How to treat Helicobacter pylori at home. Symptoms and treatment of the bacterium Helicobacter pylori (Helicobacter pylori) Helicobacter one plus, is it necessary to treat

You're lucky with your observations. Anything can happen. Agree. But in clinics, statistically, the situation is often close to the bearded joke, when one tablet was used to treat headaches and diarrhea. Breaking into two halves.
As for the seriousness of the basis on which I relied, judge for yourself -
1. Warren J.R., Marshall B.J. Unidentified curved bacilli on gastric
epithelium in active chronic gastritis. Lancet. 1983; 1: 1273-5.
2. Marshall B.J., Rouce H., Anner D.I. Original isolation of Campylobacter pyloridis from human gastric mucosa. Microbios Lett. 1984; 25: 803-10.
3. Warren J.R., Marshall B.J. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet. 1983; 1: 1311-5.
4. Sidorenko S.V. Trends in the spread of antibiotic resistance among gram-positive microorganisms and prospects for overcoming them. Clinical pharmacology and therapy. 2006; 15 (2): 7-13.
5. Baranskaya E.K. History of discovery Helicobacter pylori. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 1999; 4:61-5.
6. Graham D.Y. Campylobacter pylori and peptic ulcer disease. Gastroenterology. 1989; 96 (Suppl.): 615-25.
7. Goodwin C.S., Armstrong J.A., Marshall B.J. Campylobacter
pyloridis, gastritis, and peptic ulceration. J. Clin. Pathol. 1986; 39: 353-65.
8. Uemura N., Okamoto S., Yamamoto S. et al. Helicobacter pylori infection and the development of gastric cancer. N.Engl. J. Med. 2001; 345(1):784-9.
9. Zimmerman Ya.S. Helicobacter pylori infection: extragastric effects and diseases (critical analysis). Clinical medicine. 2006; 4: 63-7.
10. Domaradsky I.V., Isakov V.A., Tomaskauskas A.A. Extragastric effects of Helicobacter pylori: continuation of the infectious “renaissance”. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2000; 2 (Appendix 10): 16-22.
11. Current European concept in The management of Helicobacter pylori infection. The Maastricht Consensus Report. Gut. 1997; 41 (1): 8-13.
12. Isakov V.A., Domaradsky I.V. Helicobacteriosis. M.; 2003.
13. Achtman M. In: Achman M., Suerbaum S., eds. Helicobacter pylori: Molecular and cellular biology, ads. Wymondham, UK: Horison Scientific Press; 2001: 311, 321.
14. Goodwin C.S., Armstrong J.A., Chilvers T. et al. Transfer of Campylobacter pylori and Campylobacter mustelae to helicobacter gennov. as Helicobacter pylori comb. nov respectively. Int. J. Syst. Bacteriol. 1989: 39: 397-405.
15. Bower H. Sequencig of Helicobacter pylori will radically after research. Br. Med. J. 1997; 7105:383-6.
16. Khin M.M., Hua J.S., Ng H.C. et al. Agglutination of Helicobacter
pylori coccoids by lectins. World J. Gatroenterol. 2000; 6 (2): 202-9.
17. Karczewska E., Konturek J.E., Konturek P.C. Oral cavity as a potential source of gastric reinfection by Helicobacter pylori. Dig. Dis. Sci. 2002; 47: 978-86.
18. Sidorenko S.V. Diagnosis and treatment of infections caused by Helicobacter pylori. In the book: Infections in outpatient practice. M.; 2002: 125-40.
19. Atherton J.C. CagA, the cag pathogenecity island and Helicobacter pylori virulence. Gut. 1999; 44 (3): 307-8.
20. Blaser M.J. Role of vacA and cagA locus of Helicobacter pylori in human disease. Aliment. Pharmacol. Ther. 1996; 10: 73-7.
21. Yamaoka Y., Kodama T., Guitierroz O. et al. Relationship between Helicobacter pylori: IceA, CagA and VacA-status and clinical outcome: Studies in four different countries. J. Clin. Microbiol. 1999; 37 (7): 2274-9.
22. Blaser M.J. Ecology of Helicobacter pylori in the human stomach. J. Clin Invest. 1997; 100 (4): 759-62.
23. Kurilovich S.A., Reshetnikov O.V. Epidemiology of diseases of the digestive system in Western Siberia. Novosibirsk; 2000.
24. Axon A.T.R. Treatment of Helicobacter pylori: Future therapeutic and prophylactic perspectives. Gut. 1998; 43(Suppl. 1): 570-3.
25. Shcherbakov P.L. Epidemiology of Helicobacter pylori infection. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 1999; 2:8-11.
26. Blaser M.J. Helicobacter pylori: Balance and imbalance. Eur. J. Gastroenterol. Hepatol. 1998; 10:15-8.
27. Blaser M.J. Helicobacter pylori and gastric disease. Br. Med. J. 1998; 316:1507-10.
28. Maev I.V., Samsonov A.A. Modern standards of treatment of acid-related diseases associated with Helicobacter pylori. Consilium medicum. Appendix: Gastroenterology. 2006; 1 (Maastricht 3 Consensus Proceedings): 3-8.
29. Morris A., Nickolson J. Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric pH. Am. J. Gastroenterol. 1987; 82 (3): 192-9.
30. Aruin L.I. Helicobacter pylori: how one pathogen causes different diseases. Experimental and clinical gastroenterology. 2004; 1: 36-41.
31. Sipponen P. Peptic ulcer disease. In: Whitehead R., ed. Gastrointestinal and oesophageal phathology. London: Churchill Livingstone; 1995: 512-23.
32. Sipponen P. Chronic gastritis and ulcer risk. Scand. J. Gastroenterol. 1990; 22 (2): 105-7.
33. Goodwin C.S. Duodenal ulcer, Campylobacter pylori and the “Leaking roof” concept. Lancet. 1988; 2: 1467-9.
34. Danesh J. Helicobacter pylori infection and gastric cancer: Systematic review of the epidemiological studies. Aliment. Pharmacol. Ther. 1999; 13: 851-6.
35. Correa P. A human model of gastric cancerogenesis/ Cancer Res. 1988; 48: 3554-60.
36. Sipponen P., Seppala K. Gastritis - atrophic gastritis - intestinal metaplasia - gastric cancer: is this sequence reversible? Russian Journal of Gastroenterology, Hepatology, Coloproctology. 1999; 2:30-5.
37. Webb P. M., Lew M., Varghese C. et al. Gastric cancer and Helicobacter pylori: A combined analysis of 12 case control studies nested with in prospective cohorts. Gut. 2001; 49: 347-53.
38. Barthes F., Traulle C., Baillet J. Lumphones gastriques et Helicobacter pylori. MALT, tissue a risk. Competences medicales. 1997; 29:22-3.
39. Wotherspoon A. Gastric lumphoma of mucosa - associated lymphoid tissue and Helicobacter pylori. Ann. Rev. Med. 1998; 49: 289-99.
40. Malfertheiner P., Megaud F., O’Morain C. et al. Current concept in
the management of Helicobacter pylori infection. The Maastricht -
2 - 2000 Consensus report. Aliment. Pharmacol. Ther. 2002; 16:
167-80.
41. Malfertheiner P., Megaud F., O’Morain C. Guidelines for the
management of Helicobacter pylori infection business briefing. Eur.
Gastroenterol. Rev. 2005: 59-60; 998-9.
42. Loginov A.F. "Maastricht-3" is a modern tactic for diagnosing and treating Helicobacter pylori infection. Pharmateka. 2006; 12 (127): 46-8.
43. Zimmerman Ya.S. Evolution of strategies and tactics for the treatment of Helicobacter pylori-related diseases (based on the Maastricht Consensus-1-3: 1996-2005. Clin. Med. 2007; 8: 9-14.
44. Zimmerman Ya.S. Maastricht Consensus-4" (2011): main provisions and comments to them. Clinical medicine. 2012; 9: 28-34.
45. Marshall B.J., Armstrong J.A., Francis J.J. et al. Antibacterial action of bismuth in relation to Campylobacter pyloridis colonization
and gastritis. Digestion. 1987; 37 (Suppl.): 16-30.
46. Zimmerman Ya.S. Alternative eradication therapy regimens and ways to overcome Helicobacter pylori resistance to treatment. Clinical medicine. 2004; 2: 9-15.
47. Peitz U., Sulliga M., Wolle K. et al. High rate of posttherapeutic
resistance after failure of macrolide-nitroimidazole triple therapy to
cure-line therapies in randomized study. Aliment. Pharmacol. Ther.
2002; 16: 315-22.
8. Gisbert J.P., Gisbert J.L., Marcos S. et al. Third-line rescue therapy with levofloxacin is more effective that rifabutin rescue regimen
after 2 Helicobacter pylori treatment failures. Aliment. Pharmacol.
Ther. 2006; 24: 1469-74.
49. Blinkov I.L. The problem of Helicobacter pylori - myth or reality. Clinical medicine. 1997; 12:71-4.
50. Bukharin O.V. A constant tension of intellectual thought is required. Medical Bulletin. 2007; 31:4-5.
51. Blaser M.J. Hypothesis: The changing relationships of Helicobacter
pylori and humans: Implications for health and disease. J. Inflect.
Dis. 1999; 179(6):1523-30.
52. Menegatti M., Holton J., Figura N. et al. Antibodies to Helicobacter pylori of subjective healthy donors: Clinical meaning of them
presence of absence. Gastroenterol. Hepatol. Update/Abstract from
the Latest publ. 1999; 1:3-4.
53. Guo F. Helicobacter pylori infection: is there a relationship between the genotype of the microorganism and the presence of the disease? In the book: Diagnosis and treatment of diseases associated with Helicobacter pylori: II International Symposium. M.; 1999: 2-3.
54. Zimmerman Ya.S. Humans and Helicobacter pylori: concept of relationships. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 1998; 5 (App. 5): 64-5.
55. Zimmerman Ya.S., Zinnatullin M.R. The concept of the relationship between the human body and Helicobacter pylori. Clinical medicine. 1999; 2:52-6.
56. Blaser M.J. Cost of commensalism (state of the art lecture). In: 6th
United European Gastroenterology Week; 1997: Abstract on disk.
57. Zimmerman Ya.S. Chronic gastritis and peptic ulcer. Permian; 2000.
58. Vorobyov A.A. Preface. In the book: Chernin V.V., Chervinets V.M., Bondarenko V.M., Bazlov S.N. Peptic ulcer, chronic gastritis and esophagitis in the aspect of dysbiosis of the esophagogastroduodenal zone. Tver; 2004: 4-6.
59. Zimmerman Ya.S., Zakharova Yu.A., Vedernikov V.E. Microflora of the gastric mucosa, its properties and role in the development of acute and chronic gastritis. Clinical medicine. 2012: 11: 41-6.
60. Maucci G., di Battista R., Abbiati C. et al. Prevalence and risk
factors of Helicobacter pylori-negative peptic ulcer: A multicenter
study. J. Clin. Gastroenterol. 2000; 31:42-7.
61. Bytzer P., Taglbjaerd P.S. Helicobacter pylori-negative duodenal
ulcers: Prevalence clinical characteristics and prognosis: Results
from a randomized trial with 2-yers fallow-up. Am. J. Gastroenterol.
2001; 96: 1409-16.
62. Laine L., Hopkins R., Gerardi L. Has the impact of the United State
been overstated? - A meta-analysis of rigorously disignet trials.
Am. J. Gastroenterol. 1998; 93 (9): 1409-15.
63. Tytgat G.N.J. No Helicobacter pylori, no Helicobacter pylori associated peptic ulcer disease. Aliment. Pharmacol. Ther. 1995; 9
(Suppl. 1): 39-42.
64. Maev G.V., Samsonov A.A., Andreev N.G., Andreev D.N. Important practical results and current trends in the study of diseases of the stomach and duodenum. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2012; 4: 17-27.
65. Niemala S., Karttunen T., Kerola T. Helicobacter pylori-associated
gastritis: Evolution of histologic changes over 10 yers. Scand. J. Gastroenterol. 1995; 30: 542-9.
66. Thoreson A.C.-E., Nosseini N., Svannerhelm A.M., Bolin I. Different Helicobacter pylori strains colonize the antral and duodenal
ulcer patients. Helicobacter. 2000; 5: 69-78.
67. Zimmerman Ya.S. The concept of the pathogenesis of peptic ulcer disease (rationale). Clinical medicine. 1994; 4:65-7.
68. Sudakov K.V. Functional systems organism in dynamics pathological conditions. Clinical medicine. 1997; 10: 4-11.
69. Zimmerman Ya.S. Etiology, pathogenesis and treatment of peptic ulcer associated with Helicobacter pylori infection: state of the problem and prospects. Clinical medicine. 2006; 3:9-19.
70. Zimmerman Ya.S. The problem of etiology and pathogenesis of peptic ulcer: rereading V.Kh. Vasilenko. Clinical medicine. 2011; 1:14-9.
71. Zimmerman Ya.S. Peptic ulcer: current problems of etiology, pathogenesis, differentiated treatment / Clinical medicine. 2012; 8:11-8.
72. Aruin L.I. Helicobacter pylori in the etiology and pathogenesis of peptic ulcer. In the book: Materials of the 7th session of the Russian group for the study of Helicobacter pylori. N. Novgorod; 1998: 6-9.
73. Zimmerman Ya.S., Shchetkin D.I. Pirocetam in complex pathogenetic therapy of duodenal ulcer. Clinical medicine. 2002; 1:48-53.
74. Zimmerman Ya.S., Mikhaleva E.N. State immune system in patients peptic ulcer duodenum and the effect on it from modern therapy and immunomodulatory agents. Clinical medicine. 2002; 1:40-4.
75. Chernousov A.F., Bogopolsky P.M. Surgery peptic ulcer of the stomach and duodenum. Clinical medicine. 2000, 8: 88-90.
76. Baranskaya E.K. Peptic ulcer and Helicobacter pylori infection. Russian medical journal. 2002; 1:48-53.
77. Rollan A., Giancaspero R., Fuster F. et al. The long-term reinfection rate and the course of duodenal ulcer disease after eradication of
Helicobacter pylori in a developing country. Am. J. Gastroenterol.
2000; 95: 50-6.
78. Correa P. Human gastric cancerogenesis: A multistep and multifactorial process. Cancer Res. 1992; 52: 6735-40.
79. Hansen S., Melby K.K., Aase S. et al. Helicobacter pylori infection
and risk of cardia cancer and non-cardia gastric cancer. Scand. J.
Gastroenterol. 1999; 34: 353-60.
80. Burakov I.I. Results of long-term observation of patients with peptic ulcer associated with Helicobacter pylori after eradication of the microorganism. Experimental and clinical gastroenterology. 2002; 3:45-8.
81. Webb P.M., Law M., Varghese C. et al. Gastric cancer and Helicobacter pylori: A combined analysis of 12 case-control studies nested
with in prospective cohorts. Gut. 2001; 49: 347-53.
82. Zimmerman Ya.S. Helicobacter pylori infection and stomach cancer. Clinical medicine. 2004; 4: 9-15.
83. Zimmerman Ya.S. Stomach cancer: a modern view of the problem. Bulletin of surgical gastroenterology. 2011; 2: 77-88.
84. Roccas F. Helicobacter pylori infection as a risk factor for gastric cancer: current evidence. Russian Journal of Gastroenterology, Hepatology and Coloproctology. 2002; 3: 66-70.
85. Weston A.P., Bard A.S., Topolovski M. et al. Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett’s dysplasia and Barrett’s adenocarcinoma.
Cancer Res. 1998; 58: 388-90.

Therapy aimed at expelling a person infected with it from the stomach is not the easiest task that a doctor sets for himself.

This is due to the fact that pathogenic microorganisms are extremely reluctant to leave their favorite places of existence - the epithelial cells of the inner lining of the stomach or the submucosa, and drug-resistant strains are formed.

Therefore, the effect on the bacterium must be complex: medication, physiotherapy, nutrition, phytotherapeutic. The main point of application is drug therapy.

The expression “treat Helicobacter pylori infection” is not entirely correct from a medical point of view. Doctors treat diseases caused by this microorganism, but the bacterium itself should be gotten rid of.

The main direction in drug therapy is eradication - a method of destroying an infectious agent with the help of drugs.

In addition to eradication therapy, it is important to correct the impaired acidity of gastric juice, restore the motor and evacuation function of the gastrointestinal tract, stabilize enzymatic activity, and calm inflammatory processes.

All these functions are assigned to specific drugs, which, in combination with proper nutrition, give positive results. The main groups of drugs, medicines and tablets for Helicobacter pylori:

Antibacterial
Preparations of bismuth salts
Proton pump blockers
M-anticholinergics
H2-histamine receptor blockers
Antacids
Antispasmodics
Prokinetics

Most common dosage form drugs - tablets, antacids can be used in the form of suspensions, powders that require dissolution in water.

What antibiotics kill Helicobacter pylori

Antibacterial medicines– “heavy artillery”, forcing the bacterium to desert and leave the patient’s body.

The standards for the treatment of Helicobacter-associated gastric pathologies indicate at least two antibiotics. With significant contamination of the mucous membrane and pronounced clinical manifestations of the disease, it is impossible to do without them.

Amoxicillin
Clarithromycin
Tetracycline
Metronidazole
Rifambutin
Levofloxacin

Rifambutin and levofloxacin are “reserve” drugs; they are not included in standard treatment regimens, but can be used if pathogenic strains develop resistance to common drugs included in the protocols.

Antibacterial drugs have side effects: allergic reactions, dysbacteriosis, nausea. Patients are often afraid to drink antimicrobials exactly because of this reason.

If you are infected with Helicobacter and have gastric diseases, you should not do this. Taking antibiotics in this case is justified.

Without these medications, the patient risks earning money, and by refusing treatment, he exposes the body to the risk of developing cancer. gastrointestinal tract. Stomach cancer is 3-6 times more likely to occur in patients infected with H. pylori who have not received proper therapy.

How to treat Helicobacter pylori with antibiotics - eradication therapy regimens

Today, 3- and 4-component treatment regimens aimed at destroying the bacteria have been developed and are actively used.

If a patient has a microbe in the stomach, there are symptoms of gastrointestinal damage, and the person has not previously received treatment, therapy is always started with a three-component regimen, which includes:

Proton pump blocker (lansoprazole, rabeprazole, pantoprazole 20 mg) 2 times a day
Amoxicillin 1000 mg 2 times a day
Clarithromycin 500 mg 2 times a day

A 3-component regimen is prescribed when a patient first seeks treatment; elderly, debilitated patients can be individually adjusted to the dosage of medications.

Assign this therapy from 7 (minimum) to 14 days. Clinical studies have shown that in some cases, taking drugs for a week is not enough to ensure eradication, and therapy is ineffective.

After two weeks of taking the drugs, on the contrary, the effect of treatment was an order of magnitude higher: in a much larger number of patients, eradication of the pathogen reached 80% or more.

Four-component treatment regimen

If the effect of the 3-component regimen is not achieved, the destruction of the infectious agent has not occurred, the doctor will recommend continuing therapy after a month and a half, consisting of:

Proton pump blocker (omeprazole, lansoprazole, rabeprazole, pantoprazole 20 mg) 2 times a day
Preparations of bismuth salts 120 mg 4 times a day
Metronidachol 500 mg 3 times a day
Tetracycline 500 mg 4 times a day

This is a 4-component eradication scheme. It is important to ensure that previously used antibacterial drugs are not repeated. If resistance to the above antibiotics is detected, “reserve” medications can be prescribed: levofloxacin, rifambutin.

Despite the developed standards, the doctor, when conducting eradication, must approach each case and disease individually, taking into account the patient’s age, concomitant pathologies, possible allergic reactions organism and the resistance of specific bacterial strains to drugs.

How many days to take antibiotics for Helicobacter pylori

A 3-component regimen is prescribed by a doctor for a period of 7 to 14 days. It is not advisable to take the drugs for less than a week; there will be no effect from such treatment.

The bacterium is difficult to treat and develops resistance to drugs, so more and more evidence is emerging that even a week is not enough to achieve a positive result and get rid of the pathogen. More and more doctors are inclined to extend antibiotic therapy to 10-14 days.

The 4-component regimen is prescribed for a period of two weeks.

The effectiveness of treatment should be assessed through diagnostic and laboratory methods no earlier than 1-1.5 months from the end of taking the medications.

If eradication is 80% or more of the initial level, or no bacteria are found in the body at all, we can speak of success in the treatment of a disease associated with this pathogen.

More about drugs

Features of taking antibiotics for the treatment of Helicobacter pylori:

Clarithromycin

This is an antibacterial drug from the macrolide group. Included in the first-line treatment of Helicobacter pylori infection. It is successfully used in gastroenterology, it is able to inhibit the synthesis of the cell wall of Helicobacter pylori, and therefore prevent its reproduction. Acid-resistant, “works” effectively under normal and increased acidity, well absorbed.

Some strains of bacteria exhibit resistance to clarithromycin. In this case, the drug must be replaced with another one to achieve a better therapeutic effect.

Amoxicillin and metronidazole

Metronidazole or trichopolum is a drug that has a destructive or bactericidal effect on H. pylori. Its activity does not depend on the pH level in the stomach; the drug can be used in both hyper- and hypoacid conditions.

Today, resistance of many Helicobacter strains to metronidazole is very common. If the drug is prescribed together with de-nol, resistance to it develops more slowly.

Amoxicillin is a penicillin antibiotic that blocks the synthesis of microbial cell walls and is well absorbed by the gastric mucosa. More active in a neutral environment than in an acidic environment. Increasing pH to 4 increases 10 times pharmacological effect of this drug.

Metronidazole and amoxicillin are first-line drugs, but can also be prescribed in a 4-component treatment regimen.

Tetracycline

Another antimicrobial agent actively used in eradication helicobacter therapy pylori The mechanism of action of tetracycline is to inhibit microbial cell protein synthesis.

The medicine is well absorbed from the gastrointestinal tract. Eating dairy foods slows down its absorption.

Proton pump blockers

The most common representative of this group is. There are other very effective means: lansoprazole, pantoprozole, esomeprazole, rabeprazole).

Medicines suppress the production of hydrochloric acid. Thus, they influence the microbe indirectly: they do not destroy it, but create unfavorable conditions for existence, have a suppressive effect on the infection: they stop bacterial growth and development.

Omeprazole and other representatives of the group, by increasing the pH of gastric contents, contribute to better job antibacterial drugs, in particular amoxicillin.

There is evidence that proton pump inhibitors can block the bacterial enzyme urease.

Doctors recommend that after completing the course of treatment with antibiotics, continue taking omeprazole for up to 4-8 weeks. Patients who continue to take proton pump blockers have better mucosal healing processes and a higher percentage of bacterial destruction compared to patients who stopped taking omeprazole after the end of the eradication regimen.

Antacids and H2 receptor blockers

Most often, the acidity of gastric juice during infection with H. pylori is normal or increased.

In addition to omeprazole, which normalizes pH, antacid drugs (Almagel, phosphalugel, Hefal, Maalox, Rennie) and H2-histamine receptor blockers (famotidine, ranitidine) also have this effect.

The mechanism of action of antacids is to neutralize gastric acid. Active ingredients These preparations contain aluminum and magnesium hydroskides.

The products effectively eliminate clinical manifestations“acidism” – heartburn, sour belching. Take them 1-2 hours after meals and at night. Release form: suspensions, or powders, tablets.

You should not combine the use of antacids with antibacterial drugs or bismuth salts, since aluminum and magnesium hydroxides interfere with the absorption of other substances in the gastrointestinal tract.

New generation H2-histamine receptor blockers (famotidine, ranitidine) have virtually no side effects. Their mechanism of action: they inhibit the production of HCL and the production of pepsin, which causes a decrease in acidity. Prescribe tablets after breakfast and before bed.

Bismuth preparations

This group of drugs, in combination with antibiotics, has a bactericidal effect - it destroys both coccal strains and vegetative forms.

Bismuth salts have many effects that positive influence when conducting complex treatment diseases caused by Helicobacter:

Prevents pathogens from attaching to epithelial cells of the gastric mucosa
Disrupt microbial ATP synthesis
Block bacteria enzymes
Promote the destruction of the cell wall of the infectious agent
Increases the synthesis of protective immunoglobulins, prostaglandins of gastric secretions
Increases the secretion of bicarbonates and protective mucus
Reduce the absorption of antibiotics in the gastrointestinal tract, thereby increasing their concentration in the gastric contents
Provide a reparative, wound-healing effect of the internal gastric wall
Improves local blood circulation

Data pharmacological properties allowed the bismuth drug to occupy its niche in the treatment of helicobacteriosis in combination with two antibiotics. One of the most effective drugs This group is de-nol.

Does de-nol kill Helicobacter or not?

Only in combination with antimicrobial agents does de-nol have a bactericidal effect. If you take this drug separately as monotherapy, such treatment will not have the desired effect.

But in a combined treatment regimen, de-nol fully reveals its therapeutic effects, while simultaneously enhancing the properties of antibacterial drugs.

The combination “de-nol + 2 antibiotics” is extremely effective, and in the case of Helicobacter sensitivity, it allows the microbe to disappear if the tablets are taken for 10-14 days.

How much to drink de-nol for Helicobacter infection

The drug is prescribed 1 tablet 4 times a day for 30 minutes. before meals and at night for a period of at least 21 days, you can take the medicine for up to 8 weeks as recommended by your doctor. You should know that when the drug is prescribed, the stool turns black.

The tablets should be taken with a glass of boiled water, but not with milk, since dairy products reduce the pharmacological effect of the drug. Tablets cannot be combined with juices either.

Antacids slow down the absorption of de-nol, so you should not drink them together.

If side effects occur: diarrhea, nausea, allergic reactions, vomiting, you should stop taking the medication and consult a doctor.

0 65 954

Scientists have found that the bacterium Helicobacter pylori is the cause of many diseases: from gastritis to stomach cancer. However, Helicobacter does not provoke diseases in all people affected by it. And, according to various sources, these constitute from 50% to 70% of the planet’s population. We tell you in what cases it is necessary to fight the Helicobacter bacteria.

Scientists have found that the bacterium Helicobacter pylori is the root cause of many diseases of the gastrointestinal tract: from gastritis to stomach cancer. However, Helicobacter does not provoke diseases in all people affected by it. And, according to various sources, these constitute from 50% to 70% of the planet’s population.

The question arises: what to do with this “mine”? Treat before the bacteria has time to cause serious illness, or wait until they start pathological changes? Nobody wants to poison the body with antibiotics once again.

In what cases is it necessary to fight the Helicobacter bacteria?

Gastroenterologists around the world have already agreed that it is unwise to fight Helicobacter on the same scale as epidemiologists once fought smallpox. To completely eradicate this bacterium from the world, antibiotics will have to be prescribed to every second person.

As a result, as the medical community believes, “we will get a mountain of corpses from pseudomembranous colitis (acute inflammation of the colon associated with taking antibiotics), but we will not eradicate the harmful Helicobacter.” After all, all bacteria have the ability to mutate while fighting for survival.

Disputes about “to treat or not to treat”, “to detect or not to detect” have been raging for so long that the debate among the luminaries of medicine eventually took shape in the so-called Maastricht Consensus. These are the recommendations of doctors developed at a consultation on the fight against bacteria.

The first meeting of doctors took place in the city of Maastricht, hence the name of the set of recommendations based on laboratory research, which are updated regularly. To date, four consensus statements have been published.

Medical conclusions made in the light of the latest scientific knowledge about Helicobacter pylori:

Treatment is required for duodenal or gastric ulcers.
Antibacterial therapy is prescribed to the closest relatives of patients with stomach cancer.
Eradication is recommended for atrophic gastritis. It is this that is considered a precancerous disease, and not a stomach ulcer.
Treatment required if detected Iron-deficiency anemia. However, doctors will first need to find out whether the patient is losing iron or whether it is not absorbed due to bacteria.

Everything listed above applies to cases where the bacterium has already been identified. However, doctors are faced with another question: is it necessary to look for Helicobacter in all people? The answer that gastroenterologists most often give is: rather no than yes. Specialists also have a list of approximate candidates for analysis.

When to look for Helicobacter bacteria

Proton pump inhibitors - drugs that reduce the aggressiveness of gastric juice - do not help with stomach pain.
Along with fatigue, iron deficiency appears - the first sign of stomach cancer.
As part of the medical examination, even if there are no complaints of pain in the upper abdomen, you can do a gastroscopy and biopsy every 7 years to identify the bacteria.
The patient is at risk: his relatives had stomach cancer.
During the study, gastric dysplasia, intestinal metaplasia or atrophic gastritis were revealed.

Scheme of eradication (destruction) of Helicobacter pylori

1–2 weeks the patient receives comprehensive drug therapy: proton pump inhibitors, bismuth preparations, antibiotics. The doctor should also prescribe medications that will compensate for the deficiency of beneficial microorganisms in the stomach and intestines after taking antibiotics. Popular remedies: “De-Nol”, amoxicillin (“Flemoxin”); clarithromycin; azithromycin; tetracycline; Levofloxacin.
The patient is tested again. If the bacteria remains, after 5-6 weeks the doctor will again prescribe a course of treatment, but with different antibiotics.
If after the second stage of treatment the Helicobacter test is again positive, the treatment method is selected on an individual basis.

What foods should be excluded from the diet if the Helicobacter bacterium is detected.

IN modern world There are many different diseases. In this article I would like to talk about how Helicobacter can be treated: a treatment regimen and getting rid of this problem.

What it is?

At the very beginning, you need to understand the concepts that will be used in this article. What is Helicobacter pylori? spiral-shaped, which lives either in duodenum, or in the stomach. The danger of Helicobacter is that it can cause various diseases, such as gastritis, polyps, hepatitis, ulcers and even cancer. It is also worth saying that the majority of the inhabitants of our planet, approximately 60%, are infected with this microorganism. Scientists say that it is in second place in terms of prevalence after herpes infection. It can be contracted through contaminated food or water, as well as through contact with a sick person through sputum or even saliva, which can be released during coughing or sneezing.

Requirements

It is very important to also consider the schemes. So, it is worth saying that for therapy there are several simple but important requirements:

The main goal of therapy is to destroy (this is not always possible to do completely) these harmful bacteria.
We must try to eliminate side effects. If they occur, the drug can be changed.
It is very important that the treatment gives positive results within 7-14 days.

Important rules that imply the treatment of Helicobacter

The treatment regimen must meet very simple but very important rules. What not only every doctor, but also the patient should remember:

If the treatment regimen does not produce the desired effect on the patient, it is not worth repeating.
If the regimen is ineffective, it may mean that the bacteria has become immune to one of the components used in the therapy.
If no treatment regimen has a positive effect on a person, it is necessary to check the sensitivity of the disease strain to the entire spectrum of antibiotics.
If a year after recovery a person becomes infected again, it should be considered as a relapse, but not as a reinfection.
If a relapse of the disease occurs, a more stringent treatment regimen must be applied.

Medications

What steps can be taken if treatment for Helicobacter is expected? The treatment regimen may consist of the following medications:

Their main goal is to reduce the acidity of the stomach and coat its walls.
You will also need substances that suppress the production of gastric juice. In this case, it is customary to talk about proton pump blockers and H2-histamine blockers.
Antibacterial agents - antibiotics. Their main goal is to destroy the harmful organism.

Scheme 1. Seven days

How can Helicobacter be treated with antibiotics? The regimen can be seven days (the so-called first line of therapy). In this case, all medications are taken twice a day for a week. In this case, the doctor will most likely prescribe the following medications to the patient:

Proton pump inhibitors. This may be one of the following drugs: Omez, Lanzoprazole, Esomeprazole.
Bactericidal agents, for example a drug such as Klacid.
You can also use the antibiotic Amoxiclav (a group of penicillins).

Scheme 2. Ten- or fourteen-day treatment

Helicobacter can be treated with antibiotics for two weeks. The scheme in this case could be as follows:

Proton pump inhibitors are taken twice daily. These will again be drugs such as Omeprazole, Pariet, Nexium.
You will need to take this four times a day drug, as "De-nol" (bismuth subcitrate).
The drug Metronidazole is prescribed three times a day.
For a complete cure, you will also need to take the drug Tetracycline, which is an antibiotic, four times a day wide range actions.

Actions after completion of treatment

Once the basic treatment regimen for Helicobacter pylori has been completed, you should not relax. Next, you need to support your body with the help of medications for a certain period of time:

Five weeks, if we are talking about duodenal localization of the microorganism.
Seven weeks, if its localization is gastric.

The subsequent treatment regimen for Helicobacter pylori with antibiotics includes the use of one of the following drugs:

Proton pump inhibitors - drugs "Omez", "Rabeprazole". You need to take these medications 1-2 times a day.
Histamine H2 receptor blockers. These may be drugs such as Ranitidine, Famotidine. Taken twice a day.
Antibiotic "Amcosiclav" - 2 times a day.

Helicobacter gastritis

Now we will consider a treatment regimen for gastritis with Helicobacter. What medications can the doctor prescribe in this case? These may be drugs such as De-Nol, as well as Metronidazole, Clarithromycin, Amoxicycline. To work more efficiently, the drug Omeprazole may be prescribed. To improve recovery processes in the stomach, you can take medications such as Solcoseryl and Gastrofarm.

Main side effects

If the Helicobacter pylori treatment regimen described above was used, it is worth mentioning that the drugs can also cause some side effects. I would like to separately talk about some of them:

If the patient took Omeprazole, bismuth, or Tetracycline, flatulence, diarrhea, dizziness, dark stools, and increased renal failure are possible.
If the patient took this medicine, like Metronidazole, the following side symptoms may occur: vomiting, headache, temperature increase.
While taking Amoxicycline, pseudomembronous colitis may develop, there may be diarrhea, and a rash.
When taking Clarithromycin, nausea, vomiting, diarrhea, headache, and pseudomembranous colitis are possible.

Efficiency mark

What is important if treatment for Helicobacter is proposed? Treatment regimen, as well as assessment of its effectiveness:

An important indicator is the disappearance of pain.
Dyspeptic syndrome should disappear ( discomfort in the upper abdomen).
Well, the most important thing is the complete disappearance of the causative agent of the disease - Helicobacter pylori.

Small conclusions

It is also worth mentioning that doctors are still arguing about which treatment regimen is best to choose. After all, complete extermination of the bacterium Helicobacter pylori is possible only with the use of large quantity the most different antibiotics(the microorganism can be resistant to most). And this is very harmful to the body. If the patient previously took a certain antibiotic, treatment with it will no longer be completely effective. In addition, this can lead to the death of intestinal microflora, which in itself is also very harmful to the patient’s health.