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Biomedical subjects

F Di Mario

Publications and source records attributed to F Di Mario.

At least 109 records · Page 6Linked to original sources
PubMed1994

Effect of age on gastric acid, pepsin, pepsinogen group A and gastrin secretion in peptic ulcer patients.

To verify the effect of age on gastric secretions in gastric (GU) and duodenal ulcer (DU) patients, we carried out a retrospective study evaluating basal and stimulated gastric acid secretion in 427 peptic ulcer subjects aged between 12 and 73 years (GU = 74, DU = 353) in addition to studying gastric juice pepsin, serum pepsinogen group A (PGA) and gastrin in 175 patients (GU = 28, DU = 147). All subjects were then divided into groups according to their sex and age (< 30, 30-39, 40-49, 50-59 and > 60 years). Basal, maximal and peak acid outputs (BAO, MAO, PAO) were unchanged in the various age groups, though MAO and PAO were higher in males than females and in DU than in those with GU, even in the elderly (> 60 years). Pepsin and gastrin levels were unchanged at the various ages in GU and DU, while PGA was higher in males with DU aged 50 or over. This demonstrates that acid, pepsin and gastrin secretions do not change with age in ulcer patients. Acid secretion retains its typical distribution according to pathology (DU > GU) and sex (males > females), and also appears to have a fundamental pathogenetic role in peptic ulcer in the elderly.

Adolescent↗
PubMed1994

A pharmacodynamic study of two omeprazole regimens suitable for long-term treatment of duodenal ulcer.

BACKGROUND: The experience with long-term treatment of peptic ulcer with omeprazole is still scant, but the possibility cannot be excluded that its better pharmacodynamic effect on gastric acidity also has a positive result in the relapse rate. Moreover, this drug acts via a mechanism other than receptorial binding, and therefore its efficacy should not dissipate with time. This study was carried out to assess the pharmacodynamic properties and the possible changes with time of two dose regimens of omeprazole that could be suitable for long-term treatment in duodenal ulcer. METHODS: Twenty patients with endoscopically proven duodenal ulcer were studied by means of 24-h gastric pH-metry both in basal conditions and on the 5th day of acute treatment with 40 mg omeprazole in the morning. All the ulcers healed after 4 weeks, and thereafter 10 patients were randomized to receive orally 20 mg omeprazole daily at 0800 h in single-blind fashion (group A) and 10 to receive 20 mg omeprazole every other day (group B) for up to 6 months. At the end of the 1st, 3rd, and 6th month of these maintenance treatments 24-h gastric pH-metry was repeated to assess the antisecretory effect of each regimen over time. In group-B patients the test was performed on 2 consecutive days (without and with medication) at each time interval. The fasting gastrin values were also determined. The patients underwent esophagogastroduodenoscopy every 2 months. RESULTS: Three patients in group B were lost to follow-up for various reasons, and only seven remained eligible for final analysis. The two long-term regimens of omeprazole were able to increase significantly pH values (p < 0.02-0.001) and the times spent at and above pH 3.0 (p < 0.001) over 24 h compared with basal conditions. In group A the 24-h pH value obtained in the 6th month was higher (p < 0.02) than that in the 3rd month of maintenance treatment. In group B the pharmacologic effect tended to decrease on the day without medication compared with the day with medication, but the difference between them was significantly (p < 0.05) only at the 6-month interval. There was no significant difference between the gastrin levels of the two groups in the long-term treatment. No ulcer relapse was detected at any long-term endoscopic control in the two groups of patients. CONCLUSIONS: The two omeprazole regimens we tested are effective in reducing gastric acidity, and their pharmacodynamic action does not decrease with time. They are therefore suitable for maintenance treatment in acid-related disorders.

Adult↗
PubMed1993

Markers of slow-healing peptic ulcer in the elderly. A study on 1,052 ranitidine-treated patients.

Little is known about ulcer outcome in the elderly. The aims of the present paper were to establish whether risk factors of slow-healing peptic ulcer can be demonstrated in the elderly and whether clinical differences exist between ulcer patients whose age of onset of the disease was before or after 65 years old. The short-term, open study, involving 1052 elderly patients (over 65 years) in 37 gastroenterology centers throughout Italy aimed to compare two schedules of ranitidine treatment: 150 mg twice daily versus 300 mg at bedtime. As nonsignificant differences were found between these two schedules, the sample was considered as a whole. It included 319 gastric ulcer (GU) patients, 699 duodenal ulcer (DU) patients, and 34 concomitant GU and DU cases. Ninety-three patients dropped out of the trial; 79/294 GU, 138/635 DU, and 10/30 GU+DU were found still unhealed after four weeks and 20 GU, 15 DU, and 1 GU+DU remained so after eight weeks. Statistical analysis was performed using likelihood-ratio and Pearson's chi-squared tests and Cox's models. Univariate analysis showed that the indicators of slow-healing GU were ulcer size (P = 0.002) and persisting ulcer symptoms (P = 0.0001); indicators of slow-healing DU were ulcer size (P = 0.0001), persisting ulcer symptoms (P = 0.0001), alcohol (P = 0.0003), and NSAID (P = 0.0088) consumption. DU patients taking antiplatelet drugs have significantly better results after four weeks and worse results after eight weeks (P = 0.0352).(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1993

Early and advanced gastric cancer in the follow-up of moderate and severe gastric dysplasia patients. A prospective study. I.G.G.E.D.--Interdisciplinary Group on Gastric Epithelial Dysplasia.

The role of gastric epithelial dysplasia (GED) as a biological and morphological precursor of gastric cancer has been widely investigated, but few studies have prospectively evaluated the risk of its evolution into gastric cancer. In 1985, a prospective multicenter follow-up study was undertaken on patients with high-grade (moderate or severe) GED. The study involved 49 patients, with a follow-up currently averaging 18.8 months (range: 1-70) and a mean number of 4 endoscopies (range: 2-10). Follow-up was abandoned when 2 subsequent control endoscopies and a 1-year period were negative for GED, or when neoplasia was detected. Gastric cancer was diagnosed in 16 cases (33%). The cancer was detected at an early stage in 10 patients (62%). Eleven cases (59%) were diagnosed within 1 year of follow-up and 5 cases after 13, 18, 21, 24 and 39 months, respectively. Cancer was associated with 36% of moderate GED cases and with 80% of severe cases. Dysplastic changes were no longer detectable at follow-up in 27% of the moderate cases and in 10% of the severe cases. The relative risks for the two lesions being associated with or evolving into gastric cancer were 26 and 132, respectively. In conclusion, high-grade (moderate or severe) GED is frequently associated with or evolves into gastric cancer. The follow-up of patients considerably enhances the chances of diagnosing gastric cancer in its early stages, thus making such an approach mandatory.

Female↗
PubMed1993

Prevalence of Helicobacter pylori infection in patients with precancerous changes and gastric cancer.

Several papers suggested a role for H. pylori infection in gastric cancer. We evaluated the prevalence of H. pylori infection in an endoscopic population of patients with gastric precancerous conditions and lesions by studying biopsies from 252 patients and recording the presence and degree of H. pylori infection. Patients were subgrouped as follows: chronic non-atrophic gastritis (CG), chronic atrophic gastritis (CAG), intestinal metaplasia (IM), epithelial dysplasia (ED) and gastric cancer (K). As control populations, patients with duodenal ulcer (DU) and patients with no endoscopic and histologic damage (CO) were investigated. H. pylori infection rate increased with age, but became significantly lower (P < 0.001) with the progression of gastric mucosal damage: DU 85%, CG 72%, CAG 58%, particularly in the antral type (39%), IM 63% overall, ED 44% and K 35%. The density of colonization showed the same trend (P < 0.001). Of the K patients, only 36% were H. pylori positive in the adjacent mucosa. Anti-H. pylori antibodies (IgG, IgA and IgM) were also tested. A concordance in the diagnosis between histology and serology was obtained in 82% of the cases. In our experience, H. pylori infection correlates inversely with the presence of gastric precancerous changes and cancer. A cautious interpretation of the epidemiological data regarding H. pylori infection and gastric cancer is therefore, in our opinion, mandatory.

Adolescent↗
PubMed1993

Peptic ulcer in the elderly--a double-blind, short-term study comparing nizatidine 300 mg with ranitidine 300 mg. GISU (Interdisciplinary Ulcer Study Group).

UNLABELLED: This was a randomized, double-blind, multicentre, short-term study comparing ranitidine and nizatidine at the standard dosages of 300 mg at bedtime. In 49 centres in Italy, all peptic ulcer patients aged over 65 years and with endoscopically documented acute disease were considered eligible for the study. Clinical check-ups were repeated every 3 weeks, while the endoscopic and biochemical assessments were scheduled at 6 and (in unhealed patients) 12 weeks. STATISTICS: chi-squared test, Fisher's exact test, Student t-test for unpaired data. The study included 170 duodenal ulcer and 75 gastric ulcer patients. Of these, 83/170 duodenal ulcer and 38/75 gastric ulcer patients were treated with nizatidine 300 mg and the remainder with ranitidine 300 mg. The groups were well-matched for common clinical data. Eight patients dropped out. Healing rates at 6 and 12 weeks were 81.9% and 91.5% for nizatidine-treated duodenal ulcer patients versus 78.1% and 94.2% for ranitidine-treated duodenal ulcer cases (P: N.S.); 6 and 12-week healing rates were 76.3% and 89.5% for nizatidine-treated gastric ulcer patients versus 67.6% and 83.8% for ranitidine-treated gastric ulcer patients (P: N.S.). No slow healing risk factors were found. Only minor adverse events were registered. IN CONCLUSION: ranitidine 300 mg and nizatidine 300 mg both proved effective and safe in the treatment of acute peptic ulceration in the elderly.

Aged↗
PubMed1993

Pathology of the gastric antrum and body associated with Helicobacter pylori infection in non-ulcerous patients: is the bacterium a promoter of intestinal metaplasia?

A series of 115 consecutive, non-ulcerous, dyspeptic patients were examined for Helicobacter pylori (H. pylori) colonization in the gastric antral and/or body mucosa using Giemsa staining. Findings were correlated with the presence and degree of activity of superficial gastritis, deep gastritis, atrophic gastritis and with the presence of intestinal metaplasia. The prevalence of H. pylori positivity was 61.7%. In 59 of the 71 positive patients (83%), H. pylori was detected in the antrum or in both the antral and oxyntic mucosa. In the remaining 12 positive patients, H. pylori was detected only in the oxyntic mucosa nad in all these cases, the antrum showed intestinal metaplasia associated with atrophic gastritis (25%). In both antral and oxyntic mucosa, the activity of the gastritis was significantly correlated with H. pylori colonization. Linear logistic regression analysis showed that in patients with intestinal metaplasia the presence of H. pylori infection was significant in predicting the presence of more extensive intestinal metaplasia after adjusting for age. The prevalence of intestinal metaplasia types II and III was 65.5% in the H. pylori positive and 25% in the H. pylori negative patients. The antral mucosa is thought to be the elective site for H. pylori related histological lesions. At a later stage, H. pylori can be detected only in the oxyntic area while the antral mucosa shows extensive metaplastic or atrophic lesions. We would suggest that H. pylori plays a promotional role in the morphogenesis of intestinal metaplasia.

Adolescent↗
PubMed1993

Chronic nicotine intake causes vascular dysregulation in the rat gastric mucosa.

Chronic cigarette smoking has adverse effects on peptic ulcer disease because the healing of ulcers is delayed and the incidence of relapses is enhanced. Short term intake of nicotine induces vascular damage in the rat gastric mucosa, but the pathophysiological mechanisms of nicotine's action in the stomach are largely unknown. In this study rats were treated with nicotine, added to their drinking water, for 50 days. They were then anaesthetised and their stomachs perfused with acidified acetylsalicylic acid (ASA). Chronic nicotine treatment failed to change the effects of acidified ASA to induce gastric mucosal acid back diffusion, haemorrhagic damage and bleeding. Basal blood flow in the gastric mucosa was also unchanged by chronic nicotine intake, whereas the mucosal hyperaemia evoked by ASA induced acid back diffusion was averted. The concentrations of sulfidoleukotrienes were significantly augmented in the gastric wall of nicotine treated rats. These data show that chronic nicotine intake causes dysregulation of the gastric microcirculation, an effect that is associated with biochemical changes in the stomach. This study thus substantiates the adverse effects of smoking on gastric mucosal pathophysiology. These data suggest that inappropriate regulation of gastric mucosal blood flow inhibits recovery from gastric mucosal injury in smokers.

Animals↗
PubMed1993

Changes in parietal and mucous cell mass in the gastric mucosa of normal subjects with age: a morphometric study.

Whether or not the gastric mucosa undergoes significant changes in normal aging subjects is still open to debate. In 51 subjects undergoing endoscopy and lacking any significant endoscopic or histologic modification we evaluated mucosal thickness, gland number, numbers of parietal, chief and mucous cells at the fundus and of mucopeptic cells at the antrum, with a morphometric method, subgrouping the patients according to their age class. Our findings demonstrate that the number of parietal cells tends to increase with age and, on the other hand, the number of mucous cells is reduced in elderly subjects (p < 0.05). When considering the parietal-to-mucous cell ratio, this is significantly increased (p = 0.0005) with age. Acid secretion being an offensive factor and mucus a fundamental component of the gastric mucosal barrier, these findings suggest an increased susceptibility of the gastric mucosa to damage in the elderly.

Adult↗
PubMed1993

Circadian acidity pattern in prepyloric ulcers: a comparison with normal subjects and duodenal ulcer patients.

We used continuous 24-h pH monitoring to compare the circadian intragastric acidity of 36 patients with prepyloric ulcers (PPU) with that of 101 normal subjects (NS) and that of 206 patients with duodenal ulcer (DU). The ulcer crater was endoscopically ascertained in all cases, and PPU were located within an area up to 2 cm proximal to the pylorus. The pH curve pertaining to DU patients ran below that of NS during most of the circadian period, whereas the pH profile of PPU patients was higher than that of NS, and this was particularly true during the evening and the night. The acidity of PPU patients was significantly lower (p < 0.01) than that of NS during the night only, whereas it was lower (p < 0.05-0.001) than that of DU patients during each time interval analysed (24 h, nighttime, and daytime). Our findings show that the gastric acidity of PPU patients differs greatly from that of DU patients, since it is lower throughout the whole 24-h period, and particularly during the night. Thus these two entities are pathophysiologically different with regard to the acidity pattern and should be considered two distinct subgroups of peptic ulcer disease instead of being incorporated, as usually happens, in the clinical group 'duodenal ulcer disease'.

Adult↗
PubMed1993

Gastric bicarbonate secretion in high-relapsing, smoking duodenal ulcer patients.

Gastric bicarbonate secretion has been evaluated by Feldman's method in 48 duodenal-ulcer patients. The relationship between smoking, clinical ulcer outcome (healing and recurrence) and bicarbonate secretion has been analysed. Heavy smokers secreted higher bicarbonate ions than did non-smokers. High-relapsing patients produced lower bicarbonate output. These preliminary data suggest that an impaired gastric bicarbonate secretion is associated with smoking, a well-known ulcer-associated factor; further-more, it may single out high-relapsing duodenal ulcer patients.

Adult↗
PubMed1993

Helicobacter pylori infection, cigarette smoking and alcohol consumption. A histological and clinical study on 286 subjects.

UNLABELLED: Helicobacter pylori (Hp) is connected with active/chronic gastritis, gastric gastric and duodenal ulcer. It is not known whether exogenous factors are involved in Hp infection. The aim of this prospective study, performed on 286 consecutive subjects undergoing upper gastrointestinal endoscopy, was to evaluate the influence of smoking and alcohol consumption on Hp infection. For each patient the following parameters were taken into account: sex, age, smoking (no, < 10, > 10 cig/day) and alcohol (no, < 40, > 40 g ethanol/day) intake, antiulcer therapy (no, H2-blockers, omeprazole, sucralfate), presence of gastric or duodenal ulcer (DU). At least two biopsies from both the antrum and the corpus were obtained for histological examination; the gastritis was classified and scored according to the Sydney system. STATISTICS: chi-squared test (corrected), Fisher's exact test. RESULTS: 43 pts had Hp (27M, 16F; age 57.8 yrs, range 23-91), 47 Hp ++ (25M, 22F; age 61.1, range 19-86), 81 Hp + (48H, 33F; age 56, range 16-84), 115 Hp- (75M, 40F; age 57.8, range 19-84). Hp infection was found to be significantly correlated with presence of ulcer symptoms, gastritis, lymphoid follicles and, among DU patients, with active DU. The other parameters considered did not influence Hp infection. In conclusion smoking habits and alcohol consumption do not affect Hp infection of the stomach.

Adolescent↗
PubMed1993

[Alcohol-dependent mast cell activation in ulcer].

Numerous studies have shown that alcohol causes both acute and chronic damage to gastroduodenal mucosa. The methods of damage differ however, and experimental studies in animals have shown that the degranulation of mast cells in gastric mucosa causes acute hemorrhagic lesions after the consumption of alcohol. It is not known whether this mechanism also operates in man. The aim of the present study was therefore to evaluate whether there is a correlation between mast-cell activation, determined by assaying tryptase levels in gastric mucosa, and the consumption of alcohol in patients with ulcerative diseases. Thirty-one patients with cicatrized ulcerative lesions (13 gastric ulcers, 18 duodenal ulcers) were included in the study. Biopsies at the level of the gastric fundus and antrum and the duodenal bulb were performed in all patients to determine tryptase levels. Biopsy material was frozen and subsequently homogenized; the enzyme was assayed in the supernatant using a radioimmunometric method. The mean daily alcohol consumption was calculated in clinical terms for each patient over the past 5 years and patients were subdivided into non-drinkers and moderate (< 60 g alcohol/day) and excessive (> 60 g alcohol/day) drinkers. It was found that tryptase concentrations were higher in the fundus compared to the gastric antrum and duodenal bulb, irrespective of alcohol consumption both in patients with gastric ulcer and duodenal ulcer. The importance of mast cells in provoking alcohol-dependent damage was studied at a gastric level. Alcohol leads to their degranulation and therefore contributes to the formation of gastric lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Evaluation of the cost of maintenance therapy (6 months) with 150 mg ranitidine vs 20 mg omeprazole vs 20 mg omeprazole every other day in duodenal ulcer].

Prevention of ulcer relapse and of its complications is a problem which remains to be solved. Our study involved 250 patients, with healed duodenal ulcer. We evaluated efficacy and costs of three different maintenance therapies: ranitidine 150 mg/day, omeprazole 20 mg/day every other day and omeprazole 20 mg/day. Six months later, we found the incidence of relapse to be 24.4% (32/131) in the once-a-day ranitidine group, 19.7% (13/66) in the day every-other-day omeprazole group, and 3.8% (2/53) in the once-a-day omeprazole group. Further, we evaluated costs relative to relapsing patients, and total costs for each treatment group. From these data, we conclude that personalized maintenance therapy with omeprazole is the most cost-effective: a dosage of 20 mg/day is extremely effective in maintaining remission, and is therefore most indicated in patients at risk; omeprazole 20 mg/day every-other-day affords better compliance, lower costs and fewer relapses with respect to standard H2-antagonist dosages.

Adult↗