Several studies have suggested that a higher degree of chronic active inflammation in the gastric mucosa is associated with H.
pylori as measured by PCR, as well as by the grade of chronic active inflammation, as evidenced by infiltration of lymphocytes and neutrophils in the gastric mucosa [16-25, 32].
Increased chronic active inflammation might trigger a favorable host response that facilitates eradication of the organism with appropriate treatment.
Administration of the four compounds was associated with increased incidences of nonneoplastic changes of the exocrine pancreas, including cytoplasmic vacuolation, chronic active inflammation, atrophy, and arteritis, variably observed in the 14-, 31-, and 53-week interim sacrifices and seen in the 2-year studies (Tables 1-4, Figures 1-8).
Chronic active inflammation was generally seen in association with atrophy and consisted of an infiltrate of mononuclear cells with occasional neutrophils within the stroma.