Table 3.

Histological features of the different forms of gastritis.

	Type A gastritis	Type B gastritis	Type C gastritis	CPI-ass Gastritis
Inflammatory infiltrate	Lymphoplasmacytic-dominant inflammatory infiltrate	Mixed inflammatory infiltrate with a usually superficial granulocytic component close to the crypt lumina	Lymphoplasmacytic inflammatory infiltrate, sparse amount of intermingling neutrophilic granulocytes possible	Mixed inflammatory infiltrate with lymphoplasmacytic and granulocytic component, foveolar abscess formation possible
apoptosis	Mild increase of apoptotic cells in the gland epithelia (average of 1 apoptotic cell per 10HPF)	Mild increase of apoptotic cells in the gland epithelia (average of 1.5 apoptotic cells per 10 HPF)	No increase of apoptotic cells in the gland epithelia	Increase of apoptotic cells in the gland epithelia, detachment of apoptotic cells and shift to the glandular lumen (average of 6 apoptotic cells per 10 HPF)
Additional characteristics	Reduction/loss of parietal cells and hypoplasia of the glandular body in corpus mucosa	Detection of Helicobacter pylori via conventional H&E- and Giemsa stain, or immunohistochemistry	Fibrotic antral changes, foveolar hyperplasia, smooth muscle fibers radiating to surface parts, potentially intestinal type goblet cell metaplasia and occurence of pseudo-Paneth cells.	Anti-caspase 3 immunohistochemistry helpful in detection of apoptotic bodies/cells.

HPF, High Power Field.