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G Testino

Publications and source records attributed to G Testino.

At least 37 records · Page 2Linked to original sources
PubMed1999

Primary malignant duodenal tumours: a point of view and a proposal of classification.

To date, malignant duodenal tumours have remained obscure subject-matter although they were first described in the eighteenth century. Recent development in technology and in anatomohistopathology makes it necessary to review the duodenal tumours classification, especially in relation to the progressive development of stromal and neuroendocrine forms. In the literature, precise epidemiological data are not reported and, as regards some duodenal tumours, simply do not exist. Series are generally either surgical, anatomopathological or gastroenterological. Hospital centres need to establish a collaboration which gathers new observed cases to avoid the dispersion of case series. Thus, a European Register will be established to report the real incidence by analyzing the specific differential elements.

Duodenal Neoplasms↗
PubMed1998

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.

Gastrointestinal Neoplasms↗
PubMed1998

Gastric foveolar immature cells (mucopeptic cells) expansion in body-fundic advanced intestinal type gastric cancer in patients with chronic non-atrophic ("superficial") gastritis: Helicobacter pylori role.

BACKGROUND: Some authors reported the relationship between Helicobacter pylori (HP) prevalence and gastric cancer incidence. It is generally agreed that HP plays a key role in altering regulatory factors affecting cellular proliferation during the disease process. This hyperproliferation is due, mainly, to active inflammation action on glandular neck cells. Neoplastic changes may arise owing to a loss of control of cell proliferation. METHODS: In the present study it has been evaluated the mucopeptic cells (immature cells) expansion in surrounding areas of body-fundic intestinal type advanced gastric cancer (GC) in patients with non atrophic gastritis: the cases have been subdivided in relation with HP infection. RESULTS: Muco-peptic expansion was present in 73.9% of HP positive GC patients. The cell expansion has not been observed either in HP negative GC or in control subjects. CONCLUSIONS: The phenomenon, a morphological manifestation of hyperproliferation, might overexpose the mucosa to environmental factors. Therefore, in subjects with genetic predisposition, HP could act as a promoter in the progression towards neoplasia independently of chronic atrophic gastritis.

Chronic Disease↗
PubMed1997

[Is active autonomous duodenitis a precursor of duodenal ulcer?].

Up to today, the relationship between autonomous nonspecific duodenitis (ANSD) has not yet been defined. ANSD has been noticed in about 26% of dyspeptic population. With reference to the presence of active inflammation, ANSD has been divided into chronic duodenitis (CD) (77.7%) and in active duodenitis (AD) (22.3%). The two duodenitis groups have been compared with a group of patients with duodenal ulcer (DU) in relation with the presence of duodenal gastric metaplasia (GM), of duodenal Helicobacter pylori (Hp) infection, of antral chronic gastritis (AG), of antral Hp infection, and in relation with the gastric secretion behaviour. The data concerning AD are superimposable to those of DU with presence of high percentage of duodenal GM, of duodenal Hp infection and of Hp positive AG. Furthermore, they present a gastric secretory profile similar to DU with prevalence of hyperchlorhydria and hyperpepsia. CD without activity, on the contrary, present values superimposable to dyspeptic population without duodenitis and DU. It is, therefore, that Hp positive AD can be considered as a possible precursor of DU. In periulcerous site, in fact, AD is present in more than 90% of cases.

Duodenal Ulcer↗
PubMed1997

Immature cells and Helicobacter pylori infection in early gastric cancer. An immunohistochemical study.

BACKGROUND: Helicobacter pylori (HP) infection has been frequently pointed out as one of factors involved in gastric carcinogenesis: in fact, the risk of developing gastric cancer is 4-6 times higher in infected than in non infected subjects. MATERIALS AND METHODS: In the present study the mucopeptic cells (immature cells) expansion was evaluated in 15 patients with intestinal type early gastric cancer (EGC): the cases were subdivided in relation with HP infection in the surrounding areas. RESULTS: Foveolar mucopeptic cells expansion was present in 63.6% of HP positive EGC patients. This phenomenon was not observed in HP negative EGC. In case of HP positive EGC there is foveolar expansion of the mucopeptic department with substitution of mature cells with immature ones. CONCLUSIONS: Therefore, HP, by means of alteration of cellular turn-over, could act as a promoter in the progression towards neoplasia, modulating the risk acting over individual genetical susceptibility. That even independently from atrophic gastritis.

Female↗
PubMed1997

Body-fundic gastric ulcer and Helicobacter pylori: muco-peptic cells expansion (immature cells) in Helicobacter pylori positive patients.

It is generally agreed that Helicobacter pylori (Hp) plays a key role in alterating regulatory factors affecting cellular proliferation during the disease process. During chronic superficial gastritis there is, in case of moderate/severe activity, a foveolar-superficial expansion of immature muco-peptic cells. In the present experience this phenomenon has been evaluated in the surrounding areas of 22 body-fundic gastric ulcer (BFGU). The 72.7% of BFGU were Hp positive. The expansion was detectable in 68.7% of Hp positive BFGU. The expansion process involves the substitution of mature cells with immature one determining a reduction of the efficacy of the mucosa barrier in association with an increment of aggressive factors (mucosal pepsins). This phenomenon in relation with host genetic susceptibility may favor peptic ulcer.

Cell Division↗
PubMed1997

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.

Adult↗
PubMed1996

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.

Duodenal Neoplasms↗
PubMed1996

Long-term therapy with interferon in anti-HCV positive chronic hepatitis: is it conceivable?

HCV positive hepatitis possesses a relevant social impact as regards national health costs. On the other hand, interferon (IFN) therapy represents to date the best therapeutic approach to this problem. However, several clinical questions have arisen regarding the efficacy and safety of long-term treatments, and above all the management of those patients who did not respond to acute therapy. Nevertheless, it is well known there is a high rate of relapse after the cessation of treatment. The goal of the present paper has therefore been to verify both efficacy and safety of a weekly single dose of IFN in maintaining an adequate remission rate in 38 outpatients who obtained a good response (either type I or II according to Marcellin's classification) to a 12 months' IFN course. Our results evidenced that a maintenance therapy with a single a weekly dose of IFN (3MU) did not seem to lead to a lower rate of relapses when compared to patients who were not given any treatment.

Adult↗
PubMed1996

[Aggressive factors in the physiopathology of peptic ulcer. Recent findings].

The peptic ulcer (PU) is characterized by definite gastric cyto-secretory profiles. In case of duodenal ulcer (DU) and pre-pyloric gastric ulcer (PPGU), there is a prevalence of hyperparietalism with hyperchloridria, while in ulcer with body-fundic localization (BFGU) normo-hypoparietalism with normo-hypochloridria prevails. As well, the total peptic activity follows a superimposable course: it increases in cases of DU and PPGU, while it remains in the normal range in case of BFGU. With reference to the qualitative variations of pepsin, in course of PU the amount of pepsin 1 increases significantly. Such pepsin has a powerful proteolytic action even at high pH: which explains the possible onset of PU even in hypochloridria conditions. Helicobacter pylori (HP) has revolutionized the pathogenetic approach towards the gastric pathology: in 75% of cases there are alterations of the mucosae superficial profile, micropapillary changes, erosions, vacuolations with cellular degeneration. In 90% of cases is present chronic active inflammation in correspondence of the glandular neck of the gastric epithelium. In 70% of cases of BFGU there are qualitative alterations of the superficial epithelium. The gastric anatomic-functional behaviour, however, has an autonomous course and it is not influenced by the presence of infection. It results, therefore, that the bacterium is an important cofactor in PU pathogenesis by means of a direct cytotoxic-enzymatic action, without influencing a secretory behaviour which, in PU, is substantially conditioned by the genetic characteristics of the patient.

Gastric Acid↗
PubMed1996

[Helicobacter pylori, chronic gastritis and precancerous gastric manifestations].

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.

Biopsy↗