Peptic ulcer inheritance in patients with elevated serum pepsinogen group A levels and without infection of Helicobacter pylori.

BACKGROUND: Peptic ulcer has multifactorial aetiology, including genetic factors. We have identified a family with pepsinogen Group A levels higher than normal, with a high prevalence of ulcer disease and a low prevalence of Helicobacter pylori infection. AIMS: Performing linkage analysis in the identified family PATIENTS AND METHODS: We examined the segregation of pepsinogens with microsatellite dinucleotide repeat DNA markers along chromosome 11 (D11S480, PYGM) for pepsinogen Group A and along chromosome 6 [D6S105, D6S 1610, TRMI) for pepsinogen Group C. RESULTS: In markers examined along chromosome 11, linkage analysis provided no evidence for significant causal mutation but, controlling for some risk factors we observed that the probability of falling ill, increases. The linkage analysis along chromosome 6 for pepsinogen Group C did not show a uniform genetic profile. CONCLUSIONS: This study evaluates the hypothesis of peptic ulcer inheritance at least in a small group of patients without the common risk factors.

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.

[Alcohol-dependent mast cell activation in ulcer]. / Attivazione delle mastcellule alcol-dipendente nella malattia ulcerosa.

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)

Intraepithelial carcinoma of the oesophagus: report of 25 cases from north-east Italy.

OBJECTIVE: To investigate the incidence and define the diagnostic aspects of intraepithelial squamous cell carcinoma of the oesophagus and to show the trend in its natural history. DESIGN: Analysis of records of more than 31000 upper gastrointestinal endoscopies in a secondary referral centre. SETTING: Gastroenterology unit, Italy. SUBJECTS: 23 men and 2 women with endoscopic and histological diagnoses of intraepithelial squamous cell carcinoma of the oesophagus. RESULTS: The incidence was 0.8/1000 patients/year. There was a coexisting oropharyngeal or laryngeal cancer in 17 patients. The endoscopic appearance was of a more or less well-defined hyperaemic area. Lesions progressed to infiltrating carcinoma in a mean of 18.3 months range 11-32). CONCLUSIONS: Intraepithelial squamous cell carcinoma is rare in this population. Endoscopy and histology are essential for diagnosis and staging.

Esaprazole effect on acid, peptic and alkaline secretion in duodenal ulcer patients.

To study the effect of Esaprazole, a new antiulcer drug, on acid, peptic and alkaline secretion a modified gastric acid test was performed in 18 duodenal ulcer patients. Pentagastrin was administered as bolus 30' and 75' after the beginning of the test, followed by Esaprazole 300 mg i.v. at 90'. Gastric juice was collected every 15' for determination of: total volume, volume of non parietal secretion, acid, bicarbonate and pepsin output. Serum pepsinogen group I was determined by radioimmunoassay. Esaprazole had a significant inhibitory effect on the total volume of gastric secretion and on volume of non parietal secretion. Pepsin output and serum pepsinogen group I were not affected by Esaprazole, while bicarbonate secretion was reduced. Antiulcer activity of Esaprazole seems to be due to the reduction of total volume of gastric secretion.