MANAGEMENT OF PATIENTS WITH ACUTE ABDOMINAL PAIN. MANAGEMENT OF PATIENTS WITH GASTROINTESTINAL BLEEDING

Chronic gastritis is defined as the presence of chronic mucosal inflammatory changes, and is characterized by violation of cellular regeneration processes leading to mucosal atrophy and intestinal metaplasia and disorders of his functions.

The epithelial changes may become dysplastic and constitute a backround for the development of carcinoma.

According to European consensensus – Maastriht 2000-2 chronic gastritis is excluded from the list of acidity – dependent diseases.

This underlines the importance of CG problem.

ETIOLOGIC FACTORS OF CHRONIC GASTRITIS

1. EXOGENOUS ( FAVORABLE ) FACTORS :

MALNUTRITION

DISORDERS OF CHEWING

SMOKING AND ALCOHOL ABUSE

CHEMICALS, used nonsteroidal anti-inflammatory drugs (NSAID)

2. ENDOGENOUS FACTORS :

HELICOBACTER PYROLI

GENETIC PREDISPOSITION

BILE REFLUX INTO STOMACH

AGE

OTHER DISEASES : DIABETES MELLITUS , HYPERTHYROIDISM , CROHN’S DISEASE , CHRONIC KIDNEY INSUFFICIENCY , ANEMIA

The diagonal line (\) shows the approximate division of the stomach into the two secretory regions: the oxyntic secretory area consisting of the fundus and the body, and the pyloric secretory area consisting of the pyloric antrum.

CLASSIFICATION OF CHRONIC GASTRITIS

ADOPTED AT THE 9^TH INTERNATIONAL CONGRESS OF GASTROENTEROLOGISTS

( SYDNEY 1990) , MODIFICATED IN HOUSTON IN 1994

1. CHRONIC NONATROPHIC ( CHRONIC HELICOBACTERIC GASTRITIS , CHRONIC ANTRIAL , TYPE «B») , WHICH REPRESENTS ALMOST 70 % OF ALL GASTRITS TYPES.

2. CHRONIC ATROPHIC GASTRITIS ( AUTOIMMUNE , DIFFUSE GASTRITIS OF STOMACH CORPUS , ASSOCIATED WITH PERNICIOUS ANEMIA , ATROPHIC , TYPE A ) , PRESENT IN 15 – 18 % CASES OF CHRONIC GASTRITIES ; CHRONIC MULTIFOCAL GASTRITIS.

3. SPECIAL FORMS OF CHRONIC GASTRITIS :

CHEMICAL ( REACTIVE CHRONIC GASTRITIS , WHICH OCCURS IN CASE OF BILE REFLUX

( ABOUT 15 % ) , AFTER NSAID THERAPY

( ABOUT 10 % ) ;

GRANULOMATOUS ( IN CASE OF CROHN’S DISEASE , SARKOIDOSIS , TUBERCULOSIS ) ;

EOZINOPHILIC ( IN CASE OF BRONCHIAL

ASTHMA , FOOD ALLERGY ) ;

LYMPHOCYTIC ( WITH MANIFESTED LYMPHOCYTIC INFILTRATION OF

EPITHELIUM ) ;

GIANT HYPERTROPHIC GASTRITIS

( MENETRIER’S DISEASE ) ;

RADIATION GASTRITIS

4. TOPOGRAPHY OF LESION

ANTRAL

FUNDAL

PANGASTRITIS

* ACUTE * CHRONIC

5. METAPLASIA OF MUCOUS MEMBRANE , INTESTINAL OR PYLORIC TYPE

INTERNATIONAL CLASSIFICATION OF DISEASES OF 10^TH REVISION

K 29.3 CHRONIC GASTRITIS

K 29.4 EROSIVE GASTRITIS

K 29.5 GIANT HYPERTROPHIC GASTRITIS

( MENETRIER’S DISEASE ) ;

Helicobacter gastritis is a primary infection of the stomach and is the most frequent cause of chronic gastritis. H pylori are gram-negative rods that have the ability to colonize and infect the stomach. The infection is usually acquired during childhood. Once the organism has been acquired, has passed through the mucous layer, and has become established at the luminal surface of the stomach, the intense inflammatory response of the underlying tissue develops.

The interaction of H pylori with the surface mucosa results in the increase of the inflammatory response leading to high levels of cytokines, particularly tumor necrosis factor-α (TNF- α) and numerous ILs (eg, IL-6, IL-8, IL-10), and may trigger the entire inflammatory process. Leukotriene levels are also quite elevated, especially leukotriene B4, which is cytotoxic to gastric epithelium. This inflammatory response leads to functional changes in the stomach. When inflammation affects the gastric corpus, parietal cells are inhibited, leading to reduced acid secretion. Continued inflammation results in loss of parietal cells, and the reduction of acid secretion becomes permanent.

People infected with H pylori strains that secrete the vacuolating toxin A (VacA) are more likely to develop peptic ulcers than people infected with strains that do not secrete this toxin. Strains that produce CagA protein (CagA) are associated with a greater risk of gastric carcinoma development and peptic ulcer.

H pylori – associated chronic gastritis progresses with the following 2 main topographic patterns that have different clinical consequences:

Antral predominant gastritis is characterized by inflammation and is mostly limited to the antrum. Individuals with peptic ulcers usually demonstrate this pattern of gastritis.

Multifocal atrophic gastritis is characterized by involvement of the corpus and gastric antrum with progressive development of gastric atrophy (loss of the gastric glands) and partial replacement of gastric glands by an intestinal-type epithelium (intestinal metaplasia). Individuals who develop gastric carcinoma and gastric ulcers usually demonstrate this pattern of gastritis.

Chemical or reactive gastritis is caused by gastric mucosa injury by bile reflux and pancreatic secretions into the stomach, but it can also be caused by exogenous substances, including NSAIDs, acetylsalicylic acid, chemotherapeutic agents, and alcohol. These chemicals cause epithelial damage, erosions, and ulcers that are followed by regenerative hyperplasia, histologically detectable as foveolar hyperplasia and damage to capillaries, with mucosal edema, hemorrhage, and proliferation of smooth muscle in the lamina propria.

In contrast to other chronic gastropathies, minimal inflammation of the gastric mucosa typically occurs in chemical gastropathy.

Infectious granulomatous gastritis. Granulomatous gastritis is a rare entity. Tuberculosis may affect the stomach and cause caseating granulomas. Fungi can also cause caseating granulomas and necrosis, a finding that is usually observed in patients who are immunosuppressed.

Chronic noninfectious granulomatous gastritis. Noninfectious diseases are the usual cause of gastric granulomas and include Crohn disease, sarcoidosis, and isolated granulomatous gastritis. Crohn disease demonstrates gastric involvement in approximately 33% of cases. Granulomas have also been described in association with gastric malignancies, including carcinoma and malignant lymphoma. Sarcoidlike granulomas may be observed in people who use cocaine, and foreign material is occasionally observed in the granuloma.

Autoimmune gastritis. This type of gastritis is associated with serum antiparietal and anti-intrinsic factor (IF) antibodies (secretory Ig A). The gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients may develop pernicious anemia.

Damages to gastric mucosa and parietal cells may occur when insufficient secretory Ig A persists. This leads to the damage factor Castle – gastromucoproteid, so as gastromoucoproteid is produced in the parietal cells. There is atrophy gastric mucosa and violation of cyanocobolomine absorption and B₁₂ development of – B₁₂deficiency anaemia.

Lymphocytic gastritis. This is a type of chronic gastritis with dense infiltration of the surface and foveolar epithelium by T lymphocytes, and associated chronic infiltrates are in the lamina propria. Because of similar histopathology relative to celiac disease, lymphocytic gastritis has been proposed to result from intraluminal antigens. High anti–H. pylori antibody titers have been found in patients with lymphocytic gastritis, and, in limited studies, the inflammation disappeared after H. pylori eradication. However, many patients with lymphocytic gastritis are serologically negative for H. pylori. A number of cases may develop secondary to intolerance of gluten and drugs such as ticlopidine.

Eosinophilic gastritis. Large numbers of eosinophils may be observed with parasitic infections such as those caused by Eustoma rotundatum and ascaridosis. Eosinophilic gastritis can be part of the spectrum of eosinophilic gastroenteritis. Although the gastric antrum is commonly affected, this condition can affect any segment of the GI tract and can be segmental. Patients frequently have peripheral blood eosinophilia. In some cases, especially in children, eosinophilic gastroenteritis can result from food allergy, usually to milk or soy protein. Eosinophilic gastroenteritis may also be found in some patients with connective tissue disorders, including scleroderma, polymyositis, and dermatomyositis.

Radiation gastritis. Small doses of radiation (up to 1500 R) cause reversible mucosal damage, whereas higher radiation doses cause irreversible damage with atrophy and ischemic-related ulceration. Reversible changes consist of degenerative changes in epithelial cells and nonspecific chronic inflammatory infiltrate in the lamina propria. Higher amounts of radiation cause permanent mucosal damage, with atrophy of fundic glands, mucosal erosions, and capillary hemorrhage. Associated submucosal endarteritis results in mucosal ischemia and secondary ulcer development.

SYMPTOMS

Nondescript epigastric distress, often aggravated by eating

Anorexia

Belch and heartburn after eating

Nausea, with or without vomiting

Significant bleeding is unusual except in hemorrhagic

gastritis

Hiccups

Abdominal indigestion

Vomiting blood or coffee-ground like material

Dark stools

Features of clinical symptoms at the definite types of gastritis

H pylori chronic gastritis, which usually is asymptomatic but may manifest as gastric pain or, rarely, with nausea, vomiting, anorexia, or significant weight loss. Symptoms may occur with the development of chronic H pylori gastritis complications, which include peptic ulcers, gastric adenocarcinoma, and MALT lymphoma.

Autoimmune gastritis: The clinical manifestations are primarily related to the deficiency in cobalamin, which is not adequately absorbed. Cobalamin deficiency affects the hematologic, gastrointestinal, and neurologic systems. Patients with pernicious anemia have an increased frequency of gastric polyps and gastric carcinoid.

Hematologic manifestations: The most significant manifestation is megaloblastic anemia, but, rarely, purpura due to thrombocytopenia may develop. Symptoms of anemia include weakness, light-headedness, vertigo and tinnitus, palpitations, angina, and symptoms of congestive failure.

Gastrointestinal manifestations: The lack of cobalamin is associated with megaloblastosis of the gastrointestinal tract epithelium. Patients sometimes report having a sore tongue. Anorexia with moderate weight loss that is occasionally associated with diarrhea may result from malabsorption associated with megaloblastic changes of the small intestinal epithelial cells.

Neurologic manifestations: These result from demyelination, followed by axonal degeneration and neuronal death. The affected sites include peripheral nerves, posterior and lateral columns of the spinal cord, and cerebrum. Signs and symptoms include numbness and paresthesias in the extremities, weakness, and ataxia.

Granulomatous gastritis: In multisystemic diseases, specific symptoms related to gastric involvement may be minor. Caseating granulomas secondary to tuberculosis may be found in the absence of lung disease in patients who are malnourished, immunosuppressed, or alcoholic. Gastric involvement in Crohn disease is almost invariably associated with intestinal disease, and intestinal manifestations predominate. Sarcoidosis of the stomach is usually associated with granulomatous inflammation in other locations, especially the lungs, hilar nodes, or salivary glands.

Lymphocytic gastritis: This type mostly affects middle-aged or elderly patients. It may be associated with chronic H pylori infection, gluten-sensitive enteropathy, and Ménétrier disease. It may represent a hypersensitivity reaction involving the gastric body. Lymphocytic gastritis has been described complicating MALT lymphoma and gastric carcinoma.

Eosinophilic gastritis: Some patients have underlying connective tissue disorders. Patients with predominant mucosal involvement may report nausea, vomiting, and abdominal pain related to the ingestion of specific foods. Many patients have a history of allergy, peripheral eosinophilia, asthma, eczema, or food sensitivity. Some patients respond to removal of these items from the diet, and they often respond to steroid treatment.

LabORATORY Studies AND DIAGNOSTIC TESTS:

The diagnosis of chronic gastritis can only be ascertained histologically. Therefore, histological assessment of endoscopic biopsies is essential. The identification of the underlying cause of chronic gastritis and the assessment of specific complications can require several laboratory tests.

Atrophic gastritis may be assessed by measuring serum levels of the pepsinogen I–to–pepsinogen II ratio. Pepsinogen I (PGA, PGI) and pepsinogen II (PGC, PGII) are synthesized and secreted by gastric chief cells. After secretion into the gastric lumen, they are converted into proteolytic active pepsins. The level of PGA in the serum decreases as loss of gastric chief cells during gastric atrophy occurs, resulting in a decreased PGI/PGII ratio. Gastric carcinoma occurs usually in association with severe atrophic gastritis. Measuring the levels of pepsinogen I and II and the pepsinogen I/II ratio in the serum is useful for screening atrophic gastritis and gastric cancer in regions with high incidence of these diseases.

Rapid urease test from gastric biopsy tissue

Urea breath test with radioactive carbon isotope (¹³C) or with radioactive carbon isotope (¹⁴C)

Diagnosis of autoimmune gastritis

Antiparietal and anti-IF antibodies in the serum

Achlorhydria, both basal and stimulated, and hypergastrinemia

Low serum cobalamin (vitamin B-12) levels (<100 pg/mL)

Possible abnormal result on Schilling test (can be corrected by IF)

Procedures:

Performing the upper GI endoscopy with sample multiple biopsies is essential to establish the gastritis diagnosis.

Videoendoscopic image chronic gastritis:

Gastritises can be classified based on the underlying etiologic agent and the histopathological pattern only at morphological research of biopsy of the mucous.

Histologic Findings:

H pylori–associated gastritis - H pylori organisms were found within the gastric mucous layer. Polymorphonuclear leukocytes infiltrate the lamina propria, glands, surface epithelium, and foveolar epithelium and forming small microabscesses.

Multiple organisms (brown) are visibly adherent to gastric surface epithelial cells.

Numerous plasma cells in the lamina propria.

Autoimmune atrophic gastritis - diffuse involvement of gastric corpus and fundus by chronic atrophic gastritis associated with little intestinal metaplasia.

Granulomatous gastritis - isolated granulomas in the mucosa and submucosa, inflammation may extend to the muscularis propria and fibrosis may be prominent.

Eosinophilic gastritis - the mucosa infiltration by numerous eosinophils, with occasional pit abscesses. Mucosal edema, congestion, and necrosis of epithelium surface with small erosions may be present.

Lymphocytic gastritis - the lamina propria and pit epithelium are infiltrated by large numbers of small mature T-cell lymphocytes. The diagnosis can be rendered when 30 or more lymphocytes per 100 cons ecutive epithelial cells are observed.

Chemical gastritis - mucosal edema, congestion, fibromuscular hyperplasia in the lamina propria, and pit or foveolar hyperplasia that may create a corkscrew pattern. The cellular proliferation is associated with reactive nuclear features and epithelial reduction of mucin.

Radiation gastritis - atrophy of fundic glands, mucosal erosions, and capillary hemorrhage and chronic inflammatory infiltrate in the lamina propria.

medical treatment

1. Antimicrobial activity against most H pylori strains - Amoxicillin (Amoxil, Trimox) 1000 mg PO bid, Clarithromycin (Biaxin) 500 mg PO bid, Metronidazole (Flagyl) 250 mg PO bid,

Omeprazole (Prilosec) 20 mg PO bid or (Rabeprazole 30 mg PO bid, Pantoprazole 40 mg PO bid, Esomeprazole (Nexium) 20-40 mg PO qd).

2. Drug Category: Bismuth compounds - Ranitidine bismuth citrate (Tritec) 400 mg PO bid; coadministered with clarithromycin (500 mg PO) and amoxicillin (1000 mg PO).

II.

In case of atrophic gastritis, either stimulating or replacement therapy is administered. Stimulating therapy includes metabolic drugs, replacement therapy includes gastric juice or acidin pepsin.

Further Outpatient Care:

If a patient was treated for H pylori infection, confirm eradication.

Evaluate eradication at least 4 weeks after the beginning of treatment.

The eradication may be assessed by noninvasive methods such as the urea breath test or stool antigen test.

Follow-up may be individualized depending on findings during endoscopy. For example, if dysplasia was found with endoscopy, increased surveillance would be necessary.

For patients with atrophic gastritis and/or dysplasia, a follow-up endoscopy is recommended after 6 months.

EFFICIENCY CRITERIA AND REQUIREMENTS FOR TREATMENT RESULTS

Absence of clinical symptoms (disappearance of pain syndrome, signs of gastric and intestinal dyspepsia), endoscopic and histological signs of inflammation activity, eradication of infectious agent (complete remission).

Table 1

Health center treatment of patients with chronic unatrophy, atrophy gastritis and special forms of chronic gastrities

Nosologic form

Frequency of inter-nist’s examination

Reviews by examination other specialists

Diagnostic inspections

Basic medical and health measures

Chronic unatrophy, atrophy gastritis, special forms of chronic gastrities.

2 times per year.

Dentist-oncologist according to necessity.

Clinical blood test, general urine test – 1-2 times per year, intragastric pH-metry, x-ray of G.I.T., gastroduodenoscopy with biopsy with it’s cytological and histological investigation for diagnose verification. Test conduction for НР finding (serological investigation of НР in blood, ureastic test, morphological investigation).

Diet, regimen, antirecidivation treatment – as necessary, healthcare resort treatment, preventive clinic, drug treatment.

Table 2

Disability examination of patients with chronic gastritis

Disease

Character of expert conclusion

Work recommendations

Antiindications to work conditions

Indications to work conditions

Chronic gastritis

In the period of exacerbation - temporary disability (as a rule 6-10 days). Out of period of exacerbation - capacity is not broken.

Work which hinders the observance of the dietary regimen.

Work which allows the observance of the dietary regimen.

PEPTIC ULCERS

(GASTRIC, DUODENUM)

Professional Motivation: Ulcers are serious social problem of modern medicine, because of high level of morbidity. Occurrence of ulcerous disease in adult population is very frequent. Most ulcers are found in the first part of the small intestine (duodenal ulcers) but they can be also formed in the stomach (gastric ulcers).

Ulcerous disease is chronic disease, which is characterized by formation of defect in the gastric and duodenal mucosa. Ulcerous disease is multietiologic disease.

FAVOURABLE FACTORS OF ULCER DISEASE :

1. AUTOSOMAL – DOMINANT GENETIC PREDISPOSITION

(INCREASED NUMBER OF PARIETAL CELLS, EXCESS OF GASTRIN SECRETION , INCREASED PEPSINOGEN 1 IN PLASMA , DEFICIENCY OF PEPSINOGEN 1 INHIBITOR , MUCOGLYCOPROTEINS , DISORDERS OF IgA SYNTHESIS , BLOOD GROUP 0 ( I ) ;

HELICOBACTER INFECTION

EXTERNAL ENVIRONMENT CONDITIONS

( STRESS , NUTRITION , BAD HABITS );

ACTION OF DRUGS ( NSAID THERAPY )

Basic pathogenic mechanism of ulcerous disease is an imbalance between factors of acid-peptic aggression elements of the stomach and and defensive factors. The aggressive link of ulcerogenesis includes: increasing the production of hydrochloric acid, pepsinogen and pepsin, presence of Helicobacter pylory in the gastric and duodenal mucosa, pelting of bilious acids in a stomach at duodenogastrum reflux. The aggressive factors conduce to violation of gastroduodenal peristalsis.

The defensive factors includes : mucus, bicarbonate secretion, mucosal blood flow, gastric mucosal barrier, cellular regeneration, level of prostaglandins.

aggression elements:

hydrochloric acid

pepsinogen and pepsin

Helicobacter pylory

bilious acids

defensive factors:

mucus

blood flow

gastric mucosal barrier

level of prostaglandins

In honour of American scientist this pathogenic mechanism was named by SHEYA (Sheya equilibrium).

Main FACTORS LEADING To PEPTIC ULCER ARE: Helicobacter pylory AND GENETIC PREDISPOSITION

FACTORS OF HELICOBACTER PYLORI VIRULENCE:

SCREW – LIKE FORM AND PRESENCE

OF ADAPTATIVE ENZYMES

TOXINS AND TOXIC ENZYMES

INHIBITION OF IMMUNE SYSTEM

STIMULATION OF INFLAMMATION

CONDITIONS OF HELICOBACTER PYLORI PERSISTENCE IN MUCOUS MEMBRANE OF THE STOMACH:

OPTIMAL LEVEL OF ACIDITY , pH : 3 – 6

PRESENCE OF UREA IN STOMACH

PRESENCE OF STOMACH EPITHELIUM

CLASSIFICATION OF ULCER DISEASE

ULCER LOCALIZATION

STOMACH ULCER

DUODENAL ULCER

ULCER OF STOMACH AND DUODENUM

GASTROJEJUNAL ULCER ( ULCER OF ANASTOMOSIS );

ETIOLOGY

HP – POSITIVE ULCER

HP – NEGATIVE ULCER

STAGE OF ULCERATION PROSSES

ACTIVE ( ACUTE , FRESH );

ULCERATION

ULCER STAGE

PERMANENT ABSENCE OF ULCERATION

LEVELS OF MORPHOLOGICAL CHANGES

LOCALIZATION AND ACTIVITY OF GASTRITIS AND DUODENITIS

PRESENCE AND STAGE OF MANIFESTED MUCOUS MEMBRANE ATROPHY

PRESENCE OF INTESTINAL METAPLASIA

PRESENCE OF EROSIONS AND POLYPS

PRESENCE OF GASTROESOPHAGEAL OR DUODENOGASTRIC REFLUX

COMPLICATIONS

HAEMORRHAGE

PERFORATION

PENETRATION

STENOSIS

MALIGNATION

The most common symptom of ulcer

PAIN:

Gnawing or burning pain in the abdomen between the breastbone and navel.

The duodenal ulcer pain is midepigastric in only 80 % of patients. About

15 % of patients have right upper quadrant pain, and 5 % have left upper

quadrant pain. In addition, about 25 % of duodenal ulcer patients have pain

that sometimes radiates into back, and up to 50 % have heartburn in

association with epigastric pain.

This pain usually occurs between meals and in early hours of the

morning. Symptoms that may suggest gastric ulcer are pain that occurs

within 30 minutes after eating and 2-3 hours after eating in duodenal ulcer.

Duodenal ulcer pain typically occurs at night, especially within the first few

hours of reclining. Duration of pain is from a several minutes to a several

hours and may be relieved by eating or taking antacids. Ulcer that lie in the

pyloric channel are subtype of gastric ulcer that are especially likely to

produce food-induced symptoms, including pain, nausea, and vomiting.

Fig. 17. This image shows localization of pain at the peptic ulcer: (1) duodenal ulcer

(2) gastric ulcer

gastric dyspepsia:

Nausea

Vomiting

Loss of appetite

Loss of weight

belch

heartburn

intestinal dyspepsia:

constipation

flatulence

PEPTIC ULCER Diagnostics

Most gastric and duodenal ulcers can be diagnosed by ordinary barium radiographic examinations. The patient drinks the solution, which coats the walls of upper digestive tract so that they may be examined under x- ray. Barium swallows are used to identify ulcers, and any abnormalities of the upper gastrointestinal tract such as tumors, hernias, pouches, strictures, and swallowing difficulties).

Endoscopy research with biopsy for discoveries H. pylori and malignancy.

Ulcer are seen as depressions with white or yellow bases surrounded by

normal gastric or duodenal mucosa, often with erythematous or edematous

edges. Endoscopic criteria distinguishing ulcer from erosions include the

appearance of depth and a size over 5 mm.

Videoendoscopic image a peptic ulcer:

Blood, breath, stomach tissue tests to detect the presence of H. pylori and

stool antigen testing for H. pylori.

Computer measurement of gastritic secretion

Blood tests

The body produces antibodies against H. pylori in an attempt to fight the bacteria. The blood tests such as enzyme-linked immunosorbent assays (ELISA) identify and measure H. pylori antibodies.

Breath tests

Breath tests measure carbon dioxide in exhaled breath. Patients are given the substance with carbon marked 13С or 14С to drink. The bacteria enzyme urease - break down urea (constant matter of the stomach) to amoniya and carbon dioxide

and carbon is absorbed into blood stream and lungs and exhaled in breath.

Tissue tests

Routine histologic analysis of biopsy samples is common and practical. This technique is helpful, because one can visualize the mucosa, permitting detection of histologic gastritis and lesions such as MALT-type lymphomas, which are tumors of lymphoid tissues. There are, however, clear drawbacks that should be considered. First, the organism may have a patchy distribution, especially at the base of the stomach, so more than two biopsy specimens are necessary for accurate results. Also, standard staining techniques (i.e., eosin staining) are usually unreliable for detection of H. pylori by microscopy. Tissue samples of the stomach have to be explored histologically. Histologycal visualizing of bacteria under the microscope. Culture involves special processing of the tissue and its observation for H. pylori organisms growth.

Adding to the impracticality of this method is that it requires endoscopy and diagnosis cannot be obtained until several days after the procedure.

Stool antigen testing for H. pylori. Trials have shown this test to be extremely accurate for initial diagnosis and for confirming cure of H. pylori infection after antibiotics. The test identifies bacterial antigens in stool with an immunoprecipitation assay. Its cost is highly competitive, and it may become the noninvasive diagnostic modality of choice if patients demonstrate willingness to provide stool (instead of breath) for diagnosis.

H. pylori testing must be done without confounding factors that may cause false-negative results. For determination of cure, testing should not be performed any earlier than 4 weeks after completion of the antibiotic regimen. Testing earlier than 4

weeks cannot distinguish between antibiotic-induced suppression of infection and true cure.

Diagnostic tests for Helicobacter pylori infections

Table 3

TEST	SENSITIVITY (%)	SPECIFICITY (%)
INVASIVE:
Histology	95	< 100⁶
Culture	-60	100
Biopsy urease test	90-95	98-100
NONINVASIVE:
Serology	95	95
Urea breath test	95-98	95-98
Stool antigen	95	95

PEPTIC ULCER COMPLICATIONS

Obstruction

Perforation

Penetration

Hemorrhage

Gastric outlet obstruction

The blockage usually occurs at the narrow part of the stomach (pyloric canal) or the upper part of the small intestine (duodenum). Duodenal ulcers give rise to this complication more often than gastric ulcers. Patients with gastric outlet obstruction usually complain of nausea, vomiting, and pain or fullness in the upper middle part of the abdomen. Laboratory findings may show anemia and potassium abnormalities, and X-ray typically shows large gastric shadow with air/fluid level. An upper GI series will show a marked delay in gastric emptying and large stomach. Endoscopy is the best test for evaluating gastric outlet obstruction.

Penetration of other organs

Often penetration can involve the pancreas, bile ducts, liver, and the small or large intestine. The pancreas is the most common site of penetration. The acute onset of associated complications, such as pancreatitis (inflammation of the pancreas), cholangitis (infection of the biliary tract), or diarrhea of undigested food, may indicate penetration. The diagnosis of penetration is made when atypical pain and clinical symptoms of damaged organ are present.

Perforation of the stomach or duodenal lining

Perforation occurs when duodenal or gastric contents spill into the abdominal cavity and contaminate the peritoneum. Initial symptoms of perforated duodenal or gastric ulcers include severe abdominal pain, worse in the upper middle portion of the abdomen, often accompanied by nausea and vomiting. Typically, the patient is acutely and severely ill. The finding of free air on the abdomen an X-ray examination.

Perforation is the contraindication for endoscopy, because the procedure may aggravate spillage of gastric contents or disrupt sealed perforation.

Hemorrhage

Bleeding is the most common complication of peptic ulcer disease. Symptoms of the bleeding are: absence of pain, vomiting by coffee-grounds, hammers.

Endoscopy is able to identify accurately bleeding source. The goal of endoscopic therapy is to "seal" blood vessel involved and stop bleeding (may be coagulation or injection therapy).

Peptic ulcer complication requires surgical treatment. The common types ulcers of surgery are vagotomy, pyloroplasty, and antrectomy.

Peptic Ulcers Treatment

Guidelines for the Management of Helicobacter pylori Infection - the Maastricht-3 2005

The European Helicobacter pylori Study Group (EHSG) was founded in 1987 to promote multi- disciplinary research into the pathogenesis of Helicobacter (H.) pylori. Since then, the EHSG has organised successful annual meetings and arranged task-forces on paediatric issues and clinical trials on H. pylori. Consensus meetings have convened on who, how and when to treat patients with H. pylori infection. The most active area of research is the link of H. pylori with gastric cancer, a major public health issue. The most recent consensus meeting held this year was divided into three panels:

• who to treat;

• how to diagnose and treat H. pylori; and

•prevention of gastric cancer by H. pylori eradication.

Chairpersons and selected experts were chosen to participate for each of these panels based on their contribution to the published literature. The chairpersons met to choose topics relevant to their panel. They developed statements that needed clarification and debate. The international faculty that attended reflected on the global problem of H. pylori infection. Each of the panelists were asked to review different topics and provide key references on these topics.

Who to Treat?

The starting point when considering who to treat is the previous guidelines published by the European Helicobacter Study Group in Maastricht 2000.

Dyspepsia.

The increasing awareness of H. pylori as a pathogen in developing countries has stimulated interest in a test-and-treat approach in these areas. A test-and-treat approach was recommended in adult patients below 45 years of age – the age cut-off may vary locally – presenting in primary care with persistent dyspepsia having excluded those with predominantly gastro- oesophageal reflux disease (GORD), non-steroidal anti-inflammatory drugs (NSAIDs) consumption or with alarm symptoms. This recommendation has been vindicated in more recent publications. The definition of low prevalence is a population with an infection rate of less than 20%.

The Cochrane Systematic Review stated that the test- and-treat principle was as effective but less expensive than endoscopy in patients not at risk of malignant disease and likely to be more effective than acid- suppressive therapy; longer term studies have confirmed this statement. The majority of patients with dyspepsia have a normal endoscopy and in the absence of predominant reflux symptoms, these patients are considered to have non-ulcer dyspepsia. The Cochrane Systematic Review confirmed that there is a small benefit of eradicating H. pylori in this context. Emperical anti-secretory treatment may be less costly if the infection rate is less than 20%.

Statements and Recommendations.

• H. pylori test-and-treat is an appropriate option for patients with non-investigated dyspepsia.
• H. pylori eradication is an appropriate option for patients infected with H. pylori and investigated non-ulcer dyspepsia.
• H. pylori test-and-treat is the strategy of choice in all (adult) patients with functional dyspepsia in high-prevalence populations.
• The effectiveness of H. pylori test-and-treat is low in populations with a low H. pylori prevalence. In this situation, the test-and-treat strategy or empirical acid suppression are appropriate options.

GORD.

The second area of controversy that was reviewed was the link between H. pylori and reflux oesophagitis. In previous guidelines, it was thought advisable to eradicate H. pylori when long-term anti- secretory treatment is necessary for the management of GORD. This recommendation was based on a report that such treatment may accelerate the progression of H. pylori-induced atrophic gastritis in the fundus of stomach. Oservational studies have suggested that H. pylori may protect against GORD, but the results could be due to bias or confounding factors.

In randomised controlled studies, the relapse rate in GORD symptoms was the same in the H. pylori- treated as the placebo-treated GORD patients (83% of both groups) and treatment of H. pylori did not affect the efficacy of proton pump inhibitors (PPIs). More recent studies fail to support the theory that H. pylori eradication leads to the development of erosive oesophagitis or worsening of symptoms in patients with pre-existing GORD.

Most H. pylori-positive GORD patients have a corpus-predominant gastritis, where treatment with a PPI eliminates gastric mucosal inflammation and induces regression of corpus glandular atrophy. H. pylori did not worsen reflux or lead to increased maintenance dose, which confirms the benefit of eradication of H. pylori in GORD patients.

Statements and Recommendations.

• H. pylori eradication does not cause GORD.

• Profound acid suppression affects the pattern and distribution of gastritis favouring corpus-dominant gastritis and may accelerate the process of loss of specialised glands leading to atrophic gastritis.
• H. pylori eradication halts the extension of atrophic gastritis and may lead to regression of atrophy. The effect on intestinal metaplasia is uncertain.
• There is a negative association between the prevalence of H. pylori and GORD in Asia, but the nature of this relationship is uncertain.
• H. pylori eradication does not affect the outcome of PPI therapy in patients with GORD in Western populations. Routine testing for H. pylori is not recommended in GORD; H. pylori testing should be considered in patients on long-term maintenance therapy with PPIs.
H. pylori and Non-steroidal Anti-inflammatory Drugs.

The relationship between H. pylori and NSAIDs is complex. Both account for nearly all peptic ulcers. They are independent factors for peptic ulcer and peptic ulcer bleeding. H. pylori eradication is insufficient to prevent recurrent ulcer bleeding in high-risk NSAID users. It does not enhance the healing of peptic ulcer in patients taking anti- secretory therapy who continue to take NSAIDs.

In one study among patients with H. pylori infection and a history of upper gastrointestinal (GI) bleeding who are taking low-dose aspirin, the eradication of H. pylori was equivalent to treatment with a PPI in preventing recurring bleeding.
However, PPI was superior to the eradication of H. pylori in preventing recurring bleeding in patients who are taking NSAIDs.
In a study from Hong Kong, H. pylori eradication reduced the risk of bleeding in H. pylori-positive patients or patients who had dyspepsia and a history of ulcer before beginning NSAID treatment. However, the eradication was insufficient to completely prevent NSAID ulcer disease. Clopidogrel is also associated with an increased risk of GI bleeding. The role of H. pylori in this situation has not been assessed. The combination of aspirin and clopidogrel merits further studies. These drugs have a synergistic beneficial effect on cerebral vascular disease. Among patients with a history of aspirin- induced ulcer bleeding whose ulcer had healed, aspirin and a PPI was superior to clopidogrel in the prevention of recurrent ulcer bleeding. Therefore, the current recommendation is that patients with GI intolerance to aspirin be given clopidogrel. However, this cannot be sustained.
An emerging topic was cyclooxygenase-2 (COX-2) inhibitor and H. pylori, but the recently published adverse events of these drugs has stopped all studies into this field.

Statements and Recommendations.

• H. pylori eradication is of value in chronic NSAIDs users but is insufficient to completely prevent NSAID-related ulcer disease.

• Patients who are naïve NSAIDs users should be tested for H. pylori and, if positive, receive eradication therapy to prevent peptic ulcer and/or bleeding.
• Patients who are long-term aspirin users who bleed should be tested for H. pylori and, if positive, receive eradication therapy.

• In patients on long-term NSAIDs and peptic ulcer and/or ulcer bleeding, PPI maintenance therapy is superior to H. pylori eradication in preventing ulcer recurrence and/or bleeding.

Table 4

Requirements for

Ideal therapy of H.pylori eradication

№	Requirements	Criteria
1.	The effectiveness of eradication	above 80 % of case
2.	Good tolerance	side effects in loss than 5 % patients
3.	Convenient drug-intake	twice a day

Table 5

Recommended indication for H. pylori eradication therapy

№	Strongly recommended indication for H. pylori eradication therapy	Pathology
1.	Necessarily	Peptic ulcer disease – active or not including complicated ulcer
2.	Necessarily	Mucosa-associated lymphoid tissue lymphoma (MALToma)
3.	Necessarily	Atrophic gastritis
4.	Necessarily	Post-gastric cancer resection
5.	Necessarily	Patients who are first-degree relatives of gastric cancer patients
6.	Necessarily	Patients’ wishes – after full consultation with their physician

Table 6

Eradication therapy according to Maastricht consensus

(3-2005)

First-line therapy (triple therapy)

Proton pump inhibitors

(PPI) bis in die (bid)

Amoxicillin 1000 мg

bid

Clarithromycin

500 мg

bid

PPI

bid

Metronidasole 500 мg

bis in die (bid)

Clarithromycin

500 мg

bid

Second – line therapy (quadriplex therapy):

PPI

bid

De Nol

120 мg qid

Metronidasole

500 мg tid

Tetracycline

500 мg qid

In most cases, anti-ulcer medications heal the ulcers quickly and effectively. Eradication of H. pylori prevents most ulcers from recurring. However, some people do not respond to medication or they develop complications. They may require surgical intervention.

The common types of surgery for ulcers are vagotomy, pyloroplasty, and antrectomy.

Vagotomy

In this surgery the vagus nerve, which transmits messages from the brain to the stomach, is cut. Interrupting these messages sent through the vagus nerve reduces acid secretion. However, there can be side effects. The surgery may also interfere with stomach emptying. The newest variation of this surgery involves cutting the only parts of the nerve that control the acid-secreting cells of the stomach. This avoids the parts of the nerve that influence stomach emptying.

Antrectomy

In this surgery, the lower part of the stomach (antrum) is removed. This section produces a hormone that stimulates the stomach to secrete digestive juices. Sometimes a surgeon may also remove an adjacent part of the stomach that secretes pepsin and acid. A vagotomy is usually done in conjunction with an antrectomy.

Pyloroplasty

This surgery enlarges the opening into the duodenum and small intestine (pylorus), which enables stomach contents to pass more freely out of the stomach. A vagotomy may also be performed along with a pyloroplasty.

EFFICIENCY CRITERIA AND REQUIREMENTS FOR TREATMENT RESULTS

1. Treatment of clinical and endoscopic displays of illness. Good antihelicobacter therapy of HP-positive ulcers (confirmed with negative tests on НР) promotes complete recovering in 80-85% cases, frequency of ulcer recidivations, as a rule, does not exceed 6%, frequency of complications 2-4%.

If ulcer cicatrized, but active gastroduodenіtis and infected H. pylori mucus is saved, it means absence of complete remission. Such patients need continuation of treatment, draw second line of therapy - quadrotherapy.

Table 7

Health center treatment of patients with peptic ulcer

Nosologic form	Frequency of internist’s examination	Reviews by examina-tion other specialitst	Diagnostic inspections	Basic medical and health measures
Ulcer disease heavy run.	4 times per year.	Surgeon 1-2 times per year, dentist 2 times per year.	Clinical blood test 2 times per year, general urine test, excrement on the hidden blood, research of gastric content, stomach X-ray investigation(gastroduodenofibroscopy) – according to necessity.	Diet, regimen, antirecidivation treatment - 2 times per year, preventive clinic, employment – according to indications, stationary treatment in the period of exacebation-, healthcare resort treatment – according to indications.
Ulcer disease, middle-heavy run.	2 times per year	Surgeon – according to indicati-ons, dentist –once a year.	Clinical blood test 2 times per year, general urine test, excrement on the hidden blood, research of gastric content, stomach X-ray investigation gastroduodenofibroscopy – according to necessity.	Diet, regimen, antirecidivation treatment - 2 times per year, healthcare resort treatment, preventive clinic, employment.
Ulcer disease, light run.	once a year.	Dentist once a year.	Clinical blood test 2 times per year, general urine test, excrement on the hidden blood, research of gastric content, stomach x-ray investigation gastroduodenofibroscopy – according to necessity.	Diet, regimen, antirecidivation treatment - 2 times per year, healthcare resort treatment, preventive clinic, employment.

P.S. If active ulcer was found primary –examis ination doone once a month during a year.

Table 8

Disability examination of patients with ulcer disease

Disease	Character of expert conclusion	Work recommendations
Disease	Character of expert conclusion	Antiindications to work conditions	Indications to work conditions
Ulcer disease, light run.	In the period of exacerbation temporary disability is observed during treatment. In the period of remission capacity for work is kept. Employment is according to recommendations of TCC. Rarely (considerable loss of qualification) – direction on MSEC (III group of disability).	The considerable or moderate physical exertion, protracted overheating of body, protracted forced position with tension of abdominal press muscles. Work, related to frequent bending, by pressure on the stomach region. Considerable nervously-emotional exertion. Impossibility of observance of the dietary regimen and conducting of antirecidivation treatment.	Facilitated physical work. Work which allows the observance of the dietary regimen, possibility of valuable night sleep, unconnected with business trips. Professions of administrative, economic, office and intellectual character of middle capacity.
Ulcer disease, middle-heavy run.	For all forms temporary (quite often is long lasting) disability on the period of treatment. At the infrequent recidivative bleeding and impossibility of operative treatment - employment (depending on qualification) makes TCC or MSEC (III or II group of disability).). At penetration employment makes TCC or MSEC (III group). At the expressed pain syndrome and uneffectiveness of therapy and impossibility of operation - stable loss of capacity (II group of disability). During a perforation depending on the volume of operation (sewing, resection), condition of a patient, subsequent run of disease - employment makes TCC or (at the decrease of qualification) through MSEC (III group). At perivisceritis - in the stage of remission, in absence of pain syndrome, workability is kept, at presence of it - partial or stable loss of workability (III,II group of disability). At complication by stenosis in the stage of compensation workability is kept. Employment is conducted on principles, that are characteristic for the uncomplicated ulcer disease in the stage of remission. At the subcompensated stenosis and impossibility of operation - stable loss of workability (II group of disability). In the stages of decompensation at impossibility of operative treatment - directions to MSEC (II, not rarely I group of disability).	Permanent and inconstant physical tension. Longlasted walking. Concussions and overheats of body. General and local vibration. Considerable neuro-psychical exertion. Forced position with tension of abdominal press muscles. Work in the set rhythm, which hinders observance of the dietary regimen.	Easy, small capacity of physical work. Work which needs insignificant emotional tension, makes mainly sitting, allows the observance of the dietary regimen, possibility of valuable night sleep. Professions of administrative, economic, office and intellectual character of middle capacity. On occasion - work in the specially created conditions.

Situation tasks with standard answers:

Task 1. Patient Т., 60 years old, complains of permanent dull pain in the epigastrium, belch with a rotten smell, the blowing of the abdomen after meals, absence of appetite, lost of 15 kg-weight during the last month , general weakness. Objectively: the patient is lean, the skin is of grey colour. During palpation pains in the epigastrium can be revealed. The liver and spleen are not enlarged. The intestine shows no peculiarities.

Gen. blood test: Er. 3,0 х 10^12, Нв 80 g/l, leuk. 6,0 х 10^9/l; SSE 72 mm/h. Previous diagnosis?

Standard answer: gastric cancer. Esophagogastroduodenoscopy with an aiming biopsy. X-ray examination of the gastrointestinal tract.

Task 2. Patient L., 30 years old, on admission to the clinic complained of "hungry pains" in the epigastrium, heartburn, belch with a sour smell, sometimes vomiting. Objectively: the skin is pail, the patient is lean, feels pains in the epigastrium, Mendel’s symptom is positive .

What disease can one suspect? What instrumental examination can be the most informative ?

Standard answer: ulcer of the duodenum in the phase of exacerbation. Esophagogastroduodenoscopy.

BIBLIOGRAPHY

1. Gastrointestinal pharmacology and therapeutics / edited by Gerald Friedman, Eudene D. Jacobdon, Richard W. McCallum; with 87 additional contrybtors,1996.-P.45-73

2. The Merck Manual of Diagnosis and Therapy /edited by Mark H., Beers, M. D., and Robert Berkow, M. D.,1999.- P. 250-256

3. Vergara V., Valve M., Gisbert J.P., Calvet X. Meta-analysis: Comparative efficacy of different proton pump inhibitors in triple therapy for Helicobacter pylori eradication // Aliment. Pharmacol. Ther. – 2003. – № 18. – P.647-654.

4. Singhal A.V., Sepulveda A.R. Helicobacter heilmannii gastritis: a case study with review of literature // Am. J. Surg. Pathol. –2005. – 29(11). – P.1537-1539.

5. Itoh T, Seno H, Kita T, Chiba T, Wakatsuki Y. The response to Helicobacter pylori differs between patients with gastric ulcer and duodenal ulcer // Scand. J. Gastroenterol. – 2005. – 40(6). – P. 641-647.