Our data testifies that hypochlorhydria of gastric juice is prevalent in the examined patients, that results in
migration of Hp from pyloroantral part of stomach, where acidity is reduced due atrophic processes in mucosa,
to upper part of stomach (corpus and cardial part) where they find more appropriate conditions for their vital
activity. At the same time reduced gastric acidity favors to Candida development that worsens disbiotic processes
in the digestive tract.
DISCUSSION
The relevance of problem erosive-ulcerous lesions in upper part of digestive tract in patients with hepatocirrhosis
and portal hypertension in clinical practice is determined by a large number of publications over many years.
Stomach function and secretions are altered significantly in patients with cirrhosis, both with or without
portal hypertension motivation by the abnormalities of gastric acid and pepsin secretion, and gastrin release.
Histological and endoscopic changes, and the impaired cytoprotection associated with cirrhosis, are discussed in
the context of abnormal gastric secretion. In addition, the symptomatology and association of Hp, and treatment
of duodenal ulceration in cirrhosis are discussed [11].
The result of many early studies is the conclusion that additional studies are needed to further understand of
erosive-ulcerous lesions in upper part of digestive tract in patients with hepatocirrhosis and portal hypertension.
Early H.ꢀpylori eradication is associated with a lower risk of recurrent peptic ulcers in cirrhotic patients. H.ꢀpylori
eradication is the mainstay for treating cirrhotic patients who have contracted peptic ulcers [12].
So high frequency of helicobacteriosis in patients with HC and PH may be caused by various general and local
factors: total decrease of resistance to infection in patients with HC, disorders in blood circulation in portal
system, contributing to local decrease of resistance in mucosa of gastroduodenal zone. In turn Hp invasion
worsens all the processes described above, causing progressive mucosa atrophy and development of hypo- and
achlorhydria. It is also necessary to remember that various strains of Hp differ by their virulence, i.e. ability for
adhesion on GM and, probably, esophagus, and some other pathogenic features that allow Hp to affect tissues of
macroorganism up to development of bleeding and other complications. This is confirmed by the studies of Wen
et al. [13] H. pylori infection impairs the expressions and functional activities of duodenal mucosal bicarbonate
transport proteins, CFTR and SLC26A6, which contributes to the development of duodenal ulcer [13].
Due to unique mobility and some other factors, Hp and products of their metabolism may penetrate into
esophagus and manifest pathogenic properties, negatively influencing changed mucosa over EVVGD.
It would be wrong to ignore a question about biological properties of isolated strains of Hp as a possible
etiological agent of pathologic processes in mucosa of the gastroduodenal zone and esophagus in patient with HC
and PH, however such data were presented in study in our center. The results of the study indicated to the
presence of eubiotic drugs characterizing by significant antagonistic activity against Hp cultures, isolated from
patients with HC and PH. The author described a group of specific preparations, which can be used in the complex
treatment of such patients. Besides correction of intestinal dysbiosis, these preparations exert antagonistic action,
direct and indirect, on Hp, persisting in an organism.
Walton [14] in one of the recent issues learn about the virulence factors that have made Helicobacter pylori
such a successful pathogen in hepatocirrhosis, when it focuses on in vitro findings that may shed light on
epithelial-mesenchymal transition that occurs during the process of fibrosis [14].
Thus, Hp are frequently found in patients with HC and PH and worsen the course of the main disease,
contributing to the development of hemorrhages from EVVGD. Pathologic process in these patients lasts for a long
time, and they admitted to hospital with advanced cases with considerable atrophy of mucosa and respectively
essentially reduced secretory activity; but at the initial phases of the process these symptoms are manifested
weaker. Hp infection is much intensive, frequency of the presence of antibodies to Hp is higher than isolation of
Hp from stomach, i.e. due to the development of some negative for Hp conditions, microorganisms are eliminated
to some extent, but antibodies against Hp continue to circulate in patients’ blood.
CONCLUSIONS
1. Distinctive features of so-called “hepatogenous ulcers” are not only their specific localization and
quantitative presentation but also some definite morphologic properties: Multiple flat ulcers in pyloroantral part
covered with a thin layer of fibrinoid necrosis with a weak development of granulations and number of venous
vessels of various diameter in fibrous layer; 2. “Hepatogenous” erosive-ulcerous process in stomach of patients
To cite this paper: Ibadov RA, Devyatov AV, Babadjanov A.Kh, Baibekov IM, Irmatov S.Kh, Djumaniyazov DO, Strijkov NA. 2016. Some Morphometric and
Microbiological Aspects of Erosive-Ulcerous Lesions in Upper Part of Digestive Tract in Patients with Hepatocirrhosis and Portal Hypertension. J. Life Sci. Biomed.
6(4): 76-82.
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