Crabtree J E, Taylor J D, Wyatt J I, Heatley R V, Shallcross T M, Tompkins D S, Rathbone B J
Department of Medicine, St James's University Hospital, Leeds, UK.
Lancet. 1991 Aug 10;338(8763):332-5. doi: 10.1016/0140-6736(91)90477-7.
The gastric IgA response to Helicobacter pylori was examined in 100 dyspeptic patients by means of immunoblotting of supernatants from antral biopsy and gastric mononuclear cell cultures. 76 of 78 patients with chronic gastritis, 2 of 8 with reactive gastritis, and 1 of 14 subjects with normal mucosa showed positive responses. Of patients with chronic gastritis, 75%, 83%, 97% and 76%, respectively, showed responses to the 120 kDa, 90 kDa, 61 kDa, and 31 kDa proteins. None of the 19 patients with chronic gastritis who did not recognise the 120 kDa protein had peptic ulcers, whereas 25 of 57 with positive recognition had peptic ulcers (p less than 0.001). Mucosal recognition of the H pylori 120 kDa protein was also positively associated with the activity of gastritis (polymorph infiltration) (p less than 0.002) and with the extent of surface degeneration (p less than 0.01). These findings suggest that 120-kDa-positive strains of H pylori have pathogenic features associated with active gastritis and peptic ulceration. Infection with 120-kDa-negative strains may explain why peptic ulceration develops in only a proportion of subjects infected with H pylori.
