LETTER

IL-1 gene cluster and TNFA–307 polymorphisms in the risk of perforated duodenal ulcer

J B Guerra, G A Rocha, A M C Rocha, C M de Castro Mendes, I E B Saraiva, C A de Oliveira, D M M Queiroz

Laboratory of Research in Bacteriology, Faculty of Medicine, UFMG, Belo Horizonte, Brazil

Correspondence to:
Correspondence to:
Professor D M M Queiroz
Laboratory of Research in Bacteriology, FMUFMG Av Alfredo Balena, 190/4026-30130-100, Belo Horizonte, Brazil; dqueiroz@medicina.ufmg.br

Keywords: duodenal ulcer; Helicobacter; interleukin 1; tumour necrosis factor ; IL-1B; IL-1RN; TNFA

The first 150 words of the full text of this article appear below.

Helicobacter pylori virulence markers have been associated with duodenal ulcer (DU) but there are few studies evaluating host factors such as cytokine polymorphisms and, to the best of our knowledge, no study has evaluated these polymorphisms as risk factors for perforated DU. We investigated associations among interleukin 1 (IL-1) cluster and tumour necrosis factor (TNFA)–307 polymorphisms, and DU and perforated DU in a non-Caucasian population. We included 223 patients with DU, 29 patients with perforated DU, and 541 blood donors. H pylori status was investigated by culture, preformed urease test, stained smear, polymerase chain reaction (PCR), and the ¹³C-urea breath test. cagA status was assessed by PCR. In the blood donors, H pylori status and cagA status were determined by serology. IL-1B–511/–31, IL-1RN, and TNFA–307 polymorphisms were genotyped by PCR, PCR/restriction fragment length polymorphism, or PCR/confronting two pair primers.¹ Data were analysed in . . . [Full text of this article]

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