Attention!

In order to establish an accurate and individual treatment regimen is recommended to pass a comprehensive survey.

Self-medication can be dangerous for your health!

PATHOLOGICAL MANIFESTATIONS OF CHRONIC HELIKOBACTERIOSIS

Gastritis type B (bacterial gastritis caused by Helicobacter pylori infection)

Chronic gastritis (CG) of type B is a chronic inflammation of the gastric mucosa caused by the bacterial flora - Helicobacter pylori (HP). HP-infection develops from an inactive (coccoid) form that enters the body with food products that are contaminated with this form when it comes in contact with dirty hands (fecal-oral route of transmission), into an active (vegetative) form only on the stomach mucosa, causing later an acute, and then a chronic inflammation of the gastric mucosa.

HP-infection releases a large number of different toxins, and also produces an ammonia gas, due to the urease enzyme, which it needs to neutralize the hydrochloric acid of gastric juice and create a neutral zone around the bacterium.

HP-infection is able to penetrate inside the parietal cell as a natural way with prolonged stress, which lasts at least 3 months, and artificial - with the use of proton pump inhibitor drugs (PPI), and block the production of these cells by hydrochloric acid, which leads to a sharp decrease in the acidity of gastric juice. The decrease in acidity leads to a violation of digestion and leads in the future to a violation of the function of not only the stomach, but also other organs involved in the digestive process: pancreas, gall bladder, liver, intestine. Prolonged violation of the whole digestive system further leads to disruption of the functions of all organs and systems of the body.

Long-term presence of HP-infection in the parietal cell can lead to the formation of precancerous changes in the gastric mucosa, which is caused by the negative effect of toxins of HP-infection on the genome of the parietal cell and can contribute to oncological process. For this reason, HP-infection since 1994 refers to carcinogens of the 1st degree.

PRECURSIC CONDITIONS OF THE GASTRIC MUCOSA

Precancerous conditions of the gastric mucosa are:

  • atrophy;
  • intestinal metaplasia;
  • dysplasia of the gastric mucosa.

Atrophy of the gastric mucosa (in the medical literature - atrophic gastritis) - is a kind of chronic gastritis, manifested in the progressive pathological changes in the gastric mucosa and the death of the glands that produce gastric juice. In the formation of atrophic gastritis, the leading role is played by HP-infection (atrophic gastritis type B), which is capable of penetrating into the parietal cell.

Intestinal metaplasia is a disease in which the gastric epithelium is replaced by the intestinal epithelium. Intestinal metaplasia is a fairly common disease. Especially often it occurs in elderly people. In 100% of cases, this pathology is diagnosed in people suffering from atrophic gastritis and stomach cancer. In 80-100% of cases it accompanies a stomach ulcer, and in 47-54% - a duodenal ulcer. Often intestinal metaplasia is diagnosed in healthy people.

Dysplasia of the gastric mucosa means a change in the work and structure of the cells of the epithelium in the affected organ. This pathology, in which normal and healthy epithelial cells are mutate, and altered, unhealthy tissues are formed on their place. As for the dysplasia of the glands epithelium of such organ as the stomach, this pathological change provokes a strong decrease in its secretion, disrupts the functioning of all healthy cells and shortens their life span.

According to the latest views, there is a certain sequence of tissue changes before the cancer is formed: atrophy small-intestinal metaplasia (I and II types) and colonic metaplasia (type III) dysplasia of the gastric mucosa adenocarcinoma (cancer) of the stomach (cascade P. Correa, 1995).

 

Gastroduodenitis

Chronic gastroduodenitis (CGD) is an inflammation of the mucous membrane of the stomach and duodenum. It is a form of chronic gastritis, in which inflammation passes to the duodenum. Duodenitis (inflammation of the duodenal mucosa) is rarely an independent disease, the combination of a joint chronic gastritis and chronic duodenitis is 94.7% of cases.

 

Stomach ulcer and 12 duodenal ulcer

Ulcer disease (UD) is a chronic disease in which gastric mucosa produces trophic disorders (disorders associated with metabolism and tissue nutrition). The etiological factor in the overwhelming majority of cases is HP-infection.

According to generally accepted views, the disturbance of the balance between aggression factors (hydrochloric acid, HP-infection, etc.) and defense factors (isolation of bicarbonates, rapid regeneration of mucosal cells, etc.) is considered to be the basis for the pathogenesis of peptic ulcer, which leads to ulceration ("scales" Neck ). However, this interpretation of the formation of ulcers does not explain a number of features of this process: the specificity of the zones and the locality of the formation of ulcers, the course of the process of ulceration at any level of acidity.

In 2007 a new theory of ulcer formation has been put forward by Ukrainian scientists-pathophysiologists Avramenko A.A. and Gozhenko A.I. - the theory of "caustic alkali spittle" (another term for the theory is the theory of "ammonia-alkaline damage"), the essence of which is that the factor of the gastric mucosa damage is not the hydrochloric acid of gastric juice, but the ammonium hydroxide that forms at high humidity in the stomach cavity (up to 96%) from the "residual" ammonia, which was not realized to neutralize the hydrochloric acid around the bacteria. Concentrating in the outlet of the stomach and in the bulb of the duodenum, ammonium hydroxide, which is caustic alkali, causes damage known as ulcers in the outlet of the stomach and duodenum (pylorobulbar zone ulcers) (such ulcers are formed at any level of acidity). The concentration of ammonium hydroxide by a small curvature in the body of the stomach causes damage, known as mediogastric ulcers (such ulcers are formed with a low level of acidity).

 

CAUSES AFFECTING THE DEVELOPMENT OF CG type B, CGD AND UD

There are a number of factors that are mistaken for the reasons for the formation of CG type B, CGD and UD. In fact, these factors are a favorable background, on which Helicobacter pylori develops better and faster. These include:

  • hormonal disorder associated with the period of puberty and extinction of sexual function;
  • hormonal disorder associated with the period of women pregnancy;
  • stress;
  • smoking;
  • long-term use of certain drugs that affect the state of the gastric mucosa (aspirin, some antibiotics);
  • long-term use of drugs that affect the acidification of gastric juice (H2 blockers - histamine receptors, proton pump inhibitors (PPI);
  • malnutrition - addiction to acute, hot and rough food, excessive use of alcohol, irregular meals, dry food;
  • intestinal infections;
  • chronic infections in the oral cavity and pharynx (carious teeth, inflammation of the tonsils).

SYMPTOMS OF CG type B, CGD AND UD

The first attack can begin quite unexpectedly. Suddenly (more often on an empty stomach) there are sharp cramping pains in the upper abdomen, there is nausea with vomiting. The first attack is often treated as banal poisoning and if the seizures do not recur, then neither the examination nor the treatment is carried out.

The first pathological manifestations from the upper parts of the gastrointestinal tract very often appear in adolescence, when hormonal changes in the body weaken the immune system, which is a good background for the activation of the latent form of chronic gastritis of type B. Very often, the physiological activator of the latent form of gastritis of women is the period of pregnancy, when hormonal regulation of the organism also changes.

The strongest factor that influences the development of chronic Helicobacteriosis is the chronic stress that a person is so much exposed to in modern society. Chronic stress leads to a decrease in immunity and acidity level of gastric juice, which is an ideal background for the development of HP infection.

Symptoms of chronic gastritis, chronic gastroduodenitis and ulcer disease are similar. They are:

  • pain in the stomach area;
  • heartburn;
  • burp;
  • nausea, up to vomiting;
  • feeling of stomach overflow;
  • unpleasant taste in the mouth;
  • appetite loss or decrease;
  • diarrhea or constipation.

DIAGNOSIS OF CG type B, CGD AND UD

The diagnosis is made by a gastroenterologist after examining and conducting a series of studies according to the order No. 271 by the Health Ministry of Ukraine from June 13, 2005:

  • intragastric step-by-step pH-metry to determine the level of acidity.
  • esophagogastroduodenoscopy (EGD);
  • testing for HP infection in at least one way (but more reliably - double testing: urease test and microscopy of stained smears-prints from one biopsy specimen of the gastric mucosa, a biopsy is taken during EGDs from 4 topographic zones of the stomach: from the middle third of the antral department and middle third of the body of the stomach for large and small curvature);
  • confirmation of the presence of an acute or chronic form of gastritis (carried out only by carrying out histological examinations of biopsy specimens of the gastric mucosa taken during the EHDS (preferably from 4 topographic zones of the stomach).

Also, to confirm the presence of patients with chronic gastritis caused by HP-infection, can be used:

  • HELIC-test (breath test) in a new modification;
  • determination of the level of immunoglobulins G to Helicobacter pylori according to IEA (by blood);
  • stool-test (for antigens of HP-infection in feces).

To determine the presence of intracellular "depot" of HP-infection two patented methods are used:

  1. Comparative characteristics of the obtained data during urease test and microscopy of stained smears-prints from one biopsy specimen of the gastric mucosa (in the presence of "depot", the time of the positive reaction of the urease test lengthens).
  2. Determination of the level of natural killer (CD-16) in the blood.

(Patent for Utility Model No. 96 920 Ukraine, UA (2015.01) А61В 1/00 "Testing of intracellular "depots" of H. pylori infection in patients with chronic Helicobacter pylori infection by Avramenko A.A. method."/А.О. Авраменко. - u 2014 09563; Заявл. 01.09.2014; Опубл.25.02.2015.; Бюл. № 4. – 3 с.)

To conduct control studies to determine the quality of treatment after anti-Helicobacter therapy , there are methods are used only:

  • HELIC-test (breath test) in a new modification;
  • stool-test (by antigens of HP-infection in feces).

but not earlier than 1 month after the end of treatment.

In the presence of patients with intracellular "depot" of HP-infection, confirmed during the initial testing, the control is performed immediately after the treatment and 1 month after the end with the help of the HELIC-test (respiratory test) in a new modification (Application for utility model № u 2017 09728 "Testing of H. pylori infection in patients with chronic Helicobacter pylori infection using HELIC-test method", Вх. № 252962 від 05.10.2017 р.).

 

TREATMENT OF CG type B, CGD AND UD

Treatment of CG type B often comes down to patterns that impose to whole world by the Maastricht consensus of all four convocations and which obliges to use the PPI without considering the acidity and the state of the gastric mucosa, which could under certain conditions contributes to the rapid development of stomach cancer. Therefore, it is safer and more physiological to apply treatment regimens based on bismuth preparations and two antibiotics. According to the experience of the laboratory of chronic Helicobacteriosis and precancerous conditions, which based on the medical center "Rea+Med", a rapid effect of the reverse development of precancerous conditions (from dysplasia and metaplasia to atrophy, as well as from atrophy to normal mucosa) occurs when a combination of eradication schemes bismuth preparations and two antibiotics) with the use of ozone therapy (intravenous and drinking the ozonated water), which is confirmed by histological and microbiological studies in patients with chronic gastric of type B before and after treatment.

Treatment of chronic gastroduodenitis does not differ from the treatment of chronic gastritis.

Treatment of ulcer disease, like treatment of CG type B, is usually based on a template whith IPP using. PPIs give a quick healing effect to ulcers, which so appeals to supporters of these schemes. However, this healing effect is realized through the effect on the hormonal system, namely, the increase of the hormone gastrin, which, in addition to stimulating hydrochloric acid, promotes the acceleration of tissue growth. Such stimulation, however, can be dangerous, since in the presence of precancerous changes in the gastric mucosa, the growth and growth of cancer cells is stimulated, which, with a low level of immunity, promotes the rapid formation of stomach cancer. Therefore, it is safer and physiological to apply the regimens based on bismuth preparations and two antibiotics (Patent for invention № 115097 С2 Ukraine, UA, МПК A61К 33/24 (2006.01), A61К 35/39 (2015.01), A61К 31/195 (2006.01), A61К 31/192 (2006.01), A61К 31/4184 (2005.01), A61К 31/7016 (2006.01), A61К 33/06 (2006.01), A61К 35/74 (2015.01), A61К 36/28 (2006.01), A61Р 1/04 (2006.01), A61Р 31/04 (2006.01) «Treatment of manifestations of chronic helicobacteriosis - chronic gastritis type B and peptic ulcer by Avramenko A.A. method"/ А.О. Авраменко – а 2016 00648; Заявл. 27.01.2016; Опубл.11.09.2017; Бюл. № 17. – 7 с.).

 

Attention!

In order to establish an accurate and individual treatment regimen is recommended to pass a comprehensive survey.

Self-medication can be dangerous for your health!