Helicobacter pylori infection sometimes leads to an antigastric autoimmunit
y that ultimately develops into complete atrophy of the glands of the gastr
ic mucosal glands. It has been found that the "classical" parietal cell ant
ibody positive and H. pylori induced autoimmune gastritis share common aspe
cts of histomorphology, stages, and pathomechanisms. Healing of H. pylori a
ssociated active preatrophic autoimmune gastritis by eradication treatment
has been confirmed both in case reports and in prospective and retrospectiv
e studies. This leads to a general practice-oriented four-step concept for
diagnosis and treatment in daily routine: (a) Histological work-up on the b
asis of: lymphocytic infiltration of the glands of the corpus and fundic mu
cosa,focal destruction in individual corpus glands, reactive hypertrophy of
the parietal cells, and search for H.pylori. (b) Additional serological wo
rk-up if histological evidence of H.pylori is lacking:determination of H.py
lori and parietal cell antibodies in the serum.(c) Initiation of an establi
shed H. pylori eradication therapy if histology and/or serology is positive
for H.pylori.(d) Histological and serological follow-up for 9-12 months to
monitor the results of treatment.