Hyperplastic gastritis: symptoms, treatment, diet, prognosis

Hyperplastic gastritis is a morphological species of chronic gastric disease, in which pathological changes in the gastric mucosa are caused by increased proliferative activity of its cells. This can lead to certain structural and functional disorders and is often accompanied by inflammation of the gastric mucosa.

[1], [2], [3]

Epidemiology

In clinical gastroenterology, hyperplastic gastritis is considered to be a very rare gastrointestinal pathology, to which - of the chronically occurring gastric diseases - there are about 3.7-4.8% of diagnosed cases.

For example, according to the Journal of Clinical Investigation, giant hypertrophic gastritis affects both children and adults; in adults, this rare form of the pathology of the gastric mucosa develops at the age of 30-60 years, and in men this condition is revealed in three to four times more often than in women.

But polypous hyperplastic gastritis, for so far unexplained reasons, much more often affects the mucous membrane of the stomach of 40-45-year-old women.

[4], [5], [6], [7], [8], [9]

Causes of the hyperplastic gastritis

If endoscopic examination of the stomach reveals areas of increased mitosis of cells of the mucous membrane lining its cavity, gastroenterologists can be diagnosed as hyperplastic gastritis.

It is precisely in the growth (hypertrophy) of the mucous membrane - due to the increase in the cells of the glandular epithelium and the change in the order of their location, as well as in the violation of the usual folded structure of the mucosa (allowing the inner surface of the healthy stomach to increase after ingestion) and is the key morphological feature of this type of lesion of the stomach. At the same time, thicker inactive (rigid) folds appear, which prevent normal peristalsis of the stomach. And in the elastin fiber containing a loose submucose (submucosal) layer of the surface of various parts of the stomach, hypertrophic nodes of different sizes (single or multiple) or polypoid formations are often found.

The process of digestion and the physiological functions of the stomach are extremely complex, and the specific causes of hyperplastic gastritis continue to be studied. The etiology of hyperplastic processes that persist in the stomach for a long time is associated with a number of factors:

• disorders of the general metabolism, negatively affecting the process of regeneration of the lining of the mucosa;
• presence of autoimmune pathologies (pernicious anemia);
• infection with cytomegalovirus and activation of the Helicobacter pylori bacterium;
• violation of neurohumoral and paracrine regulation of the production of mucoid secretions of mucosal mucosa and fundal glands of the stomach;
• peripheral eosinophilia of blood (due to parasitic diseases, for example, ascariasis, anisakidosis or lymphatic filariasis);
• genetically determined predisposition to polyposis of the stomach's base glands and adenomatous polyposis (due to mutations in the β-catenin and APC genes);
• autosomal dominant Zollinger-Ellison syndrome, in which there are mutations of the suppressor gene of the MEN1 tumor;
• various congenital abnormalities of the stomach and differentiation of its tissues (eg, Cronkheid-Canada syndrome ).

[10], [11], [12]

Risk factors

Experts call such risk factors for the development of hyperplastic gastritis, as eating disorders; allergy to certain foods; deficiency of essential vitamins; toxic effects of alcohol and carcinogenic compounds, severe renal failure and hyperglycemia. And in the treatment of hyperacid gastritis and gastroesophageal reflux disease with the help of potent drugs inhibiting the secretion of acid (omeprazole, pantoprazole, rabeprazole, etc.), the risk of activating the growth of polyps appearing in the zones of the main glands and foveal (gastric pits into which gland ducts emerge) . Probably, such a localization of the pathological process is due to the fact that the regeneration of the gastric mucosa during its damage occurs just due to the cells of the mucous membrane covering the areas of the gastric pits.

[13], [14]

Pathogenesis

Specialists also associate the pathogenesis of atrophic-hyperplastic gastritis of the body and antrum of the stomach in cases of prolonged use of the aforementioned inhibitors of the proton pump with the possibility of the development of nodular hyperplasia of neuroendocrine enterochromaffin-like cells (ECLS).

Almost 40% of cases of hyperplastic gastritis in a child has the form of lymphocytic gastritis with erosion and the presence of infiltrates of T-lymphocytes (CD4 and CD8 T cells) in the upper layer of the gastric mucosa. This pathology is detected with a greater frequency in children with gluten intolerance (celiac disease) or malabsorption syndrome.

The pathogenesis of hyperplastic gastritis is seen in an excess of epitheliocytes of the gastric mucosa secreting gastric mucus. Obviously, this is due to the increased production of the mitogenic TGF-α polypeptide (transforming growth factor alpha), the molecules of which bind to epidermal growth factor receptors (EGFR), stimulating cell division of the gastric mucosa and the production of mucin, while inhibiting the synthesis of acid by parietal cells.

[15], [16], [17], [18]

Symptoms of the hyperplastic gastritis

Symptoms of hyperplastic gastritis are nonspecific, vary greatly, but gastroenterologists include: heartburn, belching with a rotten taste, plaque on the back of the tongue, nausea, increased gas formation, pain in the epigastric region (aching, pressing or spastic), vomiting in the list of possible clinical manifestations of this pathology.

However, often the disease is latent, and the first signs for almost all types of hyperplastic gastritis are manifested by an unpleasant feeling of heaviness in the stomach that occurs soon after eating (especially if the food is fatty and acute, and the acidity level of gastric juice is increased).

So, with erosive-hyperplastic gastritis patients complain of stomach pains, which can become stronger when walking or bending the body. Some people have exacerbations of the disease in the spring with the appearance of impurities of blood (melena) in the stool. Also, blood can be in the vomit.

In most cases of giant hypertrophic gastritis, there is no symptomatology. But some patients may have pain in the pit, nausea with vomiting, diarrhea. There is also a decrease in appetite and body weight, hypoalbuminemia (low albumin in the blood plasma) and associated puffiness of the stomach tissues. Not excluded and gastric bleeding.

[19], [20], [21], [22]

Forms

A single classification of hyperplastic gastritis is not available at present, but gastroenterologists use the so-called Sydney system of gastritis classification (which was adopted by the participants of the 9th World Congress of Gastroenterology).

Experts emphasize that - regardless of localization, degree of severity and stage (exacerbation or remission) - this is a chronic hyperplastic gastritis. In the domestic gastroenterology, the following types of this pathology are distinguished:

• Focal hyperplastic gastritis or nodal endocrine-cell hyperplasia is the development of a basally located benign carcinoid gastric tumor (<1-1.5 cm in size) resulting from hyperplasia of endocrine enterochromaffin cells, the proliferation of which is stimulated by hypergastrinemia (an excess of the hormone gastrin). Most often, this pathology is observed in patients with chronic atrophic gastritis, vitamin B12 deficiency (pernicious anemia), as well as mutations of the suppressor gene of the MEN1 tumor (leading to multiple endocrine neoplasias).
• Diffuse hyperplastic gastritis is diagnosed in cases where the hypertrophic changes in the gastric mucosa of any etiology are of a multiple nature.
• Superficial hyperplastic gastritis is characterized by involvement in the pathological process of only the upper single-layer prismatic epithelium of the gastric mucosa.
• Polypous hyperplastic gastritis, which many specialists define as atrophic-hyperplastic, but officially it is called multifocal atrophic gastritis with focal hyperplasias. The appearance on the mucosa of the body walls of the stomach of multiple, consisting of cells of glandular tissue of polyps, is associated with infection with Helicobacter pylori infection, as well as hypochlorhydria and hypergastrinemia of autoimmune etiology. As a rule, pathology begins to manifest itself in adulthood; has both a focal and diffuse form.
• Erosive-hyperplastic gastritis or lymphocytic-erosive gastritis (which has already been mentioned above) differs not only in leukocyte infiltrates in the gastric mucosa and hypertrophies of its folds. Nodular formations and areas of chronic erosion of the mucosa can also be observed (especially in the foveal region of the cardial, fundal and pyloric glands). The level of acidity of gastric juice can be different.
• Hyperplastic granular gastritis (or granular) is attributed to focal mucosal hypertrophies when multiple 1-3 mm hemispherical outgrowths are formed on it, which causes the mucous membrane to swell and become bumpy. At the same time, the stiffness of her muscular plate, the submucosa, and also the folds of the mucosa and the muscular membrane of the stomach are noted. Typical localization is the antral department, the mucosa of which has a large amount of secretory cells producing additional mucosal secretions with a granular cytoplasm and the incorporation of mucous granules. According to clinical observations, this pathology is more often detected in middle-aged men.
• Hyperplastic reflux gastritis is accompanied by a throw into the stomach of the contents of the duodenum, causing the mucosal epithelium of the stomach to be damaged by the components that make up the duodenal secretion (in particular, bile acids).
• Antral hyperplastic gastritis or rigid antral gastritis manifests itself in the disturbance of the physiologically normal relief of the mucosa, up to the change in the direction of the folds, and also in the presence of polyposic lesions on their surface. Because of this, the main and lining cells of the fundal glands can be atrophied, which leads to achlorhydria (stopping the production of hydrochloric acid). In addition, the pyloric part of the stomach becomes deformed and the gastric peristalsis decreases.

Among the rare hereditary pathologies, there is a giant hypertrophic gastritis - chronic hypertrophic polyadenomatous gastritis or Menetrier's disease. It is characterized by hypertrophy of the mucous membrane in the gastric fossa and a significant increase in gastric folds, inadequate secretion of HCl and excessive production of protective gastric mucin. A low level of hydrochloric acid leads to an inability to digest proteins and absorb nutrients, causing diarrhea, weight loss, peripheral swelling of soft tissues. However, since inflammation is minimal or completely absent, in the medical literature, Menetries disease is classified as a form of hyperplastic gastropathy.

Finally, distinguish active hyperplastic gastritis, which has three degrees of leukocyte (neutrophilic) infiltration of focal mucosal hyperplasia. In fact, this is a chronic hyperplastic gastritis, in which the severity of the inflammatory process, determined by the histological examination of tissue samples, is ranked according to the scale of the penetration of polynucleated T cells into the structures of the gastric mucosa.

[23], [24], [25], [26], [27]

Complications and consequences

The most common consequences and complications of hyperplastic gastritis:

• changes in the structure of the gastric mucosa with atrophy of varying severity;
• damage and reduction of the number of parietal cells, decreased synthesis of acid and deterioration of the digestive functions of the stomach;
• atony and violation of gastric motility, leading to persistent dyspepsia and partial gastroparesis;
• hypoproteinemia (a drop in the level of whey protein);
• anemia;
• loss of body weight.

The launched hyperplastic granular gastritis threatens the development of gastric ulcer and even cancer. Giant hypertrophic gastritis leads to hypochlorhydria; experts note the ability to degenerate this form of pathology into a cancerous stomach tumor.

With focal hyperplasia of enterochromaffin-like cells, the mucosa can also develop carcinoma of the stomach. Polypous hyperplastic gastritis, according to some sources, is malignant in almost 20 cases out of a hundred.

[28], [29], [30], [31], [32]

Diagnostics of the hyperplastic gastritis

The main method on which the diagnosis of hyperplastic gastritis is based is endogastroscopy (endogastroduodenoscopy). Endoscopic instrumental diagnostics allows not only visualizing pathologically altered areas of the gastric mucosa, but also conducting a biopsy: take tissue particles for subsequent histochemical examination. Also use radiography, ultrasound of the stomach, electrogastrography.

There are laboratory tests for which such tests are taken as:

• clinical and biochemical blood test;
• blood test for eosinophils;
• IF-analysis of blood for the presence of Helicobacter pylori;
• gastric juice to determine the pH level;
• a blood test for cancer cancer cancer marker CA72-4;
• stool analysis.

[33], [34], [35]

Differential diagnosis

Differential diagnosis is carried out in order to distinguish all the mentioned types of hyperplasia of the gastric mucosa from other gastritis, gastroduodenal diseases and gastric oncology.

Treatment of the hyperplastic gastritis

To date, symptomatic treatment of hyperplastic gastritis, which takes into account the etiology of the disease, its variety and basic manifestations. And, of course, the level of acidity of gastric juice.

With a positive analysis on H. Pylori, a course of eradication of the bacterium is scheduled, including antibiotic-azalide Azithromycin (Sumamed) - three days in two capsules (1 g), as well as an antibacterial drug of the macrolide group Clarithromycin (Aziklar, Claricin) - for 14 days 500 mg twice a day. Among the side effects of these drugs are violations in the work of the stomach, gallbladder and intestines, headache, tachycardia, paresthesia, etc.

If pH <5-6, drugs are needed to reduce acid secretion: Ranitidine tablets (0.3 g once daily); Kvamatel (20 mg twice daily); Misoprostol (Saitotec) - three times a day for one tablet.

Protect the damaged mucous membrane from the action of gastric juice acid with agents containing bismuth sub-citrate (Ventrisol, Bismofal, De-Nol Sukralfa, etc.), as well as aluminum compounds (Gelusil, Compensane, Gastal, etc.). Help to relieve pain Bruskopan and Pirentsepin (Gastrotsepin, Gastril, Riabal). More details on dosage, contraindications and side effects of these medications - in the material Tablets from stomach ulcers and article - Tablets from abdominal pain

When mucous atrophy, doctors recommend taking vitamin P and B vitamins, especially cyanocobalamin (B12). To correct the condition associated with hypoproteinemia, Methionine can be used (within two to three weeks, 0.5-1.5 g three times a day).

Homeopathy in this pathology offers a multicomponent agent for parenteral and internal use (daily or every other day) - a solution in ampoules of Mucosa compositum.

Surgical treatment can be performed with expressed focal and polypous hyperplastic gastritis, as well as in cases of periodic gastric bleeding.

And how to conduct physiotherapeutic treatment, described in detail in the publication - Physiotherapy for chronic gastritis

The great therapeutic potential - as with most diseases of the digestive system - has a diet with hyperplastic gastritis of the stomach, read the article - Diet for gastritis

Alternative treatment

Alternative treatment for hyperplastic gastritis involves the treatment of herbs in the form of broths and water infusions, which are prepared from the tablespoon of vegetable raw materials for 200-250 ml of water.

Most often, phytotherapy recommends the use of: chamomile pharmacy (flowers), plantain large (leaves), calendula officinalis (flowers), crescent straight and thyme (grass).

Decoction of the roots of any two-leafed and derbennika acts as an enveloping agent (taken 50-60 ml three times a day). And infusion of willow-tea (kipreya), taken on a tablespoon 4 times a day, helps to remove inflammation of the stomach mucosa.

[36], [37]

Prevention

So far, prophylaxis concerns only the order and regularity of nutrition, which should be five-time and include slightly more protein products. Important enough vitamins (but in vegetables and fruits without coarse fiber) and water (no less than five glasses per day).

[38], [39], [40]

Forecast

The prognosis for patients diagnosed with hyperplastic gastritis depends on the type of the pathology: there is a threat of malignant degeneration of cells of polypoid formations and carcinoid gastric tumors, as well as hyperplastic granular gastritis.

[41], [42]