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Гастроэнтерология (анг,рус)

H. PYLORI ERADICATION-antibiotic regimens  

'RCTs show that first-line therapy should include a proton pump inhibitor at standard dose (12-hourly), clarithromycin 500 mg 12-hourly, and amoxicillin 1 g 12-hourly or metronidazole 400 mg 12-hourly, for 7 days. In case of failure recommended second-line therapy is a proton pump inhibitor at standard dose (12-hourly), bismuth 120 mg 6-hourly, metronidazole 400 mg 12-hourly, and tetracycline 500 mg 6-hourly, for 7 days.'


General measures 

Cigarette smoking, aspirin and NSAIDs should be avoided. Alcohol in moderation is not harmful and no special dietary advice is required. 


Short-term management 


Drugs commonly used in peptic ulcers and other acid dyspeptic disorder


Short term



Drugs which inhibits acid secretion



150 mg 12-hourly or 300 mg at night

150 mg at night


Famotidine (Cvamatel)

20 mg 12-hourly or 40 mg at night

20 mg at night

Confusion, dry mouth, fever, constipation etc.

Proton pump inhibitors


20-40 mg once daily

20 mg at night

Hypergastrinaemia, diarrhoea


30 mg once daily

15 mg at night

Hypergastrinaemia, diarrhoea


40 mg once daily

Not recommended

Hypergastrinaemia, fever, headache, rashes


20 mg once daily

Not recommended

Hypergastrinaemia, fever, headache, rashes

Drugs which enhance mucosal defence and prokinetic agents


200 μg 6-hourly

200 μg 6-hourly

Abortificient, diarrhoea in up to 20%


2 g 12-hourly

Not recommended

Cramps, diarrhoea, redu-ce absorbtion of digoxin


10-20 mg 8-hourly

Not recommended

Hyperprolactinaemia, acute dystonia


Antacids. These are widely available for self-medication and are used for relief of minor dyspeptic symptoms. The majority are based on combinations of calcium, aluminium and magnesium salts, all of which have individual side-effects. Calcium compounds cause constipation, while magnesium-containing agents cause diarrhoea. Aluminium compounds block absorption of digoxin, tetracycline and dietary phosphates. Most have a high sodium content and can exacerbate congestive heart failure. 

Histamine H2-receptor antagonist drugs. These are competitive inhibitors of histamine at the H2-receptor on the parietal cell. Dyspeptic symptoms remit promptly, usually within days of starting treatment, and 80% of duodenal ulcers will heal after 4 weeks. These drugs do not inhibit acid secretion to the same degree as the proton pump inhibitors but are useful for the short-term management of acid dyspeptic symptoms prior to investigation. They are moderately effective for the management of reflux disease. They have a proven safety record and several can now be purchased in the UK without prescription. 

H+/K+ ATPase ('proton pump') inhibitors. These are substituted benzimidazole compounds that specifically and irreversibly inhibit the proton pump hydrogen/potassium ATPase in the parietal cell membrane. They are the most powerful inhibitors of gastric secretion yet discovered, with maximal inhibition occurring 3-6 hours after an oral dose. They have an excellent safety profile. After a few days of treatment virtual achlorhydria is achieved and rapid healing of both gastric and duodenal ulcers follows. Omeprazole and lansoprazole are important components of H. pylori eradication regimens. Proton pump inhibitors are also much more effective than H2-antagonists for healing and maintenance of reflux oesophagitis. 

Colloidal bismuth compounds. Colloidal bismuth subcitrate (CBS) is an ammoniacal suspension of a complex colloidal bismuth salt. It has little, if any, effect on gastric acid secretion and its ulcer-healing effect is probably due to a combination of activity against H. pylori and enhancement of mucosal defence mechanisms. 

Sucralfate. This is a basic aluminium salt of sucrose octasulphate. It has little effect on acid secretion but probably acts to protect the ulcer base from peptic activity in a number of ways. It binds to fibroblast growth factor and to the ulcer base, reducing the access of pepsin and acid. It may also enhance epithelial cell turnover. It should be taken 30-60 minutes before meals. 

Synthetic prostaglandin analogues (misoprostol). Prostaglandins exert complex effects on the gastroduodenal mucosa. In low doses they protect against injury induced by aspirin and NSAIDs by enhancing mucosal blood flow, and by stimulating mucus and bicarbonate secretion and epithelial cell proliferation. At high doses acid secretion is inhibited. Misoprostol is effective for the prevention and treatment of NSAID-induced ulcers, but in clinical practice proton pump inhibitors are preferred, since they are at least as effective and have fewer side-effects. 


Maintenance treatment 

Continuous maintenance treatment should not be necessary after successful H. pylori eradication. For the minority who require maintenance treatment the lowest effective dose should be used. 

Surgical treatment 

The cure of most peptic ulcers by H. pylori eradication therapy and the availability of safe, potent acid-suppressing drugs have made elective surgery for peptic ulcer disease a rare event. The indications are listed in Box 17.33. 

The operation of choice for a chronic non-healing gastric ulcer is partial gastrectomy, preferably with a Billroth I anastomosis, in which the ulcer itself and the ulcer-bearing area of the stomach are resected. The reason for this is to exclude an underlying cancer. Definitive anti-acid surgery in the form of vagotomy and drainage (pyloroplasty or gastroenterostomy) or highly selective vagotomy is no longer indicated for duodenal ulcer disease. In the emergency situation 'under-running' the ulcer for bleeding or 'oversewing' (patch repair) for perforation is all that is required. In the presence of giant duodenal ulcers partial gastrectomy using a 'Polya' or Billroth II reconstruction may be required.