Gastric cancer and Helicobacter pylori: biologic and epidemiologic inconsistencies.

In this report we examine biologic and epidemiologic data with the aim of understanding any correlations between Helicobacter pylori infection and preneoplastic and neoplastic changes. As far as biologic data are concerned, some elements point to the role of H. pylori in the development of preneoplastic and neoplastic changes, such as intestinal metaplasia and dysplasia. The relationship with H. pylori would mainly be due to an increased cellular proliferation with the presence of immature cells in the superficial layers, susceptible to metaplastic or dysplastic modifications. The subsequent passage toward cancer is probably caused by other factors inasmuch as H. pylori is not able to colonize metaplastic or dysplastic areas and hyperproliferation remains at comparable levels, even in the absence of infection. In fact, available epidemiologic data show a high prevalence of H. pylori infection in some geographic areas with a high incidence of gastric cancer. It is also true, however, that there are several populations in which a low neoplastic risk is associated with a high prevalence of infection. We stress the methodologic weaknesses of several studies that attempt to establish a strict association between cancer and H. pylori. Therefore, epidemiologic data are still contradictory and do not permit identifying a precise role of H. pylori as a predominant causative agent in the onset of preneoplastic and neoplastic changes. We conclude that H. pylori behaves as a possible cofactor of other known damaging agents to the gastric mucosa, contributing to the risk of developing neoplastic modifications that may also be subject to individual genetic susceptibility.

Duodenal gastric metaplasia, gastric anatomic-functional correlations (parietal cell mass and hydrochloric acid secretion) and Helicobacter pylori. Any differences between chronic autonomous non-specific duodenitis ("non active") and duodenal ulcer?

BACKGROUND AND METHODS: Aim of the present experience was to carry out a study on a dyspeptic population in order to verify the role of Helicobacter Pylori (HP), duodenal gastric metaplasia (GM), hydrochloric acid secretion in the genesis of chronic autonomous non-specific duodenitis (ANSD). A comparison with duodenal ulcer (DU) was effected. RESULTS: Histology showed the presence of ANSD in 24.6% of dyspeptic population. GM was present in 15.1% of ANSD, in 12.8% of dyspepsia without ANSD and in 78.1% of DU. HP in duodenum was present in 12.1% of ANSD, in 10.8% of cases of dyspepsia and in 75% of DU. Concerning parietal cell mass and acid secretion in ANSD and in dyspepsia was found a prevalence of normoparietalism with normochlorhydria, while in DU was found a prevalence of hyperparietalism with hyperchlorhydria. This study shows that the role of HP has not a well defined etiologic weight in ANSD. CONCLUSIONS: The observations of the present experience, which differentiate ANSD and DU, lead to exclude a pathogenetic relation between ANSD and DU.

Duodenal tumours.

Duodenal tumours is an extremely fragmentary topic since the experience of various specialists: gastroenterologists, pathologists, radiologists and surgeons is involved. At present, correct epidemiologic data is lacking whereas much progress has been made in the diagnostic field, thanks to the endoscopic, histologic and radiologic techniques. Thus a different classification scheme has been suggested in the attempt to codify the fundamental aspects of this lesion. An interdisciplinary data base has been proposed in order to provide useful data for an epidemiological evaluation.

[Helicobacter pylori, chronic gastritis and precancerous gastric manifestations]. / Helicobacter pylori, gastrite cronica e manifestazioni precancerose gastriche.

Helicobacter Pylori (HP) has been noticed in about 80% of cases of superficial chronic gastritis. In about 75% of HP positive biopsies degenerative lesions of superficial gastric epithelium, represented by irregularities of the superficial profile, micropapillar-transformation and erosions have been observed. Furthermore, it is possible the observation, in areas of high bacterial colonization, of vacuoles which are the result of a direct action of HP strains producing vacuolating cythotoxin. In correspondence with the glandular necks active inflammation is present in about 90% of cases. Hp is responsible, by means of direct cytotoxicity and inflammatory cell aggression, of most superficial gastritis, it may help the evolution towards atrophic gastritis and may superimpose on an already noted gastritis situation, promoting their inflammatory exacerbation. The presence of HP infection decreases with the increase histological damage: superficial gastritis (SG) 89%, atrophic gastritis (AG) 58%, intestinal metaplasia (IM) 51% and dysplasia (D) 47%. The founding of the bacterium in conditions such as AG or in surrounding zones IM or D is the demonstration of a possible role of the bacterium in the development of the phases subsequent to AG or of phenomena like IM and D, and not confined to the already verified passage SG/AG. The continuous rearrangement in correspondence with the glandular necks induced by active inflammation HP induced and the subsequent hyperproliferation may help mytotic error, giving rise to metaplastic or dysplastic cellular lines. Therefore, HP in the progression towards IM and D should act as promoter by means of the increase of cellular kinetics.

Levosulpiride in functional dyspepsia: a multicentric, double-blind, controlled trial.

Abnormalities in gastrointestinal motility have been reported in a substantial proportion of patients with functional dyspepsia, supporting the use of prokinetic drugs for treatment of dyspeptic symptoms. To evaluate efficacy and safety of levosulpiride in short-term treatment, 1298 patients were enrolled in a double-blind multicentric study carried out in 45 Italian Gastroenterology Departments. Patients were randomly assigned to either levosulpiride (25 mg tid), domperidone (10 mg tid), metoclopramide (10 mg tid) or placebo (1 tablet tid) for 4 weeks. Patients were selected on the basis of: a) occurrence in the last 4 weeks of at least 5/10 selected symptoms (anorexia, nausea, vomiting, upper abdominal pain, postprandial bloating, abdominal fullness, early satiety, belching, heartburn, regurgitation), severity of which should reach/exceed a total score of 8, as assessed by a specific scale ranging from 0 (absent) to 3 (severe); b) normal results of routine biochemical, ultrasound and endoscopic examinations. In addition, each patient subjectively evaluated efficacy of treatment by a visual analogue scale. Significant improvement was recorded for all symptoms at days 10 and 28 in all groups (p < 0.001), but levosulpiride was significantly (p < 0.01) superior to domperidone, metoclopramide and placebo both in the overall clinical improvement scale as well as in a subgroup of symptoms (postprandial bloating, epigastric pain, heartburn). Active treatments and placebo were comparable as far as concerns occurrence of side-effects (12-20%) including galactorrhoea, breast tenderness and menstrual changes.

Gastric ulcer and cancer ulcer. Retrospective evaluation of the current endoscopic diagnosis.

Aim of this experience has been to evaluate the current diagnostic potentiality of the endoscopy in the framework of the gastric ulcerous pathology. On the total of the gastric ulcers 17.9% have resulted to be neoplastic with the hystologic examination. The diagnostic accurracy of the endoscopy has resulted to be of the 87% compared to hystology. From our data it is evidenced how the endoscopy examination has a relevant diagnostic accuracy in defining the nature of the gastric ulcer which however has to be confirmed by the histology which seems to be diriment.

[Influence of Helicobacter pylori on gastric secretion. Study on variously associated gastric body, fundus and antrum chronic gastritis]. / Influenza dell'Helicobacter pylori sulla secrezione gastrica. Studio in corso di gastrite cronica corpo-fundica ed antrale variamente associate.

Among the various themes related to Helicobacter pylori (HP) which is still a subject of discussion, there is the possible influence of this bacterium on gastric secretory physiology. In the present study, an evaluation has been carried out of stimulated gastrinemia, stimulated acid secretion and total peptic activity in gastric juice in the course of a paradigmatic condition, as autonomous chronic gastritis, in order to reveal possible modifications induced by the HP infection. In cases of HP positive chronic superficial antral gastritis associated either with normal body-fundic mucosa or with superficial gastritis, there is a significant increase of stimulated gastrinemia in comparison to HP negative groups and controls. In the course of body-fundic atrophic and preatrophic chronic gastritis associated either with antral superficial chronic gastritis or with antral atrophic gastritis, there are no statistically significant differences between HP positive and HP negative subjects. As regards acid and pepsin secretion no significant differences emerge in any group between HP positive and HP negative subjects. In the HP positive subjects with antral superficial gastritis and higher gastrin values the study of acid and pepsin secretion has yielded no significant variations. From the results of this study it emerges how gastric secretory parameters vary exclusively according to the histologic state of gastric mucosa. Therefore, the lesion action of HP may mainly be attributed to a direct action, rather than to substantial gastric secretory changes.

Chronic gastritis: its clinical and physiopathological meaning.

Chronic gastritis (CG) is the chronic inflammation of gastric mucosa associated with varying degrees of damage of superficial and glandular epithelia. The causes of CG are exogenous (mainly Helicobacter pylori) and endogenous. The process is concluded by atrophy of parenchyma. CG is associated with dyspepsia in approximately 50% of cases, but frequently with gastric and duodenal ulcer. The role of chronic atrophic gastritis (AG) is relevant in development of cancer or of other tumors like carcinoids and polyps. The specific secretive cells of the glandular parenchyma and of the superficial epithelium reveal a good correlation with secretory component behavior, but they are only partially influenced by H. pylori. It emerges that CG is an anatomic-functional condition. The cytofunctional profile in AG causes achlorhydria and therefore chronic luminal alkalosis. This condition favors intestinal metaplasia (IM) and important intraluminal troubles. Finally, nutritional deficiencies or H. pylori seem to interfere with the intragastric metabolism and therefore play a relevant role in the rise of IM.

[Total peptic activity in gastric juice and peptic cell mass (chief fundic cells and mucopeptic fundic-antral cells): cellular-secretory correlations in normal subjects]. / Attività peptica totale nel succo gastrico e massa cellulare peptica (cellule principali fundiche e cellule mucopeptiche fundico-antrali): correlazioni cito-secretorie in soggetti normali.

The aim of this experience has been to evaluate cytosecretory correlations between total peptic activity in gastric juice and gastric peptic cell mass (chief cells and fundic-antral mucopeptic cells) in normal subjects. Gastric peptic cell mass and total peptic activity do not change depending on sex. Concerning age, in spite of a significant decrease of gastric peptic cell mass, peptic activity does not significantly decrease. This apparent disagreement between decreasing anatomic data and functional data, remaining unchanged, may be explained by analyzing the behaviour of fundic and antral peptic cell masses in detail. A difference emerges in the behaviour of chief and mucopeptic cells. The first decrease significantly after 50 years, while the second ones do not show variations, regardless of their fundic and antral location. In particular, fundic mucopeptic cell component increase, but not significantly. The lack of variation in peptic activity in gastric juice after 50 years may be assumed to be connected with the unchanged integrity of mucopeptic cells.

Stimulated gastrinemia, parietal cell mass and stimulated acid secretion in autonomous chronic gastritis: Helicobacter pylori influence.

BACKGROUND/AIMS: In the present experience, an evaluation has been carried out of stimulated gastrinemia, parietal cell mass, and acid secretion in the course of a paradigmatic condition, such as autonomous chronic gastritis, in order to reveal possible changes induced by the presence of Helicobacter Pylori (HP). MATERIALS AND METHODS: We evaluated 153 patients with chronic gastritis of the antrum and/or body fundus, in different combinations not associated with peptic pathology. RESULTS: In the group of subjects with antral superficial chronic gastritis associated with normal body-fundic mucosa or with body-fundic superficial chronic gastritis, about 40% of the subjects in the HP positive group show gastrinemia values which are higher than the norm. The evaluation of parietal cell and stimulated acid secretion yielded no differences between the HP positive and HP negative groups: it emerges that these parameters vary exclusively according to the histologic state of the body-fundic mucosa. In the patients group with hypergastrinemia, the study has revealed no variations in parietal cell mass and acid secretion. CONCLUSION: Evidently the increase in gastrinemia in these subjects was not important enough to induce an increase in parietal cell mass and acid secretion. It emerges how the presence of HP does not imply substantial changes on the gastric cyto-functional parameters: these variations depend mainly on the histologic state of the gastric mucosa.

Epidemiology and etiology of "autonomous" nonspecific duodenitis.

In this prospective study we looked for possible epidemiological and etiological factors in "autonomous" nonspecific duodenitis. Of 136 dyspeptic patients who entered the study, duodenitis was found in 25.6% (94.4% chronic duodenitis and 5.6% isolated active duodenitis). Men predominated with a significant prevalence of 74%; 49% of them had white-collar jobs, but age, psychological factors, and the season of the year played no role. We found that smoking and alcohol and coffee intake bore no relation to duodenitis. Helicobacter pylori (HP) was present in only 17.1% of patients with duodenitis, little different from the 10% prevalence in dyspeptic patients without duodenitis. HP was always associated with gastric metaplasia and inflammatory activity.