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Toronto Notes 2019 Stomach and Duodenum H. pylori-Induced Peptic Ulceration
Pathophysiology
• H.pylori:Gram-negativeflagellatedrodthatresideswithinthegastricmucosa,causingpersistent infection and inflammation
• acid secreted by parietal cells (stimulated by vagal acetylcholine, gastrin, histamine) necessary for most ulcers
• theoriesofhowH.pyloricauseulcers:nonesatisfactory,butpatternofcolonizationcorrelateswith outcome
• gastritisonlyinantrum(15%ofpatients),highgastricacid,associatedwithduodenalulcer,may progress to gastric metaplasia of duodenum where ulcer forms
• gastritis throughout stomach (“pangastritis” – 85% of patients), low gastric acid, associated with stomach ulcer and cancer
Epidemiology
• H.pyloriisfoundinabout20%ofallCanadians
• highestprevalenceinthoseraisedduring1930s
• infectionmostcommonlyacquiredinchildhood,presumablybyfecal-oralroute
• highprevalenceindevelopingcountries,lowsocioeconomicstatus(poorsanitationandovercrowding)
Outcome
• gastritis(non-erosive)in100%ofpatientsbutasymptomatic
• pepticulcerin15%ofpatients
• gastriccarcinomaandmucosalassociatedlymphomatoustissue[MALT]lymphomain0.5%ofpatients • mostareasymptomaticbutstillworthwhileeradicatingtolowerfutureriskofpepticulcer/gastric
malignancy and prevent spread to others (mostly children <5 yr of age)
Gastroenterology G13
Helicobacter pylori Therapy for the Prevention of Metachronous Gastric Cancer
N Engl J Med 2018;378:1085-1095
Purpose: To evaluate the role of H. pylori eradication in the prevention of metachronous gastric cancer.
Study: Double-blinded randomized controlled trial. Population: 470 patients with a subtotal gastrectomy for gastric cancer and H. pylori infection with or without antibiotic treatment. Outcome: Incidence of metachronous gastric cancer.
Results: After almost 6 yr, 7.2% of the antibiotics- treated group developed another cancer in the gastric remnant vs. 13.4% in the placebo control group.
Conclusions: This provides definitive evidence that H. pylori is worthwhile treating no matter how advanced the gastric carcinogenic process.
Diagnosis
Table 7. Diagnosis of H. pylori Infection
Test
Non-invasive Tests
Urea breath test
Serology Fecal antigen
Sensitivity Specificity
90-100% 89-100% 88-99% 89-95%
Comments
Affected by PPI therapy (false negatives)
Can remain positive after treatment Only rarely used in clinical practice
Gold standard; affected by PPI therapy (false negatives) Rapid
Research only
Invasive Tests (require endoscopy)
Histology 93-99% 95-99% Rapid urease test (on biopsy) 89-98% 93-100% Microbiology culture 98% 95-100%
Treatment: H. pylori Eradication
• bismuthquadrupletherapyrecommendedfor10-14d:PPI(e.g.lansoprazole30mgbid)+bismuth525
mg qid + metronidazole 250 mg qid + tetracycline 500 mg qid
• alternatively,concomitantnonbismuthquadrupletherapyfor10-14d:PPI+amoxicillin+
metronidazole + clarithromycin
NSAID-Induced Ulceration
• NSAIDusecausesgastricmucosalpetechiaeinvirtuallyall,erosionsinmost,ulcersinsome(25%)
• erosionsbleed,butusuallyonlyulcerscausesignificantclinicalproblems
• mostNSAIDulcersareclinicallyasymptomatic:dyspepsiaisascommoninpatientswithulcersasin
patients without ulcers; NSAID-induced ulcers characteristically present with complications (bleeding,
perforation, obstruction)
• NSAIDsmorecommonlycausegastriculcersthanduodenalulcers
• mayexacerbateunderlyingduodenalulcerdisease
Pathophysiology
• direct:erosions/petechiae–areduetolocal(direct)effectofdrugongastricmucosa
• indirect:systemicNSAIDeffect(intravenousNSAIDcausesulcers,butnoterosions).NSAIDsalso inhibit mucosal cyclooxygenase, leading to decreased prostaglandin synthesis. This results in ulcers
from reduced secretion of protective bicarbonate and mucous, and decreased mucosal blood flow