Helicobacter pylori infection with gastrointestinal

Helicobacter pylori infection with gastrointestinal

    * Introduction
    * Causes and Risk Factors
    * Signs and symptoms
    * Diagnosis
    * Treatment
H. pylori is a pathogen that causes gastritis, peptic ulcer, gastric adenocarcinoma and gastric-MALT lymphoma. The infection is very common, according to some estimates over half the world population is affected, the prevalence of infection varies greatly from one country to another, is almost universal in adults in developing countries and considerably lower in countries with high economic level.
As a pathogenic factor is still regarded with reservation in non-ulcer dyspepsia appearance, portosistemice encephalopathy, diarrheal disease in children and many digestive and extra-digestive. WHO defines as a type I carcinogen, its role in producing gastric cancer is supported by renowned scientists.
Methods at their disposal to determine the epidemiology of this infection with H. pylori are varied, each technique having advantages and disadvantages. Standard method for determining the status of a person on the infection and that would allow for possible correlations with lesions is endoscopic biopsy sampling from different parts of the stomach, in particular gastric antrum. The method is considered ideal for the serological epidemiological studies. The development of kits which are able to quantify this antiH IgG antibodies. pylori in serum were made serological method to reach a specificity of 83% and 96% senzivitate. H. pylori infection is one of the most common chronic infections in humans. The incidence is greatest in the first years of life, risk of acquiring it during adult life is decreasing exponentially.
Patients experiencing complications of infection with H. pylori eradication therapy needs. Eradication can even cure some cases of MALT lymphoma. Treatment of asymptomatic infections is controversial, but recognition of the role of microorganism in cancer led to his recommendation. Immunizations, preventive and therapeutic research.
Eradication of infection requires multi-drug therapy, antibiotics and antacids. It is recommended triple therapy, two antibiotics and a proton pump inhibitor. Treatment is difficult, hard penetrating antibiotics and gastric mucosa dimimua acidic environment of their action. This explains why it takes a combination of two antibiotics and antacid. The possibility of reinfection after eradication is significant because cantonarii bacteria in certain areas, such as dental plaque. Reinfection occurs with a rate of 1-4% and is defined by the reappearance of H. pylori showed at least one method at different time intervals after the confirmation of eradication.
Pathogenesis
Gastric acidity and peristalsis should normally prevent bacterial colonization of the stomach. But natural selection has endowed the H. pylori species with mechanisms for circumventing the defense acesteiei primary barriers to determine a persistent infection.
Molecular mechanisms of defense against stomach acid: -Presence of two membranes that delimit a periplasmic space with a pH important for their survival -Adherence to the mucosa through interaction between sialic acid and bacterial adezinele, phosphatidyl-ethanolamine, gangliozidul GM1, heparin and Lewis antigen Generation of urease, which hydrolyzes urea into ammonia and canned carbon dioxide, making it possible to neutralize the acidity and gastric colonization -Motility by flagella allows different regions of stomach colonization Gastrin-use, a product of human acid secretion for its proliferation, especially bacteria colonize the stomach entrepre densest population of G cells and the result is the appearance of gastrin hypersecretion and loss of physiological control of secretion.
The effects of colonization with H. pylori include gastric inflammation, degenerative lesions of epithelial cells. Another effect is the disruption of the gastrin and somatostatin secretion. Experimental data showed that hipergastrinemia existence may be due to low secretion of somatostatin. Also ammonia generated by the action of urease secreted by bacteria may inhibit the production of somatostatin from D cells may also use and disruption of histamine metabolism, secreting histamine N-methyltransferase that converts histamine N-metilhistamina meet unusual catabolic, powerful gastric secretagogue and inhibitor secretion somatostatin. Alteration of cell cycle and increased rate of apoptosis is a characteristic feature of H. pylori infection. These changes could provide a stimulus for cell proliferation and explain the epitelilui hiperproliferativ host response associated with infection. The bacteria induce changes in the phospholipid layers of gastric mucous membrane by lipolytic enzymes.
Adherence to the mucosal surface is through close contact with mucous membranes and fiber cells. Surface mucous cells, in the vicinity of H. pylori suffer various degenerative changes such as loss microvililor, cell swelling, depletion of mucus granules, appearance and protuzii vacuolelor degenerative cytoplasmic.