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UTC: 616.009/33/34-002.44
VEGETATIVE DYSTONIA SYNDROME AS ETIOLOGY ULCER
DISEASE
(LITERATURE REVIEW)
Kadirov Bekhruzbek Saidovich
Bukhara State Medical Institute, Department of Faculty and
Hospital Therapy, Uzbekistan, Bukhara, Gijduvan 23
e-mail: kadirov.bexruzbek@bsmi.uz
ORCID ID 0009-0009-1552-6367
Resume.
The article discusses the nosology of gastric ulcer and duodenal ulcer,
pathogenetic mechanisms of their occurrence, pathomechanisms of their connection
with the syndrome of vegetative dystonia, the main cause of which is the endogenous
factor of the disease development - dysfunction of the autonomic nervous system. The
main causative agent of the disease, Helicobacter pylori, was not left without
attention..
Keywords:
gastric ulcer and duodenal ulcer, autonomic nervous system,
autonomic dystonia syndrome, helicobacter pylori, vagotonia.
Gastric ulcer disease (GUD) and duodenal ulcer disease (DUD) are chronic
polyetiological recurrent diseases, which are associated with complex changes in the
nervous,
hypothalamic-pituitary,
hypothalamic-pituitary-adrenal
and
local
gastroduodenal processes, leading to changes in trophic processes in the mucous
membrane of the stomach and duodenum. In turn, the resulting ulcer defect is a source
of interoreceptor stimulation, which supports the disruption of neuro-hormonal
control. Thus, the resulting "vicious circle" leads to the chronic course of gastric ulcer
[15].
One of the ideas about changes in the mucous membrane of the stomach and
duodenum in pathophysiology is based on the doctrine of the role of the nervous
system in the regulation of metabolic and trophic processes, which ensure the
structural integrity and physiological (functional) state of cells, tissues and organs [6].
The emergence of this view was based on the concept of I.P. Pavlov "on the trophic
function of the nervous system", the teachings of L.A. Orbeli "On the adaptive-trophic
role of the sympathetic nervous system" [10]. and P.K. Anokhin's studies "on
functional systems" [15].
The role of the hypothalamus, hypothalamus-pituitary-adrenal system in the
pathogenesis of gastric and duodenal ulcers has been studied by a number of scientists
[6]. Therefore, many scientists believe that the hypothalamus-pituitary-adrenal
system plays an important role in the development of dysregulation of the stomach
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Volume-39_Issue-1_May-2025
368
and duodenum and the appearance of dystrophic lesions, but in our opinion, the
mechanisms of such effects have not been fully explored.
In the pathogenesis of peptic ulcer disease, the syndrome of vegetative dystonia
always occurs with an increase in the parasympathetic system [12]. Increased activity
of the gastric mucosa, accompanied by hypersecretion, leads to hyperplasia of the
gastric glands and simultaneous disruption of trophic activity, as a result of which the
mechanism of development of peptic ulcer disease is based not only on an increase in
the tone of the parasympathetic nervous system, but also on a decrease in the
sympathetic nervous system [11]. When assessing the nature of autonomic tone
changes in patients with peptic ulcer disease, relying on autonomic indicators,
electrocoagulogram, gastric secretion data, and electrogastrogram (EGG) data gave
conflicting results [12]. According to the Curdo index, vagotonia was often detected
in patients with DUD, and according to the minute volume index, sympathotonia was
detected. Both of these tests are common in patients with peptic ulcer disease. In
DUD, vagotonia was detected by this examination. At the same time, EGG and
electrocoagulogram data showed the importance of sympathetic influence.
It is known that the onset of an emotional state is mainly carried out through the
nervous system, that is, through nerve stimuli transmitted from the cerebral
hemispheres to the hypothalamus, reticular formation and limbic systems. The first
mediator responsible for this reaction is believed to be acetylcholine, and the
subsequent implementation of the stress response occurs through neurogenic and
hormonal pathways [5]. The sympathetic and parasympathetic subzones of the
reticular formation are located at different levels of the CNS [12]. Through each of
them, its own group of adaptive loops is closed, directed to a group of effector devices.
Each type of receptor has its own adaptive reflex loop. Reticular neurons capable of
autonomic activity are sources of a constant background signal in both parts of the
autonomic nervous system. Each lower zone of the reticular formation and its
microzones have effector loops aimed at activating their own group with a specific
spectrum of warning afferent signals. Based on this, it is advisable to assess not the
general vegetative tone, but its components in different organs [1].
The increase in acid-peptic activity is also influenced by the participation of
endocrine hormones from the parasympathetic nervous system (ACTH, cortisol,
thyroxine, insulin, etc.) and hormones of the gastrointestinal system (histamine,
gastrin, bombesin), as well as factors that physiologically activate "substance P" -
gastrin [2]. The aggressive action of the above hormones, as a rule, is manifested in a
decrease in hormonal activity, inhibition of gastric secretion. Such hormones include
somatostatin, glucagon, calcitonin, sex hormones, secretin, cholecystokinin,
urogastrone, serotonin, prostaglandins, as well as endogenous opioids, enkephalins
and endorphins.
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In 1983, the discovery of campylobacter pylori, now known as Helicobacter
pylori (HP), led to the development of a large-scale study of the infectious theory of
the etiology of peptic ulcer disease [7]. It is known that the presence of metaplasia in
the gastric field in the duodenum is a cellular marker for HP. According to research,
the formation of foci of gastric metaplasia in the duodenum occurs as a result of
prolonged damage to its mucous membrane with hydrochloric acid. Increased acid
production in the stomach and prolonged acidification of the duodenum lead to the
development of foci of gastric metaplasia in it, creating conditions for HP
colonization.
Despite the large number of theories and theories of the development of peptic
ulcer disease, there is no explanation for the origin of peptic ulcer disease in half of
HP-negative patients [4]. The possibility of Helicobacter pylori infection in peptic
ulcer disease can be diagnosed in no more than 2/3 of patients with duodenal ulcer,
and in 2/5 of all patients with gastric ulcer. Thus, the author concludes that there is no
data on the 100% bacterial infection of patients with gastric ulcer, HP infection acts
as a local factor that affects the mucosa from the outside and acts as an activating
factor of aggression. The authors of this article agree with this point of view, namely,
due to a decrease in local immunity and other variable factors in the gastroduodenal
system, HP is considered only a pathogenetic link [13].
Шу нарса аниқки, ошқозон-ичак тизимига Helicobacter pylori инвазияси
does not lead to ulcerative processes, and, for example, the presence of HP in a large
proportion of gastritis cases without gastric ulcer is reliable evidence that HP is not
an etiological factor in the development of gastric ulcer or duodenal ulcer. This is
confirmed by a number of studies [3]. Currently, there is no experimental model of
gastric ulceration by Helicobacter pylori introduction [9].
According to Soshina A.A. et al., gastric ulcer associated with Helicobacter
pylori occurs in 22.7% of patients, and OBJECTIVES - in 80.9% of patients.
Zhernakova N.I. [4] studied the clinic, pathogenesis and treatment of the disease in
elderly patients with gastric ulcer, and out of 178 patients, 147 were diagnosed with
gastric ulcer associated with Helicobacter pylori, and 31 patients did not have
infection. At the same time, the author noted that the infection increases during the
course of gastric ulcer. The leading indicators are ensuring a favorable course of the
disease by eliminating Helicobacter pylori and normalizing the neuroendocrine state.
According to our data [8], in patients with peptic ulcer disease, cortisol
concentration during the exacerbation period was higher than in patients in the control
group (p<0.05).
According to some literature data [3], the association of peptic ulcers with
Helicobacter pylori accounts for 70-80% of duodenal ulcers and 50-60% of gastric
ulcers. Therefore, we must understand that association does not imply causation.
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Currently, none of the theories of the pathogenesis of peptic ulcer disease covers
the diversity of functions involved and the changes that lead to their development
[12].
Ярали касаллик билан оғриган беморларнинг физиологик жараёнларини It
is urgent to study the complex in the context of various methods of treatment at
different stages of the disease. Therapy, the author continues [14], “Diagnosis and
treatment of diseases of the digestive system taking into account quality standards”
(Order of the Ministry of Health of the Russian Federation of April 17, 1998 No. 125)
from a modern point of view is considered to be able to really affect only the local
factors of ulcer pathogenesis - HP and peptic factor.
Conclusion.
Thus, we should consider the existence of very diverse mechanisms
of development of gastric and duodenal ulcers. Perhaps none of the listed mechanisms
plays an independent role in determining the formation and chronicity of gastric and
duodenal ulcers, and only their combination can determine the nosological form of
gastric and duodenal ulcers.
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2. KB Saidovich. Autonomic dystonia syndrome as one of the etiofactors in the
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