Helicobacter Pylori Infection

Helicobacter Pylori Infection

HELICOBACTER PYLORI INFECTION Dr Maryam Soheilipour Assistant Professor of Gastroenterology DEFINITION Helicobacter pylori colonizes the stomachs of 50% 50% of the worlds human population

throughout their lifetimes. Colonization with this organism is the main risk factor for: Peptic ulceration Gastric adenocarcinoma Gastric MALT(mucosa-associated lymphoid tissue) lymphoma .

Increasing evidence indicates that lifelong H. pylori colonization may offer some protection against complications of GERD, including esophageal adenocarcinoma. ETIOLOGIC AGENT H.

pylori is a gram-negative bacillus . It lives in gastric mucus. its distribution is never systemic.

Its spiral shape and flagella render H. pylori motile in the mucus environment. The organism has several acid-resistance mechanisms, most notably a highly expressed urease that catalyzes urea hydrolysis to produce

buffering ammonia. H. pylori is microaerophilic (requiring low levels of oxygen), is slow-growing. EPIDEMIOLOGY The

prevalence of H. pylori among adults is 50% 30% in the United States and other developed countries. In developing nations, where the majority of children are infected before the age of 10, the prevalence in adults peaks at more than 80 percent before age 50. Humans are the only important reservoir of H.

pylori. The risk of acquiring H. pylori infection is related to socioeconomic status and living conditions early in life. Factors such as density of housing, overcrowding, number of siblings, sharing a bed, and lack of running water have all been linked to

a higher acquisition rate of H. pylori infection. Children may acquire the organism from their parents(more often from the mother) or from other children. The

route by which infection occurs remains unknown . Person-to-person transmission of H. pylori through either fecal/oral or oral/oral exposure seems most likely. Contaminated water supplies in developing countries may serve as an environmental source of bacteria.

Most H. pyloricolonized persons do not develop clinical sequelae. Developing overt disease is related to a combination of factors: bacterial strain differences host susceptibility to disease environmental factors( Smoking increases the risks

of ulcers and cancer in H. pyloripositive individuals). The pattern of gastric inflammation is associated with disease risk: Antral-predominant gastritis is most closely

linked with duodenal ulceration Pangastritis is linked with gastric ulceration and adenocarcinoma. DIAGNOSIS Tests for the presence of H. pylori can be divided

into two groups: Invasive tests, which require EGD and are based on the analysis of gastric biopsy specimens noninvasive tests . If

endoscopy is performed, the most convenient biopsy-based test is the biopsy urease test, in which one large or two small antral biopsy specimens are placed into a gel containing urea and an indicator. The presence of H. pylori urease leads to a pH

alteration and therefore to a color change, which often occurs within minutes but can require up to 24 h. Histologic examination of biopsy specimens for H. pylori also is accurate, provided that a special stain (e.g., a modified Giemsa or silver stain) permitting

optimal visualization of the organism is used. Microbiologic culture is most specific but may be insensitive because of difficulty with H. pylori isolation. Noninvasive H. pylori testing are:

Urea breath test (the most consistently accurate test ): The patient drinks a solution of urea labeled with the nonradioactive isotope 13C and then blows into a tube. If H. pylori urease is present, the urea is hydrolyzed and labeled carbon dioxide is detected in breath samples. The

stool antigen test, is more convenient and potentially less expensive than the UBT but has been slightly less accurate in some comparative studies. Measuring specific IgG levels in serum is the

simplest tests for ascertaining H. pylori status . Tests can be used to assess the success of treatment : UBT the stool antigen test biopsy-based These

tests are unreliable if: performed within 4 weeks of intercurrent treatment with antibiotics or bismuth compounds or within 2 weeks of the discontinuation of PPI treatment. In

the assessment of treatment success, noninvasive tests are normally preferred. After gastric ulceration, endoscopy should be repeated to ensure healing and to exclude gastric carcinoma by further histologic sampling.

Serologic success. tests are not used to monitor treatment TREATMENTH Who need to treath?

Testing for H. pylori should be performed only if the clinician plans to offer treatment for positive results. Indications for testing include: Low grade gastric mucosa associated lymphoid tissue (MALT) lymphoma. Active peptic ulcer disease or past history of peptic ulcer if cure of H. pylori infection has not been documented. Early gastric cancer

Other indications for testing for H. pylori are more controversial: Uninvestigated dyspepsia in patients <60 years without alarm features . Prior to chronic treatment with NSAIDs or longterm, low-dose aspirin use Unexplained iron deficiency Adults with immune thrombocytopenia first-degree relatives of family members with gastric cancer What is your recommendation for H.pylori treatment? No single agent is effective in eradicating the

organism. Combination therapy for 14 days provides the greatest efficacy, although regimens based on sequential administration of antibiotics also appear promising.

The agents used with the greatest frequency include amoxicillin, metronidazole, tetracycline, clarithromycin, and bismuth compounds. H. PYLORI ERADICATION IN IRAN Amoxicillin(1gr,BID)

+ Bismuth subcitrate(250mg BID)+PPI (BD) + one of these drugs for 14 days: Clarithromycin (500mg ,BD) Tetracycline(500mg,QID) Furazolidone (200mg BD) Choice of a particular regimen will be influenced by several factors, including:

efficacy patient tolerance existing antibiotic resistance cost of the drugs. The aim for initial eradication rates should be 8590%. Clarithromycin-based triple therapy should be avoided in settings where H. pylori resistance to this agent

exceeds 1520%. Additional regimens considered for secondline therapy include : levofloxacin-based therapy furazolidone-based therapy Unfortunately, there is no universally accepted

treatment regimen recommended for patients who have failed two courses of antibiotics. If eradication is still not achieved in a compliant patient, then culture and sensitivity of the organism should be considered.

Additional factors that may lower eradication rates include the patients country of origin (higher in Northeast Asia than other parts of Asia or Europe) and cigarette smoking. One

promising approach is sequential therapy. Regimens examined consist of 5 days of amoxicillin and a PPI, followed by an additional 5 days of PPI plus tinidazole and clarithromycin or levofloxacin. Reinfection

after successful eradication of H. pylori is rare. If recurrent infection occurs within the first 6 months after completing therapy, the most likely explanation is recrudescence as opposed to

reinfection. Association between Helicobacter pylori infection and peptic ulcer The majority of patients with duodenal ulcer (DU) are infected with Helicobacter pylori.

reviews confirmed that H. pylori is detectable in 70 to 95 percent of these patients gastric ulcers (65 to 95 percent) H. PYLORI NEGATIVE ULCERS they

have generally had a shorter duration of symptoms and that many had regularly used nonsteroidal anti-inflammatory drugs. Such patients have a significantly worse outcome, especially if treated empirically for H. pylori infection. Thus, H. pylori status should be determined in all ulcer patients before initiating treatment.

While H. pylori infection remains very common in patients from Asia with DU, it is becoming less common in patients from the United States and parts of Europe. Treatment

of H. pylori infection in patients with DU decreases the incidence of ulcer recurrence. PATHOGENESIS OF ULCER FORMATION INCREASED GASTRIC ACID SECRETION GASTRIC METAPLASIA IMMUNE RESPONSE MUCOSAL DEFENSE MECHANISMS

OTHER CONTRIBUTING FACTORS ONLY 10 TO 15 PERCENT OF PATIENTS WITH H. PYLORI INFECTION DEVELOP ULCER DISEASE OTHER FACTORS ARE PROBABLY IMPORTANT BACTERIAL STRAIN; ONLY STRAINS WITH THE CYTOTOXIN-ASSOCIATED GENE A (CAGA), COEXPRESS VACUOLATING CYTOTOXIN (VACA),

APPROXIMATELY 85 TO 100 PERCENT OF PATIENTS WITH DU HAVE CAGA+ STRAINS, COMPARED WITH 30 TO 60 PERCENT OF INFECTED PATIENTS WHO DO NOT DEVELOP ULCERS

A SPECIC H. PYLORI GENE, DUPA, APPEARS TO BE ASSOCIATED WITH DEVELOPMENT OF DU. THOSE INFECTED WITH DUPA BACTERIA HAD MORE INTENSE ANTRAL INFLAMMATION, HIGHER LEVELS OF IL-8 AND LESS GASTRIC ATROPHY, INTESTINAL METAPLASIA, AND GASTRIC CANCER, A CYTOKINE AND HISTOLOGIC

PROLE ASSOCIATED WITH DU DISEASE IN ADDITION, GENETIC FACTORS MAY HELP DETERMINE THE SUSCEPTIBILITY TO INFECTION WITH H. PYLORI. IT HAS BEEN SUGGESTED THAT PATIENTS WITH H. PYLORI WHO DEVELOP DU HAVE AN INTRINSICALLY HIGHER PARIETAL CELL

MASS OR SENSITIVITY TO GASTRIN THAN H. PYLORI-POSITIVE HEALTHY ADULTS ENVIRONMENTAL FACTORS SUCH AS SMOKING AND NSAID USE MAY ALSO INCREASE THE RISK OF ULCER FORMATION IN PATIENTS WITH H. PYLORI

A 54 years old man admited with cc of melena from 2 days ago.His hemodynamic was stable.EGD was done and bulbar clean base ulcer (10*5mm) was detected.He was discharged with order of pantoprazole .What is your recomendation for this patient?

The physicians goal in treating PUD is: to provide relief of symptoms (pain or dyspepsia) promote ulcer healing prevent ulcer recurrence and complications. The greatest influence of understanding the role of H. pylori in PUD has been the ability to prevent recurrence. Eradication of the organism may lead to diminished recurrent ulcer bleeding. The effect of its eradication on ulcer perforation is

unclear. THANKS FOR YOUR ATTENTION

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