Intestinal Metaplasia, High-Grade Epithelial Dysplasia and Gastric Cancer

TO THE EDITOR: Although the progression Helicobacter pylori non-atrophic gastritis (NAG) ® atrophic gastritis (AG) ® complete intestinal metaplasia (IM type I) ® incomplete IM (type III) ® epithelial dysplasia (ED) ® gastric cancer (GC) evolution (1–3) has been documented in several studies in recent years, it cannot be considered the only pathway for gastric oncogenesis. Many complex biological factors are involved and epidemiological data suggest the importance of environmental factors such as diet. Excessive intake of NaCl and nitrosamines and de ciency of vitamins C and E may be relevant in the development of preneoplastic/ neoplastic changes (4). Retrospective or perspective studies have indicated a close association between type III and GC, whereas types I and II have been prevalent in both benign and malignant conditions (5–8). In order to better understand the role of IM in the development of GC, we used a casuistry of epithelial high-grade dysplasia (HGD) (9, 10) composed of 50 consecutive cases of HGD (31 M, average age 58 years) (9). Gastric biopsy specimens obtained during the course of gastroscopy were studied for dyspepsia; at least 8 specimens were obtained from each patient (range 8–16) (9). HGD diagnosis was done by an experienced pathologist (MC) in accordance with well-de ned criteria (9, 11). The histological study of gastric mucosa in gastritis (haematoxylin-eosin) was effected in accordance with Dixon’s classi cation (updated Sydney system — Houston), consideration being taken of the in ammatory aspects and epithelial and glandular alterations. The presence of atrophy was evaluated and the cases were subdivided into ‘nonatrophic gastritis’ (NAG) and ‘atrophic gastritis’. Gastric atrophy was de ned as loss of glandular tissue and  brous replacement of lamina propria, and was graded as mild/ moderate chronic atrophic gastritis (MCAG) or severe chronic atrophic gastritis (SCAG) (12). When any area of IM was identi ed on a slide, additional sections were prepared and stained with alcian blue pH 2.5/ periodic acid-Schiff and high-iron diamine/alcian blue pH 2.5 to identify subtypes of IM. Subtypes were classi ed as described by Filipe et al. (8, 13). The clinical outcome subdivision of HGD was made using the criteria of Rugge et al. (14) as follows: association with GC (AGC), carcinoma diagnosed within 1 year; progression (PGC), GC diagnosed 1 year after; persistence (P), degree of dysplasia remained the same in at least two subsequent controls; and regression (R), not con rmed or of lower degree (low-grade dysplasia) in at least two subsequent controls. Pathological diagnosis and classi cation of neoplastic tissues were carried out according to the Union Internationale Contre le Cancer TNM system. The results for clinical behaviour were: AGC, 33 patients (66%) (pT1/pN0, 27 cases; pT2/pN0 4 cases; pT4/pN1 2 cases); PGC, 4 patients (8%) (pT2pN0 4 cases); P, 5 patients (10%); R, 8 patients (16%). The histological results are expressed in Tables I and II. Analysis of the data indicates how the association between IM type III with HGD (5/50: 10%) or cases of early GC (4/35: 11.4%) is limited to a low percentage of cases. However, also the percentage presence of SCAG is low (HGD 9/50: 18%; early GC 8/35: 22.8%). It can therefore be seen how the evolution SAG ® IM type III ® HGD ® GC cannot be taken for granted.