Does CagA contribute to ulcer pathogenesis in a developing country, such as Sudan?

In Western populations, peptic ulcer disease is closely associated with Helicobacter pylori (H. pylori) strains expressing the CagA antigen. In Africa the prevalence of H. pylori infection and peptic ulcer disease is high, although information regarding potential virulence factors is lacking. This study examines the prevalence of antibodies to CagA both in African patients with dyspepsia who are undergoing gastroscopy, and in asymptomatic healthy African volunteers.

Eighty two consecutive patients (median age 34 years, range 15-73 years), attending for gastroscopy were studied, of whom 78 (95.1%) were subsequently found to be Helicobacter positive. Three antral biopsies were obtained from each patient and 5 ml of blood was taken for determination of CagA seropositivity using western blot analysis. CagA seropositivity was also determined in 65 H. pylori positive healthy volunteers (median age 30 years, range 18-70 years), with no symptoms or previous history of gastroduodenal disease.

Of the 78 H. pylori positive patients, CagA seropositivity was present in all 22 patients with active peptic ulcer disease (100%), in eight of nine patients with duodenitis (89%), in 15 of 19 patients with macroscopic gastritis (78.9%), and in 24 of 28 patients with a normal endoscopy (85.7%). On histological assessment, 46 patients had chronic active gastritis, 29 patients had gastritis with atrophy and three patients had intestinal metaplasia. CagA seropositivity rates were 84.7%, 93% and 100%, respectively, for these groups. In the 89 healthy volunteers studied, 57 of the 65 H. pylori positive subjects (87.7%) were seropositive for the CagA protein.

As in Western countries, CagA seropositivity in this African population was closely related to endoscopic gastroduodenal disease, and to the presence of more advanced histological lesions in the antrum. However, there was also a high prevalence of CagA seropositivity in asymptomatic healthy individuals, suggesting that factors other than CagA predominate in ulcer pathogenesis in this population.