diabetic Association 2009; 26
Publication Date
Jan 1, 2009
Issn Electronic
1464-5491
Pages
70-5
Brief description/objective

AIMS: To assess whether, based on its relationship with complications of peptic ulcer disease (PUD), directed Helicobacter pylori serological screening is justified in diabetic patients prior to commencement of antiplatelet therapy. METHODS: We analysed data from the longitudinal, community-based Fremantle Diabetes Study (FDS). The present substudy included (i) 1301 patients (91.2% of the total FDS sample; mean age 62.0 +/- 13.3 years, 49.5% male) with available sera from baseline assessment between 1993 and 1996, and (ii) a subset of 40 patients admitted to hospital for complicated PUD (bleeding and/or perforation) between baseline and end of June 2006. All hospital admissions for complicated PUD in the population of Western Australia were identified over the same period. Helicobacter pylori IgG antibodies were measured in all patients at baseline and in the subset at the FDS visit prior to hospital admission. RESULTS: Helicobacter pylori seropositivity was present in 60.6% of FDS patients at baseline and was independently associated with increasing age and non-Anglo-Celt/non-Asian ethnicity. There were 2.9 (95% confidence interval 2.1, 3.9) first admissions for complicated PUD per 1000 patient-years, an incidence more than seven times that in the local general population. Independent baseline predictors of hospital admission were increasing age, serum urea, non-aspirin anticoagulant therapy, sulphonylurea therapy, peripheral arterial disease and diabetic retinopathy, but not aspirin use, H. pylori seropositivity or their interaction. CONCLUSIONS: There are diabetes-specific risk factors for complicated PUD, including sulphonylurea use and vascular complications. Knowledge of H. pylori serological status does not predict complicated PUD in diabetes regardless of use of antiplatelet therapy.