Critical pathogenic steps to high risk Helicobacter pylori gastritis and gastric carcinogenesis

Table 1 Atypical vs typical malgun cell change

	“Typical” malgun cell	Atypical malgun cell
Location	Proliferative/surface zone	Proliferative zone
Pits	Elongated proliferative zone	Irregular with crowding
Cell size	Enlarged	Enlarged
Perinuclear halo	+	+
Nuclei	Clear	Hyperchromatic
Chromatin	Euchromatin	Heterochromatin
Nucleoli	1 (or 2)	2 (or multiple)
Nuclear envelope	Smooth	Folded
Mulberry cells	-	+
In metaplasia	-	+/-
Malignant transformation	-	+

Table 2 Pathologic diagnosis system of gastritis/gastropathy

Superficial congestive gastritis (SCG)

SCG with epithelial regenerative change (SCG-Ad)

Erosive gastritis (EG)

EG with prominent neutrophilic proliferative zone foveolitis (EG-PNF)

EG with superficial neutrophilic foveolitis (EG-SNF)

EG, advanced (EG-Ad)

EG with atypical Malgun cell change (EG-AMC)

Chronic atrophic gastritis (CAG)

CAG, advanced (CAG-Ad)

CAG with AMC (CAG-AMC)

Chronic follicular gastritis (CFG)

CFG, advanced (CFG-Ad)

Chronic metaplastic gastritis (CMG)

CMG-Ad

CMG-AMC

Epithelial dysplasia (DYS)

DYS-high grade (DYS-H)

General addendum, if necessary

H. pylori +/-

dominant infiltrate, etc.

H. pylori: Helicobacter pylori.