Regression of Precancerous Epithelial Alteration in Patients with Helicobacter Pylori Chronic Gastritis GIANINA MICU 1 , FLORICA STĂNICEANU 1,2 , SABINA ZURAC 1,2 , CRISTIANA POPP 1 , ALEXANDRA BASTIAN 1 , ELIZA GRĂMADĂ 1 , T. TEBEICA 1 , IRINA TUDOSE 1 , R. MATEESCU 2,3 , R. VOIOSU 2,3 1 “Colentina” Clinical Hospital, Department of Pathology, Bucharest, Romania 2 “Carol Davila” University of Medicine, Bucharest, Romania 3 “Colentina” Clinical Hospital, Department of Gastroenterology, Bucharest, Romania As a Group 1 carcinogen for gastric cancer, Helicobacter pylori (H. pylori) was involved in many studies and researches focused on physiopathology and morphopathologic changes induced by this bacterium. The study included 3069 gastric endoscopies performed between January 2005 and December 2009 in “Colentina” Clinical Hospital. During upper endoscopy biopsies from antro-pyloric and corporeo-fundic region were collected. Histopathologic diagnosis of these biopsies was made using Sydney criteria. The patients were divided in two groups, based on the presence or absence of H. pylori: group A included 1414 H. pylori positive patients and group B included 1653 H. pylori negative patients. We evaluated several histopathological parameters, correlating the degree of inflammation, atrophy, metaplasia, regenerative hyperplasia and dysplasia with the presence of H. pylori infection. Our study identifies an overall tendency towards regression of premalignant lesions of gastric epithelium (regenerative epithelial hyperplasia, atrophy and intestinal metaplasia) after H. pylori eradication, as well an increasing number of patients diagnosed with early gastric cancer, thus consolidating the results of studies who foretell the significant decrease of gastric cancer mortality. These lesions are present years before becoming clinically manifest, and consequently treatable. In respect of carcinogenic mechanisms, some of our results confirm the carcinogenic cascade triggered by the H. pylori infection, as it was proposed by Correa et al. in 1975. However, we obtained data leading to the idea that the “precursor lesions” could appear (and subsequently histopathologically evaluated) independent one to the other, through other steps then Correa’s model. Key words: Helicobacter pylori, gastric atrophy, intestinal metaplasia, epithelial dysplasia. The inclusion of Helicobacter pylori (H. pylori) in Group 1 carcinogen for gastric cancer [1] has already made history. Many studies focused on physiopathologic and histopathologic changes induced by this bacterium aim both academic interest of establishing the main characteristics of the infection and the improvement of evolution or even finding the cure of gastric cancer which was until recently one of the leading causes of death [2]. Recent studies of the last decade have reported a decreasing incidence of gastric cancer as well as a decrease of mortality due to this disease [2][3]. This decrease is significant especially in Western countries, where the disease is three times less frequent than it was in 1990s [4]. Also, countries with higher risk, as Korea and Japan, are reporting decreasing mortality due to gastric cancer as well [2][4]. In the last century several directions were recommended in order to prevent the unfavorable evolution of gastric lesions [3–5]: nutritional guidelines (limitation of salt intake, reducing smoked aliments intake, increasing percentage of fresh fruits and vegetables in daily diet); therapeutic protocols (early detection and eradication of Helicobacter pylori infection, since it is a well proven fact that it is the first step towards cancer via atrophic gastritis, intestinal metaplasia and intraepithelial neoplasia), prophylactic direction (anti-H. pylori vaccination) [6] as well as new protocols for screening and clinical and endoscopic surveillance aiming diagnostic and treatment of premalignant lesions, especially in countries with higher risk among their population. Our study confirms an overall regression of premalignant lesions of gastric epithelium after H. pylori eradication [7][8], as well as the increased number of patients diagnosed with the only stage of perfectly curable gastric cancer (early gastric cancer ) [9], are consolidating the results of studies ROM. J. INTERN. MED., 2010, 48, 1, 89–99