Hypertrophic gastritis: chronic, granular, erosive, antral

A key feature that allows of all types of inflammation of the gastric mucosa to release hypertrophic gastritis is the pathological proliferation of cells of the mucous epithelium, resulting in its excess thickness.

In this case, the thickening of the mucosa is accompanied by the formation of more pronounced but inactive creases and the formation of single or multiple cysts, polypoid nodes and epithelial-glandular tumors of the adenoma type.

It is clear that without an endoscopic examination or ultrasound of the stomach, no expert will reveal any morphological changes in the mucosa in this pathology.

[1], [2]

Epidemiology

As clinical practice shows, hypertrophic gastritis is diagnosed much less often than other types of gastric diseases.

According to experts from the American Society for Gastrointestinal Endoscopy, among patients with giant hypertrophic gastritis, there are many more middle-aged men.

45% of patients with chronic alcohol dependence have superficial hypertrophic gastritis.

According to some studies, hypertrophy of the mucosa is found in 44% of cases of H. Pylori-induced gastritis, and in 32% of patients with intestinal metaplasia in the antral part of the stomach.

Gastric polyps with this type of gastritis occur in 60% of patients, and this is predominantly women over 40 years of age. Up to 40% of patients have multiple polyps. In 6% of cases, they are found in endoscopic operations on the upper gastrointestinal tract. Hyperplastic polyps and adenomas occur more often in the presence of H. Pylori, and the polyposis of the underlying glands, as a rule, develops after the use of drugs of the proton pump inhibitor group.

[3], [4], [5], [6]

Causes of the hypertrophic gastritis

Chronic hypertrophic gastritis is associated with a fairly wide range of causes of infectious, parasitic and non-infectious nature.

Hypertrophy and inflammation of the mucosa are associated with its infection by the bacteria Helicobacter pylori, Haemophilus influenzae, Treponema pallidum; with a persistent Cytomegalovirus hominis virus. Mushroom infections are much less likely (Candida albicans, Candida lusitaniae, Histoplasma capsulatum, Cryptococcus neoformans). Also, the causes of the pathology can be covered in perennial invasion (Giardia lamblia, Ascaris, Anisakidae, Filariidae, Cryptosporidium), which eventually manifests itself as eosinophilic inflammation of the stomach and small intestine.

In many cases, the development of hypertrophic gastritis with multiple granulomas in the gastric mucosa is caused by the response of humoral immunity in such systemic autoimmune diseases as lupus, scleroderma, granulomatous enteritis.

It should be borne in mind the presence of a genetic predisposition to mutations of the gastrointestinal mucosa associated with certain mutations. In addition to  Zollinger-Ellison syndrome, hypertrophy of the folds of the gastric mucosa in the background of multiple polyps simulating malignant neoplasms is attributed to the syndrome of familial adenomatous polyposis. In 70% of cases, the true cause of this pathology is the mutation of the APC / C membrane protein gene (adenomatous polyposis coli) acting as a tumor suppressor. See also -  Polyposis of the stomach

Hypertrophic processes are susceptible to gastric mucosa in food allergies, celiac disease or glucose-galactose intolerance; with long-term treatment with non-steroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors (reducing the production of hydrochloric acid in the stomach), anti-cancer cytostatics (colchicine), iron preparations, corticosteroids.

Malignant neoplasms can also lead to an increase in the folds inside the stomach.

[7], [8], [9]

Risk factors

Risk factors predisposing to the appearance of hypertrophic gastritis include the negative consequences of malnutrition, smoking and alcohol abuse, and reduced immunity (especially in the elderly). This also includes frequent stresses, in which pathological changes in the interstitial membrane of the stomach begin because of an increase in the production of gastrin and hydrochloric acid due to the increase in the level of adrenaline and norepinephrine.

[10], [11]

Pathogenesis

The pathogenesis of increased proliferation of cells of the mucous epithelium, because of which it thickens and alters the relief of the stomach cavity, is not clearly defined in all cases. But, as gastroenterologists note, all studies connect it with the features of the structure of the mucosa and its functions.

Secretory exocrine cells of the superficial layer of the mucosal epithelium (producing an alkaline mucoid secret) have increased regenerative properties and quickly repair damaged areas. Below is its own plate (lamina propria mucosae) - a basal layer formed by fibroblasts with the inclusion of diffusely located micro nodules of lymphoid tissue.

The main cells of this tissue - B-lymphocytes, mononuclear phagocytes, plasmacytoid dendrites and mast cells - provide local protection of the stomach by secretion of antibodies (IgA), interferon (IFN-α, IFN-β and IFN-γ), histamine. Therefore, almost any pathogenic factor, disrupting the surface layer of the epithelium, acts on these cells, causing an inflammatory reaction.

The pathogenesis of gastritis with mucosal hypertrophy is explained by increased expression of transforming growth factor (TGF-α) and activation of its transmembrane receptors (EGFR), which leads to an expansion of the proliferation zone of secretory exocrine cells and acceleration of differentiation of basal fibroblasts with excessive mucus secretion and gastric acid deficiency.

In addition, with hypertrophic gastritis during gastroendoscopy, a significant increase in apoptotic epithelial cells and lymphocyte infiltrates in the basal layer - at the bottom of the pits (foveol) in the outlet of the gastric glands. It is these seals (often diagnosed as lymphocytic gastritis) that cause a thickening of the mucosal folds.

[12], [13]

Symptoms of the hypertrophic gastritis

From the pathological point of view, gastritis is defined as an inflammation of the gastric mucosa, but in the case of hypertrophic gastritis - with minimal pathological changes in the mucosa at the initial stage of the disease - clinical symptoms may be absent.

This type of gastritis is a chronic disease, and the first signs of thickening of the mucosa may be manifested by a feeling of severity and discomfort in the epigastric region, especially after eating (due to a slowing of digestive processes).

Further common symptoms are manifested by nausea, eructation, spontaneous vomiting, bouts of dull pain in the stomach, intestinal disorders (diarrhea, flatulence).

Appetite significantly worsens, so the patient grows thin and feels a general weakness accompanied by dizziness. And the appearance of swelling of the soft tissues of the extremities indicates a decrease in the protein content in the blood plasma (hypoalbuminemia or hypoproteinemia).

When erosion of the sites of the gastric mucosa or polyposis nodes in the stool, blood may appear, melena is possible.

By the way, about polyps, which in themselves are usually asymptomatic and many doctors are considered as a possible complication of the chronic form of an ordinary gastritis. In the case of ulceration of the polyp, symptoms may resemble a stomach ulcer, and large formations can become malignant.

[14], [15], [16],

Forms

Despite the presence of an international classification of gastritis, many types of this disease are defined in different ways. Moreover, gastritis is predominantly an inflammatory process, but this term is often used to refer to non-inflammation of the mucosa, but to describe its endoscopic characteristics. And this still causes considerable terminological confusion.

Specialists distinguish such types of hypertrophic gastritis as:

• Focal hypertrophic gastritis, which has a limited area of damage.
• Diffuse hypertrophic gastritis (common throughout much of the mucosa).
• Superficial hypertrophic gastritis with damage to the upper layer of the mucosal epithelium of the stomach.
• Hypertrophic antral gastritis is determined by its location in the antrum of the stomach. The primary detection may be thickening and consolidation of antral folds, as well as nodules in the upper layer of the mucosa, similar to polyps, erosion and changes in contours of low curvature.
• Polyposis hypertrophic gastritis (according to another version - multifocal atrophic). Usually, several hypertrophic oval polyps are present simultaneously; sometimes they ulcerate, which causes swelling surrounding it mucosa. Less common type of  polyposis of the stomach  (10% of cases) include adenomas, consisting of an anomalous columnar epithelium of the intestine; most often they are found in the antrum part of the stomach (which is closest to the duodenum).
• Hypertrophic granular gastritis is determined when there are single or multiple cystic formations protruding into the cavity of the stomach against the peritoneal mucosa and limiting its peristalsis and mobility of the folds.
• Erosive hypertrophic gastritis is characterized by the presence of lesions in the gastric mucosa in the form of ulceration (erosions), arising either from the effect of an increased concentration of hydrochloric acid, or from infection (H. Pylori), which causes an intense inflammatory response with neutrophilic leukocytosis.
• Atrophic hypertrophic gastritis arising in persistent infections and caused by circulating autoantibodies (IgG) against the microsomes of parietal cells producing hydrochloric acid and the Castle factor. The destruction of these cells leads to hypochlorhydria and a decrease in the activity of pepsin in gastric juice. Endoscopically revealed infiltrates of lymphocytes and plasma cells penetrating the entire thickness of the mucosa with a violation of the structure of the fundal glands and a reduction in their number.

Separate consideration requires a giant hypertrophic gastritis - an abnormal thickening of the gastric mucosa due to the resembling polyps of inflammatory cell clusters. This pathology is also called tumor-like or folded gastritis, adenopapillomatosis, polyadenoma creeping or Menetries disease. Among the prospective causes of its occurrence is an increased level of epidermal growth factor (EGF) produced by the salivary glands and glands of the pyloric stomach, and the activation of its gastrointestinal receptors.

To date, many gastroenterologists (primarily foreign) consider giant hypertrophic gastritis synonymous with Menetries disease. However, with Menetriet's disease, excessive growth of secretory cells leads to the formation of thickened folds, but very rarely accompanied by inflammation. On this basis, some experts classify this disease as a form of hyperplastic gastropathy, seeing in it the cause of giant hypertrophic gastritis.

[17], [18],

Complications and consequences

In addition to the perceived reduction in digestive functions of the stomach - chronic maldigestion - the consequences and complications of hypertrophic gastritis include:

• irreversible loss of a significant portion of the glandular tissue with  atrophy of the gastric mucosa;
• reduction of acid synthesis in the stomach (hypochlorhydria);
• slowing of gastric motility;
• an increase in the stomach (in 16% of patients) or a narrowing of its cavity (9%).

Hypoproteinemia with giant hypertrophic gastritis can lead to ascites. There is also a development of anemia associated with a lack of vitamin B12, which is impeded by the production of immunoglobulin G (IgG) against the internal factor of the Castle. It is not excluded the progression of pathology in malignant megaloblastic anemia.

Localized in the body or bottom of the stomach, atrophic hypertrophic gastritis causes physiological hypergastrinemia, which in turn stimulates proliferation into the submucosal layer of neuroendocrine enterochromaffin-like (ECL) cells of the fundal glands. And this is fraught with the development of neuroendocrine tumors -  carcinoids.

[19], [20], [21], [22], [23]

Diagnostics of the hypertrophic gastritis

Diagnosis of hyperplastic gastritis is possible only by visualizing the state of the gastric mucosa.

Therefore, instrumental diagnostics - using endogastroscopy and endoscopic ultrasonography - is the standard of the technique for detecting this pathology.

Blood tests are also needed - clinical, biochemical, H. Pylori, antibodies and oncology marker CA72-4. The feces are analyzed, the pH of the stomach is determined.

[24], [25], [26]

Differential diagnosis

Differential diagnosis (which may require CT and MRI) is performed to identify pathologies with the same symptomatology, and to identify - based on the result of a histological examination of the biopsy material - sarcoma, carcinoma, gastrointestinal stromal tumors.

Treatment of the hypertrophic gastritis

Treatment prescribed for hypertrophic gastritis takes into account the causes of pathology, the nature of structural changes in the mucosa, as well as the intensity of symptoms and concomitant diseases of patients.

If the analysis showed the presence of Helicobacter infection, then begin the triple therapy (for the destruction of the bacterium) with antibiotics Amoxicillin, Clarithromycin, etc., for more details read -  Antibiotics for gastritis

When pains in the stomach are traditionally assigned No-shpa or Besalol pills, but it dries out in the mouth and the pulse may become more frequent, moreover, this remedy is contraindicated for glaucoma and problems with the prostate gland. Drugs that reduce the production of hydrochloric acid (H2-histamine receptor blockers and m-cholinolytics), with this type of gastritis do not apply. For more details, see -  Pills from abdominal pain

To improve digestion, drugs based on pancreatic enzymes are used: Pancreatin (Pancreasim, Pancral, Pancitrat, Penzital, Pancreon, Creon, Festal, Mikrazim and other trade names). Dosage: one to two tablets three times a day (before meals). Possible side effects are dyspepsia, rashes on the skin and increased levels of uric acid in the blood and urine.

For more information, see  Treatment of Gravity in the Stomach.

When the protein content in the blood plasma decreases, Methionine is prescribed, which should be taken one tablet (500 mg) three times a day, the course of treatment - 14-21 days.

Patients with hypertrophic gastritis are prescribed vitamins B6, B9, B12, C and P.

With hypertrophic gastritis surgical treatment is necessary if there is a suspicion of oncology: a laparotomy with a biopsy and urgent histology is performed, after which the suspicious lesions are removed.

Physiotherapy treatment is described here -  Physiotherapy with chronic gastritis

Diet with hypertrophic gastritis is needed, and, taking into account the decrease in the production of hydrochloric acid in the stomach, it should not only help maintain the integrity of the epithelial layer of the gastric mucosa, but also normalize the digestion process. Therefore, the most suitable  diet for gastritis with low acidity

Alternative treatment

Alternative treatment of hypertrophic gastritis uses, mainly, herbal treatment. From the mixture of chamomile pharmacies, plantain leaves and peppermint, water extract is prepared; from flowers of calendula and immortelle sandy, watch three-leaved, gold-bearing, dill seed, roots of ayr marsh, sporicha and dandelion - broths (a glass of water is taken a tablespoon of grass). During the day, infusion or decoction is taken several sips about 30-40 minutes before meals. Detailed information in the material -  Herbs that increase appetite

[27], [28], [29], [30], [31], [32],

Prevention

Standard prevention includes compliance with hygiene rules and proper nutrition: in small portions up to five times a day, without fatty and fried, canned and semi-finished products and, of course, without alcoholic beverages.

Be sure to drink water (not carbonated) - at least a liter a day.

[33], [34], [35]

Forecast

Gastroenterologists emphasize that hypertrophic gastritis is a chronic disease, and its development can not be predicted, especially since there is a risk of serious complications - up to the transformation into oncology.

[36], [37], [38],