Is gastric inflammation enhanced in children with CagA-positive Helicobacter pylori infection?
H. pylori-infected children with CagA antibodies seem to have a more severe inflammation in the gastric antrum than CagA-negative children as shown by an increase in the density of antral mononuclear cells. A finding of higher serum antibody titers to H. pylori in CagA-positive children may be related to this enhancement of inflammation.
The PRSS1 p.R122H mutation, SPINK1 p.N34S, and PRSS3 p.E32del variants were associated with recurrent, but not sentinel AP. The genetic background could possibly be different between sentinel and recurrent AP.