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Med j club nejm h pylori.
 

Med j club nejm h pylori.

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Journal club NEJM H Pylori

Journal club NEJM H Pylori

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    Med j club nejm h pylori. Med j club nejm h pylori. Presentation Transcript

    • Prepared by: Dr.Mohammad Shaikhani. MBChB-CABM-FRCP.
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    • Introduction:
      • HP, a gram-negative bacterium found on the luminal surface of the gastric epithelium, first isolated by Warren/ Marshall in
      • It induces chronic inflammation of the underlying mucosa.
      • The infection is usually contracted in the first few years of life& persist indefinitely unless treated.
      • Its prevalence increases with older age&with lower socioeconomic status during childhood& thus varies markedly around the world.
      • At least 50% of the world’s population has H. pylori infection.
      • The organism can survive in the acidic environment of the stomach partly owing to its remarkably high urease activity; urease converts the urea present in gastric juice to alkaline ammonia& carbon dioxide.
      • H. pylori is a cofactor in the development of three important UGl diseases: DU or GU (in 1- 10% of infected patients), gastric cancer (in 0.1- 3%), & gastrice (MALT) lymphoma (in <0.01%).
    • Introduction:
      • The risk of these disease outcomes in infected patients varies widely among populations.
      • The great majority of patients with H. pylori infection will not have any clinically significant complications.
    • DU:
      • In DU, the inflammation of the gastric mucosa induced by the infection is most pronounced in the non–acid-secreting antral region of the stomach& stimulates the increased release of gastrin.
      • The increased gastrin levels in turn st imulate excess acid secretion from the more proximal acid-secreting fundic mucosa, which is relatively free of inflammation.
      • The increased duodenal acid load damages the duodenal mucosa, causing ulceration&gastric metaplasia.
      • The metaplastic mucosa can then become colonized by H. pylori, which may contribute to the ulcerative process.
      • Eradication of the infection provides a long-term cure of duodenal ulcers in more than 80% of patients whose ulcers are not associated with the use of NSAIDs.
      • NSAIDs are the main cause of H. pylori–negative ulcers.
    • GU:
      • Ulceration of the gastric mucosa is believed to be due to the damage to the mucosa caused by H. pylori.
      • As with duodenal ulcers, eradicating the infection usually cures the disease, provided that the gastric ulcer is not due to NSAIDs.
    • Gastric cancer:
      • There is strong associations between H. pylori infection& noncardia gastric cancers (distal to the gastroesophageal junction).
      • The infection is classified as a human carcinogen by WHO.
      • The risk of cancer is highest among patients in whom the infection induces inf lammat ion of both the antral& fundic mucosa&causes mucosal atrophy& intestinal metaplasia.
      • Eradication of H. pylori infection reduces the progression of atrophic gastritis, but there is little evidence of reversal of atrophy or intest inal metaplasia& it remains unclear whether eradication reduces the risk of gastric cancer.
    • Gastric MALTOMA:
      • There is a strong associations between H. pylori infect ion and the presence of gastric MALT lymphomas&eradication of the infection causes regression of most localized gastric MALT lymphomas.
    • Others:NUD
      • At least 50% of persons who undergo endoscopy for UGI symptoms have no evidence of esophagitis or DU/GU ( NU or functional dyspepsia)& biopsy of the gastric mucosa often reveal H. pylori& inflammation,
      • This f inding is also common in persons without UGIsymptoms.
      • Most CRTs of HP trt shown no significant or marginal benefit regarding symptoms
      • There is thus little evidence that chronic H. pylori infection in the absence of GU/DU causes UGI symptoms.
    • Others:GERD
      • The prevalence of H. pylori infection is lower among patients with (GERD)&esophageal adenocarcinoma (which may arise as a complication of GERD) than among healthy controls.
      • H. pylori–associated atrophic gastritis, which reduces acid secretion, may provide protection against these diseases.
      • A recent meta-analysis showed no significant association between H. pylori eradication&an increased risk of GERD.
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