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Title: Porównanie obrazu makroskopowego i mikroskopowego błony śluzowej żołądka w przebiegu ostrego zatrucia i zespołu odstawienia u osób uzależnionych od alkoholu etylowego


Concentrated ethanol is one of many xenobiotics which cause injury to upper gastrointestinal tract mucosa but the mechanism of this action is still incompletely established. In cases of acute alcohol poisoning the direct necrotizing effect of consumed alcohol on the mucous membrane epithelium as well as the vascular reaction caused by vasoactive mediators (histamine, leukotrienes) released from mastocytes by the action of alcohol seems to be of principle significance. In the course of chronic alcohol consumption, in addition to lesions arising on acute intoxication, induction of an inflammatory reaction occurs in the form of mucosal inflammatory infiltrations particularly in the gastric antrum. The inflammatory process of the gastric mucosa has various activity and intensification and clinical signs. The recession of symptoms of acute poisoning or withdrawal syndrome does not stay in direct relation to the resolution or intensity of gastrointestinal tract disorders. The assessment of gastrointestinal injury in alcohol dependent patients is difficult due to the coincidence of different exogenic factors which cause gastric mucosal injury such as: smoking, Helicobacter pylori infection, malnutrition, abuse of medication or the coincidence of other alcohol related organ injury, especially of the liver and pancreas. In these cases the connection of an etiological factor to a certain micro and macroscopic feature found in the gastric mucosa and to the clinical state in extremely difficult. The facts mentioned above were the direct cause of attempting to find an answer to whether such varied clinical findings of acute alcohol intoxication and withdrawal syndrome can be reflected in endoscopic and histologic findings in the gastric mucosa of alcohol dependent patients. The additional aim of this study was the examination of the dynamics of gastric mucosa lesions following controlled alcohol abstinence and the procurement of data based on analysis of endoscopic and histologic findings of gastric mucosa adaptation to chronic stress of alcohol abuse. This study involved 66 alcohol dependent patients hospitalised in the Department of Toxicology CMUJ who were divided into two groups: one group of 28 patients admitted due to acute alcohol intoxication and another group of 38 patients admitted with variously intensified withdrawal syndrome. In each group following history taking and physical examination the indications for endoscopy within the first 24 hours post admission to the department were established. During gastrofiberoscopy biopsy specimens from the corpus, antrum and pylorus were collected for histological examination and for ureaze test to confirm or exclude Helicobacter pylori infection. Macro and microscopic findings were classified according to the actualised Sydney System. In 46 patients (26 with withdrawal syndrome and 20 with acute alcohol poisoning) in which, despite controlled abstinence, clinical sings concerning the gastrointestinal tract were still present, control gastrofiberoscopy was performed after 14 days with the aforementioned tests. The following features were characterised in both groups: age, period of alcohol dependence, alcohol blood level, withdrawal syndrome intensity according to CIWA scale, presence of gastrointestinal signs, incidence of Helicobacter pylori infection and incidence of smoking. The presence of micro and macroscopic gastric mucosa lesions and their topography and level of injury was studied according to group dependence. Next the differences in gastric mucosa lesion degree according to topography, taking into account both time and group examined (interaction assessment) were analized. The influence of Helicobacter pylori infection and smoking on specific histological findings taking into account lesion topography and patient age were assessed. ; The obtained results were analysed using computer assisted statistic tests: randomised, based on constant model bifactor analysis taking into account the complete model – with two direct effects (time effect, group effect) and the primary interaction effect (time/group effect), Chi squared and Q Cochrane. Statistically significant differences were qualified by a significance level of p<0.05. In the obtained results the percentage of patients with gastrointestinal signs (clinical and in history) in both studied groups was similar. Clinical signs during acute alcohol poisoning and withdrawal syndrome did not correlate with the degree of intensification of gastrointestinal mucosa, macro and microscopic lesions and with presence of Helicobacter pylori and smoking. The percentage of smokers and Helicobacter pylori infection in both study groups was similar but significantly higher than in the general Polish population. On gastrofiberoscopy in 24% of all study patients normal gastric mucosa was found and this percentage was identical in both groups. In the other patients primarily 1 degree changes dominated and 2 degree changes were also found (no 3 degree changes were found). Changes in the distal parts of the stomach (antrum and pylorus) were found twice as often. Both groups did not significantly differ in gastrofiberoscopy in any part of stomach topography during the first as well as control gastrofiberoscopy, no significant changes were found on gastrofiberoscopy in macroscopic dynamic change of the gastric mucosa. On histopathology chronic inflammation of the gastric mucosa was found in all topographic sites in all patients. Similarly to gastrofiberoscopy histologically both groups were dominated by first and second degree lesions which were assessed using the following parameters: intensity of inflammation, activity, atrophy and intestinal metaplasia. In both groups significant changes in the average degree of corpus gastric mucosa inflammation were not found. In the group of patients with acute alcohol poisoning a significantly higher degree of antral and pyloric gastric mucosa inflammation intensity and of inflammatory activity of the gastric mucosa of the corpus and pylorus as compared to the withdrawal syndrome group was found. No significant differences were found between groups in the average level of gastric mucosa atrophic changes in each particular topographic site, however the average level of intestinal metaplasia was significantly higher in the gastric mucosa of the corpus in the group of patients with acute alcohol poisoning. In follow up gastrofiberoscopy after controlled abstinence the group differences in the degree of antral gastric mucosa inflammation decreased due to the fact that in the withdrawal syndrome group the indicator of average gastric mucosa inflammation increased in control gastrofiberoscopy. An opposite interaction was found in the pyloric gastric mucosa where the average indicator of pyloric inflammation in the withdrawal syndrome group significantly decreased in comparison the group of acute alcohol poisoning patients. In the case of analysis of the indicator of mean inflammatory activity a significant interaction was observed only in the corpus gastric mucosa. In the group with withdrawal syndrome the inflammatory activity of the gastric corpus mucosa decreased over time while in the acute alcohol poisoning group this activity rose over time. Also significant changes were between groups were found in atrophic lesion dynamics and metaplastic lesions of the gastric corpus and pyloric gastric mucosa. In the acute alcohol poisoning group atrophic lesions of the pyloric gastric mucosa increased over time while in the withdrawal syndrome group these lesions decreased over time. In the case of the pylorus in both groups a significant decrease in the indicator of gastric mucosal atrophy over this time was found. In the case of intestinal metaplasia a significant decrease in the indicator of average

Level of degree:

2 - studia doktoranckie

Degree discipline:

choroby układu trawiennego ; toksykologia

Degree grantor:

Wydział Lekarski


Janusz Pach

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tylko w bibliotece

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Biblioteka Medyczna Uniwersytetu Jagiellońskiego - Collegium Medicum

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Last modified:

May 13, 2019

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Nov 21, 2012

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Edition name Date
ZB-99773 May 13, 2019


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