Helicobacter Pylori Infection

H. pylori is causing a widespread Magenpathogen that gastritis, peptic ulcer disease, adenocarcinoma of the stomach and a low-grade lymphoma of the stomach. The infection may be asymptomatic or manifest itself in various forms of dyspepsia. The diagnosis is made with the urea breath test and an endoscopically obtained biopsy. Treatment is with a proton pump inhibitor plus two antibiotics.

(See also the American College of Gastroenterology’s guidelines for the management of Helicobacter pylori infection.)

H. pylori is causing a widespread Magenpathogen that gastritis, peptic ulcer disease, adenocarcinoma of the stomach and a low-grade lymphoma of the stomach. The infection may be asymptomatic or manifest itself in various forms of dyspepsia. The diagnosis is made with the urea breath test and an endoscopically obtained biopsy. Treatment is with a proton pump inhibitor plus two antibiotics. (See also the American College of Gastroenterology’s guidelines for the management of Helicobacter pylori infection.) H. pylori is a spiral-shaped Gram-negative organism that is accustomed to thrive in acid. In developing countries, it often causes chronic inflammation and is usually acquired in childhood. In the US, the infection is less common in children, but increases with age to: At the age of 60 years, about 50% of people are infected. The infection is especially common among blacks, Hispanics and Asians. The pathogen could be obtained from cultures of stool, saliva and dental plaque, suggesting an oral-oral or fecal-oral transmission. Infections seem to accumulate in families and among prisoners. Nurses and gastroenterologists seem to have a higher risk because the bacteria can be transmitted through insufficient disinfected endoscopes. Pathophysiology H. pylori infection has, depending on the location in the stomach different effects. A V. a. the antrum infesting infection results in increased gastrin, probably through a local reduction of somatostatin. The resulting hypersecretion of acid predisposed to the formation of prepyloric and duodenal ulcers. Infections, mainly in the body, leading to Magenschleimhautatrophie and decreased acid production, possibly via a locally increased production of IL-1?. Patients with predominantly existing in the body of infection are predisposed to the development of gastric ulcers and adenocarcinomas. Some patients have a mixed infection with involvement of the antrum and corpus and different clinical impact. Many patients with H. pylori infection show no significant clinical effects. The ammonia formed by H. pylori allows the pathogen to survive in the acidic environment of the stomach and erode the mucosal barrier. The cytotoxins formed by H. pylori and mucolytic enzymes (eg., Bacterial protease, lipase) play a role in the mucosal damage and subsequent ulceration. Infected people carry a 3- to 6-times greater risk of developing a gastric carcinoma. The H. pylori infection is associated with adenocarcinoma of the corpus and antrum of the intestinal type, but not with carcinoma of the cardia. More associated malignant diseases are gastric lymphoma and lymphoid mukosaassoziierte lymphoma (MALT), a monoclonal B-cell tumor. Diagnosis For the initial diagnosis: serological tests to confirm the treatment: A screening of asymptomatic patients urea breath test or stool antigen test is not justified. The detection methods used in the evaluation of a peptic ulcer and gastritis. Following the treatment, the test procedures are carried out to ensure the eradication of the pathogen. For the initial diagnosis and for monitoring after treatment different tests are used. Non-invasive testing methods Serological tests for antibodies to H. pylori have a sensitivity and specificity of> 85% and are considered non-invasive method of choice for the initial diagnosis of H. pylori –Infektion. However, qualitative tests up to 3 years after successful therapy remain positive and quantitatively not significantly decrease the antibody levels over 6-12 months after treatment, serological detection methods are generally not used to detect a cure. Urea breath test using an oral dose of 13C-or 14C-labeled urea. In an infected patient metabolizes the excitation urea and sets labeled CO2 free, the exhaled in breath samples and quantitatively 20-30 can be determined by recording min. The sensitivity and specificity is> 90%. Urea breath tests are well suited to ensure the eradication of the pathogen after treatment. In recent of past antibiotic therapy and concomitant treatment with proton pump inhibitors false-negative results are possible, so the follow-up ? 4 weeks after completion of antibiotic treatment and one week is performed after discontinuation of proton pump inhibitors. H2 blockers do not affect the test. Chair antigen tests seem to have a sensitivity and specificity that is comparable to that of urea breath tests, especially for the initial diagnosis; a stool test for surgeries is Entwicklung.Invasive tests Endoscopic mucosal samples for a rapid urease test (RUT) and recovered for histological staining. Bacterial cultures because of the sensitive nature of the pathogen is limited value. Endoscopy is not recommended only for diagnosis of H. pylori; non-invasive tests are preferred unless an endoscopy is indicated for other reasons. The rapid urease test, existing bacterial urease caused in the tissue sample a color change in a special medium is the diagnostic method of choice for tissue samples. Histologic staining of the biopsy material was recently stattgehabtem use of antibiotics or after treatment are carried out with proton pump inhibitors in patients with negative rapid urease test, but suspicious clinical findings. Both the rapid urease test and histological staining each have a sensitivity and specificity of> 90%. Antibiotics (various therapies) plus a proton pump inhibitor in patients with complications (eg. As gastritis, ulcer, cancer) of the pathogen should be eradicated. The eradication of H. pylori may even some cases of MALT lymphoma cure (but no other infection-associated cancers). Treatment of asymptomatic infections is controversial, but the realization of the importance of H. pylori for the development of carcinoma has led to a recommendation for therapy. Vaccines, both preventive and therapeutic (i. E. As an adjunct to treatment of infected patients), are in development. The H. pylori eradication requires treatment with several drugs, antibiotics and typically Säuresuppressoren. Proton pump inhibitors suppress H. pylori and the higher gastric pH value occurring during treatment, the tissue concentration and the effectiveness of antimicrobial substances can increase, and thus a for H. pylori. create hostile environment. We recommend a triple therapy. Orally administered omeprazole 20 mg 2 times daily or lansoprazole 30 mg 2 times a day, in combination with clarithromycin 500 mg 2 times daily plus additional amoxicillin 1 g 2 times daily for 14 days (for Penizillinallergiker metronidazole 500 mg 2 times daily ) cure the infection from in> 95% of cases. This regimen is tolerated excellent. Ranitidine bismuth citrate 400 mg p.o. can be used instead of proton pump inhibitors 2 times a day. The quadruple therapy with a proton pump inhibitor, given two times a day, tetracycline 500 mg and bismuth subsalicylate or -subcitrat 525 mg four times daily and metronidazole 500 mg three times daily, is as effective, but cumbersome. Infected patients with duodenal or gastric ulcers require a continuation of acid suppression, for at least 4 weeks. The treatment is repeated when H. pylori was not eradicated. Although two treatment cycles are not successful, an endoscopy to obtain cultures for sensitivity testing is recommended by some specialists. Important points H. pylori is a gram-negative organism that is well suited to an acidic environment, and often infects the stomach; The incidence of infection increases with age, the age of 60 years, about 50% of people are infected. An infection favors the development of gastric, duodenal ulcers and prepyloric and increases the risk of Magenadenokarzinoms and -lymphoms. Initial serological tests or a urea breath test should be carried out; if an endoscopy is performed for other reasons, the biopsies taken by Ureaseschnelltest or histological staining are examined. A treatment is carried out in patients with complications for eradication of the organisms (for example, gastritis, peptic ulcer, cancer.); A typical regimen comprises a proton pump inhibitor and antibiotics (eg. B. clarithromycin and amoxicillin or metronidazole). Treatment success is confirmed by a Ureaseschnelltest.

Health Life Media Team

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