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Helicobacter pylori, NSAIDs, autoimmune gastritis, PPI treatment, and management in Quebec.\">\n<meta name=\"keywords\" content=\"gastrite traitement, gastrite Helicobacter pylori, gastrite AINS, gastrite chronique sympt\u00f4mes, gastrite auto-immune, IPP gastrite, gastrite atrophique Qu\u00e9bec, gastrite \u00e9rosive\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap * { font-family: 'Poppins', sans-serif; box-sizing: border-box; }\n.co-wrap { max-width: 1100px; margin: 0 auto; padding: 30px 0 60px; }\n.co-label { font-family: 'Cinzel', serif; font-size: 14px; font-weight: bold; letter-spacing: 1px; text-transform: uppercase; color: #4D6577; margin-bottom: 14px; display: block; }\n.co-wrap h1 { font-size: 32px; font-weight: 500; color: #323C52; margin: 0 0 22px; line-height: 1.2; }\n.co-intro { font-size: 16px; line-height: 1.75; color: #4D6577; margin-bottom: 36px; padding-bottom: 32px; border-bottom: 1px solid rgba(77,101,119,.2); }\n.co-wrap h2 { font-size: 20px; font-weight: 600; color: #323C52; margin: 32px 0 12px; }\n.co-wrap p { font-size: 15px; color: #4D6577; line-height: 1.7; margin-bottom: 14px; }\n.co-list { list-style: none; padding: 0; margin: 12px 0 24px; }\n.co-list li { font-size: 15px; color: #4D6577; padding: 10px 14px 10px 38px; margin-bottom: 8px; border-radius: 6px; position: relative; background: rgba(77,101,119,.06); border-left: 3px solid #4D6577; }\n.co-list li::before { content: \"\u2713\"; position: absolute; left: 12px; font-weight: 700; color: #4D6577; }\n.co-table { width: 100%; border-collapse: collapse; margin: 14px 0 22px; font-size: 14px; border-radius: 8px; overflow: hidden; table-layout: fixed; }\n.co-table thead tr { background: #323C52; color: #fff; }\n.co-table thead th { padding: 11px 16px; text-align: left; font-weight: 600; font-size: 13px; }\n.co-table tbody tr:nth-child(even) { background: rgba(77,101,119,.06); }\n.co-table tbody tr:nth-child(odd) { background: #fff; }\n.co-table td { padding: 10px 16px; color: #4D6577; border-bottom: 1px solid rgba(77,101,119,.12); font-size: 14px; vertical-align: top; }\n.co-table td:first-child { font-weight: 600; color: #323C52; }\n.co-infobox { display: flex; gap: 12px; background: rgba(77,101,119,.06); border-radius: 8px; border-left: 4px solid #4D6577; padding: 14px 18px; margin: 18px 0 28px; font-size: 14px; color: #4D6577; line-height: 1.65; }\n.co-infobox .ico { font-size: 18px; flex-shrink: 0; }\n.co-urgence { background: #fff8f8; border-left: 5px solid #c0392b; border-radius: 6px; padding: 20px 26px; margin: 24px 0 32px; }\n.co-urgence .co-urgence-titre { font-size: 13px; font-weight: 700; color: #c0392b; letter-spacing: 1.5px; text-transform: uppercase; margin-bottom: 10px; }\n.co-urgence p { color: #5a2020; font-size: 14px; margin: 0 0 10px; line-height: 1.7; }\n.co-urgence p:last-child { margin-bottom: 0; }\n.co-disclaimer { font-size: 13px; color: #8a9aaa; font-style: italic; border-top: 1px solid rgba(77,101,119,.15); padding-top: 24px; margin-top: 40px; line-height: 1.6; }\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Gastroent\u00e9rologie & M\u00e9decine de famille & M\u00e9decine interne<\/span>\n <h1>Gastritis<\/h1>\n\n <div class=\"co-intro\">\n La gastrite d\u00e9signe une inflammation de la muqueuse de l'estomac, confirm\u00e9e histologiquement par la pr\u00e9sence d'un infiltrat inflammatoire \u00e0 la biopsie gastrique. Elle se distingue de la dyspepsie fonctionnelle \u2014 syndrome clinique de douleurs \u00e9pigastriques sans l\u00e9sion muqueuse identifiable \u2014 et de la gastropathie, terme d\u00e9signant des l\u00e9sions muqueuses sans infiltrat inflammatoire significatif (comme la gastropathie \u00e0 AINS ou hypertensive). Les gastrites se classifient selon leur \u00e9volution (aigu\u00eb ou chronique), leur topographie (antrale, fundique ou pangastrite), leur aspect histologique (superficielle, atrophique, m\u00e9taplasique) et leur \u00e9tiologie. <em>Helicobacter pylori<\/em> remains the most frequent cause of chronic gastritis worldwide\u2014responsible for over 90% of active chronic gastritis\u2014and its eradication is one of the most cost-effective treatments in medicine. Atrophic chronic gastritis, whether secondary to <em>H. pylori<\/em> or autoimmune in origin (type A gastritis \u2013 Biermer's disease), represents a recognized precancerous state that can progress to intestinal metaplasia, dysplasia, and then gastric adenocarcinoma in the Correa cascade.\n <\/div>\n\n <h2>Classification, etiologies, and clinical presentation<\/h2>\n <ul class=\"co-list\">\n <li><strong>Classification histologique des gastrites \u2014 syst\u00e8me de Sydney r\u00e9vis\u00e9 :<\/strong> the Sydney System (revised in 1994 \u2013 Houston) is the reference classification for gastritis \u2014 it integrates topography + histology + etiology; topography: antral gastritis (predominant in the antrum \u2014 gastritis with <em>H. pylori<\/em> classic) + fundic gastritis (predominantly in the fundus\/body - autoimmune gastritis) + pangastritis (involvement of the entire mucosa - advanced stage of gastritis) <em>H. pylori<\/em> or diffuse chemical gastritis); histological parameters graded (0 to 3 \u2014 absent\/mild\/moderate\/severe): chronic inflammation (lymphocytes + plasma cells) + activity (neutrophil polymorphonuclear leukocytes) + atrophy (loss of specialized glands) + intestinal metaplasia (replacement of gastric epithelium by intestinal-type epithelium \u2014 goblet cells) + presence of <em>H. pylori<\/em> ; score OLGIM (Operative Link on Gastric Intestinal Metaplasia): staging of gastric cancer risk according to the extent and severity of intestinal metaplasia \u2014 stages 0 to IV \u2014 stages III\u2013IV \u2192 high risk \u2192 intensified endoscopic surveillance; Correa cascade (intestinal-type gastric carcinogenesis): normal mucosa \u2192 superficial gastritis \u2192 atrophic gastritis \u2192 intestinal metaplasia \u2192 dysplasia \u2192 gastric adenocarcinoma \u2014 each stage is influenced by <em>H. pylori<\/em> + tobacco + salty food + lack of fruits and vegetables<\/li>\n <li><strong>\u00c9tiologies principales des gastrites :<\/strong> gastritis <em>Helicobacter pylori<\/em> (type B \u2014 antrale pr\u00e9dominante) : cause la plus fr\u00e9quente mondialement (50 % de la population mondiale infect\u00e9e \u2014 pr\u00e9valence variable : <30 % dans les pays d\u00e9velopp\u00e9s + 70\u201390 % dans les pays \u00e0 bas revenus) \u2014 au Qu\u00e9bec : pr\u00e9valence estim\u00e9e \u00e0 20\u201335 % (population g\u00e9n\u00e9rale) \u2192 plus \u00e9lev\u00e9e dans les communaut\u00e9s autochtones + immigrants de premi\u00e8re g\u00e9n\u00e9ration \u2014 transmission oro-f\u00e9cale ou oro-orale (enfance surtout \u2014 conditions socio\u00e9conomiques + promiscuit\u00e9 + eau non trait\u00e9e) \u2014 <em>H. pylori<\/em> Microaerophilic spiral Gram-negative bacillus - colonizes gastric mucosa (superficial mucus layer) - virulence factors: urease (neutralizes local acidity) + CagA (oncoprotein - cagA+ strains \u2192 risk of ulcer + cancer ++) + VacA (vacuolating cytotoxin - epithelial apoptosis + immunosuppression) + BabA (adhesin - Lewis b); chemical \/ reactive gastritis (type C): NSAIDs and aspirin (COX-1 inhibition \u2192 reduced synthesis of gastroprotective prostaglandins \u2192 altered mucus + reduced mucosal blood flow) + bile reflux (partial gastrectomy + gastric bypass + incompetent pylorus) + alcohol (direct caustic effect) + corticoids (potentiate effect of NSAIDs - alone \u2192 low risk of gastritis); autoimmune gastritis (type A - fundic): anti-parietal cell + antiintrinsic factor antibodies \u2192 destruction of fundus parietal cells \u2192 achlorhydria + intrinsic factor deficiency \u2192 vitamin B12 malabsorption \u2192 Biermer anemia (macrocytic megaloblastic anemia) + risk of gastric carcinoids (hyperplasia of ECL cells by reactive hypergastrinemia) + frequent association with other autoimmune diseases (Hashimoto's thyroiditis + type 1 diabetes + vitiligo + lupus); acute gastritis : <em>H. pylori<\/em> (acute phase - transient - often unrecognized) + NSAIDs\/alcohol (acute erosive gastritis) + stress (stress gastritis - ICU patients + burn victims + trauma patients - mucosal ischemia + stress acid hypersecretion) + viral infections (CMV + EBV + HSV - in immunocompromised patients) + other bacteria (<em>*H. heilmannii*<\/em> + gastric phlegmon - rare but serious); rare causes: Crohn's disease (Crohn's granulomatous gastritis) + gastric sarcoidosis + eosinophilic gastritis + collagenous gastritis + lymphocytic gastritis (associated with celiac disease + <em>H. pylori<\/em>)<\/li>\n <li><strong>Pr\u00e9sentation clinique et particularit\u00e9s :<\/strong> gastritis <em>H. pylori<\/em> : often asymptomatic (70\u201380 % of carriers) \u2014 when symptomatic: dyspepsia (epigastric pain or discomfort + early satiety + bloating + nausea) \u2014 gastritis <em>H. pylori<\/em> does not systematically cause symptoms \u2014 but to eradicate <em>H. pylori<\/em> chez les dyspeptiques am\u00e9liore les sympt\u00f4mes dans 10\u201315 % des cas suppl\u00e9mentaires vs placebo (effet modeste mais r\u00e9el \u2014 \u00ab test and treat \u00bb recommand\u00e9 en dyspepsie non investigu\u00e9e <60 ans sans signes d'alarme au Qu\u00e9bec) ; gastrite \u00e9rosive aigu\u00eb aux AINS : souvent asymptomatique \u2014 sympt\u00f4mes si pr\u00e9sents : \u00e9pigastralgies + naus\u00e9es + vomissements \u2014 risque de complications (ulc\u00e8re + h\u00e9morragie digestive haute) souvent sans sympt\u00f4mes pr\u00e9curseurs (paradoxe des AINS \u2192 analg\u00e9siques \u2192 masquent la douleur) \u2192 surveillance et pr\u00e9vention importantes chez les patients \u00e0 risque ; gastrite auto-immune de Biermer : insidieuse \u2014 sympt\u00f4mes de la carence B12 : asth\u00e9nie progressive + p\u00e2leur + glossite (langue rouge verniss\u00e9e + d\u00e9papill\u00e9e) + signes neurologiques (paresth\u00e9sies + ataxie + signe de Lhermitte \u2014 syndrome de d\u00e9g\u00e9n\u00e9rescence combin\u00e9e subaigu\u00eb de la moelle) + achlorhydrie (perte de l'acidit\u00e9 gastrique \u2192 dyspepsie + diarrh\u00e9e + malabsorption de fer et de calcium) ; signes d'alarme devant une dyspepsie n\u00e9cessitant une endoscopie urgente (r\u00e8gles \u00abALARM\u00bb): An\u00e9mie + L\u00e9sion palpable (masse abdominale) + Amaigrissement inexpliqu\u00e9 (>5 % du poids en 3\u20136 mois) + R\u00e9gurgitations persistantes + M\u00e9l\u00e9na \/ h\u00e9mat\u00e9m\u00e8se \u2192 FOGD urgente (<2 semaines) quel que soit l'\u00e2ge<\/li>\n <\/ul>\n\n <h2>Diagnosis, treatment, and monitoring<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Clinical situation<\/th><th>Diagnosis<\/th><th>Treatment and follow-up<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Gastrite \u00e0 <em>H. pylori<\/em><br><small style=\"font-weight:400;color:#7a8fa0;\">D\u00e9pistage \u2014 \u00e9radication \u2014 contr\u00f4le<\/small><\/td>\n <td>M\u00e9thodes diagnostiques de l'infection \u00e0 <em>H. pylori<\/em> : non-invasive tests (recommended as a first-line treatment in the absence of an indication for EGD): \u00b9\u00b3C-labeled urea breath test (UBT): 95% sensitivity % + 96% specificity % \u2014 mechanism: ingestion of labeled urea \u2192 urease from <em>H. pylori<\/em> \u2192 CO2 marqu\u00e9 expir\u00e9 \u2192 d\u00e9tection par spectroscopie infrarouge \u2014 conditions : arr\u00eat des IPP depuis \u22652 semaines + arr\u00eat des antibiotiques depuis \u22654 semaines (faux n\u00e9gatifs) \u2192 test de r\u00e9f\u00e9rence non invasif pour le contr\u00f4le post-\u00e9radication + test antig\u00e9nique f\u00e9cal (Ag f\u00e9cal \u2014 ELISA monoclonal) : sensibilit\u00e9 94 % + sp\u00e9cificit\u00e9 97 % \u2014 aussi performant que l'UBT \u2014 conditions identiques (arr\u00eat IPP + antibiotiques) \u2014 pratique + peu co\u00fbteux \u2014 recommand\u00e9 par plusieurs algorithmes qu\u00e9b\u00e9cois (INESSS) comme 1re ligne diagnostic en dyspepsie non investigu\u00e9e chez <60 ans sans signes d'alarme + s\u00e9rologie <em>H. pylori<\/em> (IgG) : moins recommand\u00e9e en pratique courante \u2014 sensibilit\u00e9 80\u201390 % + sp\u00e9cificit\u00e9 75\u201390 % \u2014 IgG restent positives des ann\u00e9es apr\u00e8s \u00e9radication (pas utile pour le contr\u00f4le post-traitement) \u2014 utile si IPP impossible \u00e0 arr\u00eater ou en \u00e9pid\u00e9miologie ; tests invasifs (biopsies lors de la FOGD) : test rapide \u00e0 l'ur\u00e9ase (CLO test) : r\u00e9sultat en 1\u201324h + sensibilit\u00e9 90\u201395 % (r\u00e9duite si IPP ou antibiotiques r\u00e9cents) \u2014 histologie + coloration sp\u00e9ciale (Giemsa + Warthin-Starry + immunohistochimie) : sensibilit\u00e9 90\u201395 % + r\u00e9f\u00e9rence pour \u00e9valuer la gastrite (atrophie + m\u00e9taplasie + grade OLGIM) \u2014 culture + antibiogramme : indispensable si suspicion de r\u00e9sistance ou \u00e9chec de 2e ligne (disponible au LSPQ + laboratoires sp\u00e9cialis\u00e9s) \u2014 PCR sur biopsie : d\u00e9tection + r\u00e9sistances (clarithromycine + l\u00e9vofloxacine) en une seule analyse \u2014 disponibilit\u00e9 croissante au Qu\u00e9bec<\/td>\n <td>Traitement d'\u00e9radication de <em>H. pylori<\/em> \u2014 recommandations canadiennes (CAG 2022 + INESSS Qu\u00e9bec) : strat\u00e9gie \u00ab test and treat \u00bb : chez le patient <60 ans avec dyspepsie non investigu\u00e9e + sans signes d'alarme + sans ATCD d'ulc\u00e8re \u2192 tester (UBT ou Ag f\u00e9cal) \u2192 si positif : traiter sans FOGD pr\u00e9alable \u2192 si sympt\u00f4mes persistent apr\u00e8s \u00e9radication \u2192 FOGD ; sch\u00e9mas de 1re ligne : quadrith\u00e9rapie bismuth\u00e9e \u00d7 14 jours (devenue 1re ligne recommand\u00e9e au Canada en raison de la r\u00e9sistance croissante \u00e0 la clarithromycine) : bismuth subsalicylate (Pepto-Bismol 2 comprim\u00e9s \u00d7 4\/j) + t\u00e9tracycline 500 mg \u00d7 4\/j + m\u00e9tronidazole 500 mg \u00d7 3\/j + IPP \u00d7 2\/j \u2192 taux d'\u00e9radication : 85\u201395 % + trith\u00e9rapie standard \u00d7 14 jours (si r\u00e9sistance faible \u00e0 la clarithromycine document\u00e9e localement \u2014 <15 %) : IPP \u00d7 2\/j + amoxicilline 1 g \u00d7 2\/j + clarithromycine 500 mg \u00d7 2\/j \u2192 taux d'\u00e9radication : 70\u201385 % (en baisse au Canada) + th\u00e9rapie s\u00e9quentielle ou concomitante (OCAP) : om\u00e9prazole + clarithromycine + amoxicilline + m\u00e9tronidazole \u00d7 10\u201314 jours \u2192 donn\u00e9es canadiennes limit\u00e9es + non recommand\u00e9e en 1re ligne par tous les experts ; sch\u00e9mas de 2e ligne (si \u00e9chec de 1re ligne) : quadrith\u00e9rapie bismuth\u00e9e si trith\u00e9rapie utilis\u00e9e en 1re ligne \u2014 ou trith\u00e9rapie \u00e0 base de l\u00e9vofloxacine (IPP + amoxicilline + l\u00e9vofloxacine 500 mg \u00d7 2\/j \u00d7 14 jours) \u2014 ou culture + antibiogramme guidant le traitement de 3e ligne + contr\u00f4le post-\u00e9radication : obligatoire 4\u20138 semaines apr\u00e8s la fin du traitement (arr\u00eat IPP \u22652 semaines avant) \u2192 UBT ou Ag f\u00e9cal \u2014 ne pas utiliser la s\u00e9rologie pour le contr\u00f4le<\/td>\n <\/tr>\n <tr>\n <td>Gastrite \u00e0 AINS et gastropathie m\u00e9dicamenteuse<br><small style=\"font-weight:400;color:#7a8fa0;\">Pr\u00e9vention \u2014 IPP \u2014 coxibs<\/small><\/td>\n <td>Les AINS sont la cause la plus fr\u00e9quente de l\u00e9sions gastroduod\u00e9nales m\u00e9dicamenteuses en dehors de <em>H. pylori<\/em> \u2014 leur utilisation est tr\u00e8s r\u00e9pandue au Qu\u00e9bec (analg\u00e9siques OTC + prescription) ; m\u00e9canismes de la gastro-toxicit\u00e9 des AINS : inhibition de la COX-1 (ubiquitaire) \u2192 r\u00e9duction des prostaglandines gastroprotectrices (PGE2 + PGI2) \u2192 alt\u00e9ration du mucus gastrique (r\u00e9duction de sa viscosit\u00e9 + de sa production) + r\u00e9duction du flux sanguin sous-muqueux + augmentation de la perm\u00e9abilit\u00e9 \u00e9pith\u00e9liale \u2192 l\u00e9sions muqueuses + ulc\u00e8res + h\u00e9morragie \u2014 effet topique direct (AINS acides lipophiles \u2192 accumulation dans les cellules \u00e9pith\u00e9liales \u2192 l\u00e9sion directe) \u2014 les coxibs (inhibiteurs s\u00e9lectifs de la COX-2 : c\u00e9l\u00e9coxib \u2014 Celebrex + \u00e9toricoxib) \u00e9pargnent la COX-1 \u2192 moins de toxicit\u00e9 gastrique (r\u00e9duction de 50 % des ulc\u00e8res endoscopiques vs AINS non s\u00e9lectifs) mais ne prot\u00e8gent pas compl\u00e8tement + risque cardiovasculaire accru ; facteurs de risque de complications gastroduod\u00e9nales sous AINS : \u00e2ge >65 ans + ATCD d'ulc\u00e8re gastroduod\u00e9nal ou d'h\u00e9morragie digestive haute + utilisation concomitante d'aspirine + cortico\u00efdes + anticoagulants + antiplaquettaires + infection \u00e0 <em>H. pylori<\/em> Coexistence with high dose NSAIDs, prolonged duration, heart or kidney failure; endoscopic evaluation of NSAID-induced lesions: erythema, erosions, ulcers - Lanza score (0 to 4) - indication for EGD: gastrointestinal bleeding (melena, hematemesis), unexplained iron deficiency anemia, alarm signs, epigastric pain persistent despite treatment<\/td>\n <td>Pr\u00e9vention et traitement des gastropathies aux AINS : gastroprotection syst\u00e9matique recommand\u00e9e si \u22651 facteur de risque : IPP en 1re ligne : om\u00e9prazole 20 mg\/j + pantoprazole 40 mg\/j + rab\u00e9prazole 20 mg\/j + \u00e9som\u00e9prazole 20\u201340 mg\/j + lansoprazole 30 mg\/j \u2192 r\u00e9duction de 80 % des ulc\u00e8res gastriques + 70 % des ulc\u00e8res duod\u00e9naux li\u00e9s aux AINS \u2014 commencer l'IPP en m\u00eame temps que l'AINS (pas apr\u00e8s l'apparition des sympt\u00f4mes) + misoprostol (Cytotec \u2014 analogue des prostaglandines) : 200 \u00b5g \u00d7 2\u20134\/j \u2192 efficace mais mal tol\u00e9r\u00e9 (diarrh\u00e9es + crampes abdominales) \u2192 r\u00e9serv\u00e9 aux patientes enceintes (propri\u00e9t\u00e9s ut\u00e9rotoniques) ou si CI aux IPP ; strat\u00e9gie si AINS indispensable malgr\u00e9 risque \u00e9lev\u00e9 : pr\u00e9f\u00e9rer un coxib (c\u00e9l\u00e9coxib) + IPP associ\u00e9 \u2192 protection maximale \u2014 \u00e9liminer et \u00e9radiquer <em>H. pylori<\/em> Before starting long-term NSAIDs (ulcer risk reduction); long-term PPIs \u2013 adverse effects to consider: hypomagnesemia + hyponatremia + bone fractures (reduced calcium absorption) + intestinal infections<em>C. difficile<\/em> + pneumonias) + B12 deficiency + interaction with clopidogrel (debate - avoid omeprazole + prefer pantoprazole if combination necessary) \u2192 re-evaluate PPI indication every 6-12 months + gradual discontinuation (withdrawal) if no longer necessary (acid rebound with abrupt stop); topical NSAIDs (diclofenac gel + patch): no significant systemic absorption \u2192 no gastroprotection needed \u2192 to be preferred for local pain + osteoarthritis of small joints<\/td>\n <\/tr>\n <tr>\n <td>Autoimmune gastritis (Biermer's disease)<br><small style=\"font-weight:400;color:#7a8fa0;\">Anti-FI \u2014 vitamine B12 \u2014 surveillance carcino\u00efdes<\/small><\/td>\n <td>La gastrite auto-immune (GAA \u2014 type A \u2014 fundique) est une maladie chronique progressive caract\u00e9ris\u00e9e par la destruction auto-immune des cellules pari\u00e9tales du fundus gastrique par des anticorps IgG anti-cellules pari\u00e9tales (ACP) et anti-facteur intrins\u00e8que (AFI) ; pathogen\u00e8se : auto-anticorps anti-ATPase H+\/K+ (cible sur les cellules pari\u00e9tales) + auto-anticorps anti-facteur intrins\u00e8que (type I = bloquants + type II = pr\u00e9cipitants) \u2192 destruction des cellules pari\u00e9tales \u2192 atrophie progressive du fundus \u2192 achlorhydrie (perte de la s\u00e9cr\u00e9tion acide) + carence en facteur intrins\u00e8que (FI \u2014 n\u00e9cessaire \u00e0 l'absorption de la B12 dans l'il\u00e9on terminal) \u2192 malabsorption de la vitamine B12 \u2192 an\u00e9mie de Biermer ; bilan diagnostique de la gastrite auto-immune : anticorps anti-cellules pari\u00e9tales (ACP) : pr\u00e9sents dans 80\u201390 % des GAA + faible sp\u00e9cificit\u00e9 (positifs dans 10\u201315 % de la population g\u00e9n\u00e9rale asymptomatique \u00e2g\u00e9e) + anticorps anti-facteur intrins\u00e8que (AFI \u2014 type I bloquant) : sp\u00e9cificit\u00e9 98\u2013100 % mais sensibilit\u00e9 seulement 50\u201360 % \u2192 positif = GAA quasi certain \u2192 n\u00e9gatif = ne permet pas d'exclure + gastrine s\u00e9rique (hypergastrin\u00e9mie r\u00e9actionnelle \u2014 >100 pg\/mL \u2014 souvent >500 pg\/mL) : l'achlorhydrie l\u00e8ve le frein sur la s\u00e9cr\u00e9tion de gastrine \u2192 hypergastrin\u00e9mie \u2192 stimule les cellules ECL \u2192 hyperplasie \u2192 risque de carcino\u00efdes gastriques (type 1 \u2014 de bon pronostic) + chromogranine A (CgA) s\u00e9rique : marqueur des cellules endocrines gastriques \u2014 \u00e9lev\u00e9e si hyperplasie ECL + carcino\u00efdes + pepsinog\u00e8ne I (bas dans la GAA \u2014 marqueur indirect de l'atrophie du fundus) + ratio pepsinog\u00e8ne I\/II bas (<3) \u2192 signe d'atrophie fundique ; FOGD avec biopsies multiples (protocole Sydney) : biopsies antrale (2 antre) + fundique (2 fundus) + incisure angulaire \u2014 histologie : atrophie fundique + m\u00e9taplasie pseudopylorique + hyperplasie des cellules ECL \u00b1 carcino\u00efdes de type 1 \u00b1 m\u00e9taplasie intestinale \u2014 absence de <em>H. pylori<\/em> (excluding co-infection) \u2014 dysplasia search<\/td>\n <td>Traitement et surveillance de la gastrite auto-immune : substitution en vitamine B12 : m\u00eame sch\u00e9ma que l'an\u00e9mie de Biermer (voir fiche Globules rouges \/ An\u00e9mie macrocytaire) \u2014 voie IM ou voie orale haute dose selon les pr\u00e9f\u00e9rences et la s\u00e9v\u00e9rit\u00e9 : cyanocobalamine 1 000 \u00b5g IM\/mois \u00e0 vie (ou 1 000\u20132 000 \u00b5g\/j PO si voie orale choisie) + surveillance h\u00e9matologique : NFS + B12 + homocyst\u00e9ine + MMA (acide m\u00e9thylmalonique) \u00e0 1\u20133 mois puis annuellement + corriger les carences associ\u00e9es : fer (fr\u00e9quent \u2014 achlorhydrie \u2192 r\u00e9duction de l'absorption du fer non h\u00e9minique) + folates + zinc + calcium (achlorhydrie \u2192 r\u00e9duction de l'absorption calcique) ; surveillance endoscopique de la gastrite auto-immune : risque de cancer gastrique \u00d7 2\u20133 + risque de carcino\u00efdes gastriques de type 1 (associ\u00e9s \u00e0 l'hypergastrin\u00e9mie) \u2192 FOGD de surveillance : FOGD initiale pour stadification (biopsies protokole Sydney + \u00e9valuation OLGIM) \u2192 si stade OLGIM 0\u2013II et pas de carcino\u00efde \u2192 FOGD tous les 3\u20135 ans (consensus MAPS II \u2014 European Society of Gastroenterology 2019) \u2192 si stade OLGIM III\u2013IV ou carcino\u00efdes (>1 cm ou multiples) \u2192 surveillance annuelle + avis gastroent\u00e9rologie + \u00e9choendoscopie si carcino\u00efde visible ; carcino\u00efdes gastriques de type 1 (associ\u00e9s \u00e0 la GAA) : petits polypes fundiques (<1\u20132 cm) + multiples + de bon pronostic (m\u00e9tastases rares <5 %) + traitement : r\u00e9section endoscopique si <2 cm + surveillance + octr\u00e9otide (analogues de la somatostatine) si multiples + envahissants \u2192 avis gastroent\u00e9rologie ; bilan des maladies auto-immunes associ\u00e9es : TSH + TPO + anticorps anti-thyroglobuline (thyro\u00efdite de Hashimoto associ\u00e9e dans 30 % des GAA) + glyc\u00e9mie + HbA1c (diab\u00e8te de type 1 associ\u00e9 dans 5\u201310 %) + NFS + bilan cutan\u00e9 (vitiligo)<\/td>\n <\/tr>\n <tr>\n <td>Gastrite atrophique et pr\u00e9vention du cancer gastrique<br><small style=\"font-weight:400;color:#7a8fa0;\">M\u00e9taplasie intestinale \u2014 OLGIM \u2014 cascade de Correa<\/small><\/td>\n <td>La gastrite atrophique avec m\u00e9taplasie intestinale (MI) constitue un \u00e9tat pr\u00e9canc\u00e9reux gastrique n\u00e9cessitant une surveillance endoscopique structur\u00e9e ; d\u00e9finitions : atrophie gastrique : perte des glandes sp\u00e9cialis\u00e9es (fundiques ou antrales) avec remplacement par du tissu fibreux ou m\u00e9taplasique \u2192 r\u00e9duction de la surface fonctionnelle muqueuse \u2014 m\u00e9taplasie intestinale (MI) : remplacement de l'\u00e9pith\u00e9lium gastrique par un \u00e9pith\u00e9lium de type intestinal (cellules absorbantes + cellules caliciformes productrices de mucines neutres ou sulfat\u00e9es) \u2192 MI compl\u00e8te (type I \u2014 ent\u00e9rique \u2014 mucines neutres \u2014 faible risque) + MI incompl\u00e8te (types II\u2013III \u2014 gastriques et sulfat\u00e9es \u2014 risque plus \u00e9lev\u00e9 de transformation maligne) ; stadification par OLGIM et OLGA : OLGA (Operative Link for Gastritis Assessment) : score d'atrophie (0\u2013IV) \u2192 stades III\u2013IV = risque \u00e9lev\u00e9 \u2014 OLGIM (Operative Link on Gastric IM Assessment) : score de MI (0\u2013IV) \u2192 stades III\u2013IV = risque cancer \u00e9lev\u00e9 (OR 10\u201315 vs stade 0) \u2192 pr\u00e9f\u00e9r\u00e9 \u00e0 l'OLGA en pratique (meilleure reproductibilit\u00e9 inter-observateurs) + chromoendoscopie haute d\u00e9finition (NBI \u2014 narrow band imaging) : am\u00e9liore la d\u00e9tection des l\u00e9sions de m\u00e9taplasie intestinale + dysplasie par rapport \u00e0 la lumi\u00e8re blanche standard \u2192 recommand\u00e9e pour la surveillance dans les centres sp\u00e9cialis\u00e9s ; facteurs aggravants le risque de cancer gastrique en contexte de MI : MI \u00e9tendue (pangastrique) + MI de type incompl\u00e8te + stade OLGIM III\u2013IV + ATCD familial de cancer gastrique au 1er degr\u00e9 + infection \u00e0 <em>H. pylori<\/em> untreated + active smoking + diet rich in salt and cured meats + antioxidant deficiency (fruits + vegetables + vitamins C + E) + residence or origin from a high-incidence country (Japan + Korea + Latin America + Eastern Europe)<\/td>\n <td>Prise en charge de la gastrite atrophique avec m\u00e9taplasie intestinale : \u00e9radication de <em>H. pylori<\/em> (if not yet done): reduced risk of gastric cancer by 30-40 % if eradication before establishment of intestinal metaplasia - lesser but real benefit even after establishment of IM + lifestyle modification: stop smoking + reduce salty and processed foods + increase fruits and vegetables (antioxidants - vitamins C + E + beta-carotene) + reduce alcohol; endoscopic surveillance - MAPS II recommendations (European Society of Gastrointestinal Endoscopy - ESGE 2019) + Quebec adaptation (CAG): OLGIM stage 0-II with no family risk factors: no systematic surveillance recommended (or FOGD every 3-5 years if MI limited to the antrum) + OLGIM stage III-IV OR extensive MI (pangastric) OR family history of 1st-degree gastric cancer + MI: FOGD every 1-2 years with chromoendoscopy (NBI) + multiple biopsies according to Sydney protocol + low-grade dysplasia (LGD): confirmatory FOGD at 6 months (eliminate missed high-grade lesion) \u2192 then annual FOGD with NBI + biopsies + endoscopic resection if visible lesion + high-grade dysplasia (HGD) or early adenocarcinoma: endoscopic resection (mucosectomy - EMR or submucosal dissection - ESD) or surgery according to Curie criteria - outside early stages : surgery (subtotal or total gastrectomy depending on location) \u00b1 perioperative chemotherapy (FLOT - fluorouracil + leucovorin + oxaliplatin + docetaxel); aspirin and gastric chemoprevention: observational data suggest a protective effect of aspirin on gastric cancer \u2192 no formal recommendation for aspirin chemoprevention in IM - statins: favorable observational data - prospective studies in progress<\/td>\n <\/tr>\n <tr>\n <td>Gastrite de stress et gastrite en r\u00e9animation<br><small style=\"font-weight:400;color:#7a8fa0;\">Pr\u00e9vention IPP \u2014 l\u00e9sions aigu\u00ebs de la muqueuse<\/small><\/td>\n <td>La gastrite de stress (l\u00e9sions aigu\u00ebs de la muqueuse gastroduod\u00e9nale \u2014 LAMGD) est une complication fr\u00e9quente chez les patients en soins critiques \u2014 potentiellement mortelle en cas d'h\u00e9morragie digestive massive ; physiopathologie des LAMGD en r\u00e9animation : isch\u00e9mie de la muqueuse gastrique (vasoconstriction splanchnique lors du choc + hypoperfusion) + hypers\u00e9cr\u00e9tion acide de stress (stimulation sympathique + vagale) + alt\u00e9ration des m\u00e9canismes de d\u00e9fense muqueux (mucus + prostaglandines + bicarbonates) + reflux biliaire en cas de gastrostase \u2192 \u00e9rosions superficielles \u2192 ulc\u00e8res h\u00e9morragiques ; facteurs de risque de LAMGD cliniquement significative (h\u00e9morragie n\u00e9cessitant une transfusion ou une intervention) : ventilation m\u00e9canique \u226548h (risque \u00d7 15 \u2014 facteur de risque majeur) + coagulopathie (TP <50 % ou plaquettes <50 G\/L) + ATCD d'ulc\u00e8re ou d'h\u00e9morragie digestive haute + traumatisme cr\u00e2nien grave (ulc\u00e8re de Cushing \u2014 hypers\u00e9cr\u00e9tion acide neurog\u00e8ne) + br\u00fblures \u00e9tendues (>35 % de la surface corporelle \u2014 ulc\u00e8re de Curling \u2014 isch\u00e9mie muqueuse) + choc + sepsis grave + insuffisance h\u00e9patique ou r\u00e9nale aigu\u00eb + cortico\u00efdes \u00e0 fortes doses + anticoagulants ; incidence de l'h\u00e9morragie digestive cliniquement significative en r\u00e9animation (avec prophylaxie) : 2\u20134 % \u2014 sans prophylaxie : 5\u201310 % ; diagnostic : endoscopie digestive haute en urgence si h\u00e9morragie suspect\u00e9e \u2014 FOGD : \u00e9rosions superficielles multiples + ulc\u00e8res fundiques ou antraux \u2192 classification de Forrest (\u00e9valuation du risque de r\u00e9cidive h\u00e9morragique + d\u00e9cision th\u00e9rapeutique endoscopique)<\/td>\n <td>Prophylaxie des LAMGD en r\u00e9animation : IPP IV : m\u00e9dicament de r\u00e9f\u00e9rence pour la prophylaxie des LAMGD en r\u00e9animation \u2014 pantoprazole 40 mg IV \u00d7 1\u20132\/j (le plus utilis\u00e9) + \u00e9som\u00e9prazole 40 mg IV \u00d7 1\/j + om\u00e9prazole 40 mg IV \u00d7 1\/j \u2192 sup\u00e9riorit\u00e9 sur les anti-H2 d\u00e9montr\u00e9e (m\u00e9ta-analyse PLOS ONE 2013) + r\u00e9duction du risque d'h\u00e9morragie cliniquement significative de 50\u201360 % ; anti-H2 (famotidine + ranitidine retir\u00e9 du march\u00e9) : alternative aux IPP si disponibilit\u00e9 ou allergie \u2014 efficacit\u00e9 moindre sur la prophylaxie des LAMGD ; sucralfate (Sulcrate) : protecteur muqueux (complexe aluminium + sulfate de saccharose \u2014 adh\u00e8re aux ulc\u00e8res + stimule PGE2 + mucus) \u2192 alternative aux IPP dans certains protocoles (avantage th\u00e9orique : pas d'\u00e9l\u00e9vation du pH \u2014 pr\u00e9servation de la flore) \u2192 m\u00e9ta-analyses r\u00e9centes : moins efficace que les IPP pour la prophylaxie \u2014 risque de pneumonie associ\u00e9e aux soins similaire avec les deux approches (\u00e9tudes PEPTIC 2020 \u2014 NEJM) ; nutrition ent\u00e9rale pr\u00e9coce : r\u00e9duit le risque de LAMGD en maintenant le flux sanguin muqueux + en tamponant l'acidit\u00e9 \u2192 recommand\u00e9e dans les 24\u201348h si possible (pr\u00e9vention des LAMGD + b\u00e9n\u00e9fice nutritionnel global) \u2014 la nutrition ent\u00e9rale pr\u00e9coce peut parfois suffire comme prophylaxie si d\u00e9but\u00e9e dans les 24h + patient \u00e0 faible risque ; traitement curatif de l'h\u00e9morragie sur LAMGD : IPP en bolus IV \u2192 perfusion continue (80 mg IV en bolus puis 8 mg\/h \u00d7 72h) si h\u00e9morragie active \u2014 h\u00e9mostase endoscopique (injection d'adr\u00e9naline + clip ou coagulation thermique) si l\u00e9sion accessible \u2014 radiologie interventionnelle (embolisation) si h\u00e9morragie massive non contr\u00f4l\u00e9e endoscopiquement \u2192 chirurgie en dernier recours (gastrectomie + vagotomie) si \u00e9chec des autres approches<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong><em>H. pylori<\/em> \u2014 Test and treat for uninvestigated dyspepsia:<\/strong> In a patient under 60 years old with dyspepsia and no alarm signs (no weight loss, no bleeding, no dysphagia, no anemia), the \u00abtest and treat\u00bb strategy\u2014testing for <em>H. pylori<\/em> by breath test or fecal antigen and treat if positive without prior EGD \u2014 is recommended by Canadian and Quebec guidelines (CAG + INESSS). This approach is cost-effective and avoids unnecessary endoscopies. EGD is only indicated upfront in the presence of alarm signs or in patients aged 60 years and older (increased risk of gastric cancer).<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>H\u00e9mat\u00e9m\u00e8se (vomissements de sang) ou m\u00e9l\u00e9na (selles noires goudronneuses) avec instabilit\u00e9 h\u00e9modynamique<\/strong> high gastrointestinal bleeding from erosive gastritis or ulcer \u2192 emergency \u2192 emergency EGD + resuscitation + IV PPI bolus + continuous infusion.<\/p>\n <p><strong>\u00c9pigastralgies + signes d'alarme (amaigrissement >5 % + dysphagie + an\u00e9mie + masse palpable)<\/strong> \u2192 FOGD urgente (<2 semaines) quel que soit l'\u00e2ge \u2192 \u00e9liminer un cancer gastrique.<\/p>\n <p><strong>Patient sous AINS + douleurs \u00e9pigastriques + an\u00e9mie ferriprive ou m\u00e9l\u00e9na<\/strong> \u2192 immediate cessation of NSAIDs + urgent EGD + IV PPI + search for <em>H. pylori<\/em> on biopsies.<\/p>\n <p><strong>Dyspepsie r\u00e9fractaire + achlorhydrie + an\u00e9mie macrocytaire + paresth\u00e9sies chez un patient avec maladies auto-immunes connues<\/strong> Autoimmune gastritis of Biermer \u2192 B12 dosage + anti-Intrinsic Factor antibodies + parietal cell antibodies + upper endoscopy + urgent B12 replacement if neurological symptoms.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Les m\u00e9decins de Clinique Omicron prennent en charge les dyspepsies et les gastrites dans le cadre de la strat\u00e9gie \u00ab test and treat \u00bb recommand\u00e9e au Qu\u00e9bec \u2014 prescription du test respiratoire \u00e0 l'ur\u00e9e ou de l'antig\u00e8ne f\u00e9cal, initiation du traitement d'\u00e9radication de <em>H. pylori<\/em>, adjustment of gastroprotection in patients on NSAIDs, and referral to gastroenterology for atrophic forms requiring endoscopic monitoring. These services are available at several service points in Quebec and through telemedicine. To make an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">Le contenu de cette page est fourni \u00e0 titre informatif uniquement et ne remplace pas l'avis d'un m\u00e9decin ou d'un gastroent\u00e9rologue. Tout sympt\u00f4me digestif persistant ou accompagn\u00e9 de signes d'alarme doit \u00eatre \u00e9valu\u00e9 rapidement par un professionnel de sant\u00e9.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p> Gastroent\u00e9rologie & M\u00e9decine de famille & M\u00e9decine interne Gastrite La gastrite d\u00e9signe une inflammation de la muqueuse de l’estomac, confirm\u00e9e histologiquement par la pr\u00e9sence d’un infiltrat inflammatoire \u00e0 la biopsie gastrique. Elle se distingue de la dyspepsie fonctionnelle \u2014 syndrome clinique de douleurs \u00e9pigastriques sans l\u00e9sion muqueuse identifiable \u2014 et de la gastropathie, terme… <a href=\"https:\/\/cliniqueomicron.ca\/en\/gastrite\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Gastrite : sympt\u00f4mes, causes et traitement | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Gastrite : causes, sympt\u00f4mes, | Brossard | Clinique Omicron","_metasync_otto_description":"La gastrite est une inflammation de la muqueuse gastrique. Helicobacter pylori, AINS, gastrite auto-immune, traitement par IPP et prise en charge au Qu\u00e9bec.","_metasync_otto_keywords":"","_metasync_otto_og_title":"Gastrite : causes, sympt\u00f4mes, | Brossard | Clinique Omicron","_metasync_otto_og_description":"","_metasync_otto_twitter_title":"Gastrite : causes, sympt\u00f4mes, | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"La gastrite est une inflammation de la muqueuse gastrique. 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\n\t\t\t\t\t\n\n\n\n\nGastritis: Causes, Symptoms, Diagnosis, and Treatment | Clinique Omicron<\/title>\n<meta name=\"description\" content=\"Gastritis is an inflammation of the stomach lining. Helicobacter pylori, NSAIDs, autoimmune gastritis, PPI treatment, and management in Quebec.\">\n<meta name=\"keywords\" content=\"gastrite traitement, gastrite Helicobacter pylori, gastrite AINS, gastrite chronique sympt\u00f4mes, gastrite auto-immune, IPP gastrite, gastrite atrophique Qu\u00e9bec, gastrite \u00e9rosive\">\n<link rel=\"preconnect\" href=\"https:\/\/fonts.googleapis.com\">\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Cinzel:wght@600&family=Poppins:wght@400;500;600;700&display=swap\" rel=\"stylesheet\">\n<style>\n.co-wrap * { font-family: 'Poppins', sans-serif; box-sizing: border-box; }\n.co-wrap { max-width: 1100px; margin: 0 auto; padding: 30px 0 60px; }\n.co-label { font-family: 'Cinzel', serif; font-size: 14px; font-weight: bold; letter-spacing: 1px; text-transform: uppercase; color: #4D6577; margin-bottom: 14px; display: block; }\n.co-wrap h1 { font-size: 32px; font-weight: 500; color: #323C52; margin: 0 0 22px; line-height: 1.2; }\n.co-intro { font-size: 16px; line-height: 1.75; color: #4D6577; margin-bottom: 36px; padding-bottom: 32px; border-bottom: 1px solid rgba(77,101,119,.2); }\n.co-wrap h2 { font-size: 20px; font-weight: 600; color: #323C52; margin: 32px 0 12px; }\n.co-wrap p { font-size: 15px; color: #4D6577; line-height: 1.7; margin-bottom: 14px; }\n.co-list { list-style: none; padding: 0; margin: 12px 0 24px; }\n.co-list li { font-size: 15px; color: #4D6577; padding: 10px 14px 10px 38px; margin-bottom: 8px; border-radius: 6px; position: relative; background: rgba(77,101,119,.06); border-left: 3px solid #4D6577; }\n.co-list li::before { content: \"\u2713\"; position: absolute; left: 12px; font-weight: 700; color: #4D6577; }\n.co-table { width: 100%; border-collapse: collapse; margin: 14px 0 22px; font-size: 14px; border-radius: 8px; overflow: hidden; table-layout: fixed; }\n.co-table thead tr { background: #323C52; color: #fff; }\n.co-table thead th { padding: 11px 16px; text-align: left; font-weight: 600; font-size: 13px; }\n.co-table tbody tr:nth-child(even) { background: rgba(77,101,119,.06); }\n.co-table tbody tr:nth-child(odd) { background: #fff; }\n.co-table td { padding: 10px 16px; color: #4D6577; border-bottom: 1px solid rgba(77,101,119,.12); font-size: 14px; vertical-align: top; }\n.co-table td:first-child { font-weight: 600; color: #323C52; }\n.co-infobox { display: flex; gap: 12px; background: rgba(77,101,119,.06); border-radius: 8px; border-left: 4px solid #4D6577; padding: 14px 18px; margin: 18px 0 28px; font-size: 14px; color: #4D6577; line-height: 1.65; }\n.co-infobox .ico { font-size: 18px; flex-shrink: 0; }\n.co-urgence { background: #fff8f8; border-left: 5px solid #c0392b; border-radius: 6px; padding: 20px 26px; margin: 24px 0 32px; }\n.co-urgence .co-urgence-titre { font-size: 13px; font-weight: 700; color: #c0392b; letter-spacing: 1.5px; text-transform: uppercase; margin-bottom: 10px; }\n.co-urgence p { color: #5a2020; font-size: 14px; margin: 0 0 10px; line-height: 1.7; }\n.co-urgence p:last-child { margin-bottom: 0; }\n.co-disclaimer { font-size: 13px; color: #8a9aaa; font-style: italic; border-top: 1px solid rgba(77,101,119,.15); padding-top: 24px; margin-top: 40px; line-height: 1.6; }\n<\/style>\n<\/head>\n<body>\n<div class=\"co-wrap\">\n <span class=\"co-label\">Gastroent\u00e9rologie & M\u00e9decine de famille & M\u00e9decine interne<\/span>\n <h1>Gastritis<\/h1>\n\n <div class=\"co-intro\">\n La gastrite d\u00e9signe une inflammation de la muqueuse de l'estomac, confirm\u00e9e histologiquement par la pr\u00e9sence d'un infiltrat inflammatoire \u00e0 la biopsie gastrique. Elle se distingue de la dyspepsie fonctionnelle \u2014 syndrome clinique de douleurs \u00e9pigastriques sans l\u00e9sion muqueuse identifiable \u2014 et de la gastropathie, terme d\u00e9signant des l\u00e9sions muqueuses sans infiltrat inflammatoire significatif (comme la gastropathie \u00e0 AINS ou hypertensive). Les gastrites se classifient selon leur \u00e9volution (aigu\u00eb ou chronique), leur topographie (antrale, fundique ou pangastrite), leur aspect histologique (superficielle, atrophique, m\u00e9taplasique) et leur \u00e9tiologie. <em>Helicobacter pylori<\/em> remains the most frequent cause of chronic gastritis worldwide\u2014responsible for over 90% of active chronic gastritis\u2014and its eradication is one of the most cost-effective treatments in medicine. Atrophic chronic gastritis, whether secondary to <em>H. pylori<\/em> or autoimmune in origin (type A gastritis \u2013 Biermer's disease), represents a recognized precancerous state that can progress to intestinal metaplasia, dysplasia, and then gastric adenocarcinoma in the Correa cascade.\n <\/div>\n\n <h2>Classification, etiologies, and clinical presentation<\/h2>\n <ul class=\"co-list\">\n <li><strong>Classification histologique des gastrites \u2014 syst\u00e8me de Sydney r\u00e9vis\u00e9 :<\/strong> the Sydney System (revised in 1994 \u2013 Houston) is the reference classification for gastritis \u2014 it integrates topography + histology + etiology; topography: antral gastritis (predominant in the antrum \u2014 gastritis with <em>H. pylori<\/em> classic) + fundic gastritis (predominantly in the fundus\/body - autoimmune gastritis) + pangastritis (involvement of the entire mucosa - advanced stage of gastritis) <em>H. pylori<\/em> or diffuse chemical gastritis); histological parameters graded (0 to 3 \u2014 absent\/mild\/moderate\/severe): chronic inflammation (lymphocytes + plasma cells) + activity (neutrophil polymorphonuclear leukocytes) + atrophy (loss of specialized glands) + intestinal metaplasia (replacement of gastric epithelium by intestinal-type epithelium \u2014 goblet cells) + presence of <em>H. pylori<\/em> ; score OLGIM (Operative Link on Gastric Intestinal Metaplasia): staging of gastric cancer risk according to the extent and severity of intestinal metaplasia \u2014 stages 0 to IV \u2014 stages III\u2013IV \u2192 high risk \u2192 intensified endoscopic surveillance; Correa cascade (intestinal-type gastric carcinogenesis): normal mucosa \u2192 superficial gastritis \u2192 atrophic gastritis \u2192 intestinal metaplasia \u2192 dysplasia \u2192 gastric adenocarcinoma \u2014 each stage is influenced by <em>H. pylori<\/em> + tobacco + salty food + lack of fruits and vegetables<\/li>\n <li><strong>\u00c9tiologies principales des gastrites :<\/strong> gastritis <em>Helicobacter pylori<\/em> (type B \u2014 antrale pr\u00e9dominante) : cause la plus fr\u00e9quente mondialement (50 % de la population mondiale infect\u00e9e \u2014 pr\u00e9valence variable : <30 % dans les pays d\u00e9velopp\u00e9s + 70\u201390 % dans les pays \u00e0 bas revenus) \u2014 au Qu\u00e9bec : pr\u00e9valence estim\u00e9e \u00e0 20\u201335 % (population g\u00e9n\u00e9rale) \u2192 plus \u00e9lev\u00e9e dans les communaut\u00e9s autochtones + immigrants de premi\u00e8re g\u00e9n\u00e9ration \u2014 transmission oro-f\u00e9cale ou oro-orale (enfance surtout \u2014 conditions socio\u00e9conomiques + promiscuit\u00e9 + eau non trait\u00e9e) \u2014 <em>H. pylori<\/em> Microaerophilic spiral Gram-negative bacillus - colonizes gastric mucosa (superficial mucus layer) - virulence factors: urease (neutralizes local acidity) + CagA (oncoprotein - cagA+ strains \u2192 risk of ulcer + cancer ++) + VacA (vacuolating cytotoxin - epithelial apoptosis + immunosuppression) + BabA (adhesin - Lewis b); chemical \/ reactive gastritis (type C): NSAIDs and aspirin (COX-1 inhibition \u2192 reduced synthesis of gastroprotective prostaglandins \u2192 altered mucus + reduced mucosal blood flow) + bile reflux (partial gastrectomy + gastric bypass + incompetent pylorus) + alcohol (direct caustic effect) + corticoids (potentiate effect of NSAIDs - alone \u2192 low risk of gastritis); autoimmune gastritis (type A - fundic): anti-parietal cell + antiintrinsic factor antibodies \u2192 destruction of fundus parietal cells \u2192 achlorhydria + intrinsic factor deficiency \u2192 vitamin B12 malabsorption \u2192 Biermer anemia (macrocytic megaloblastic anemia) + risk of gastric carcinoids (hyperplasia of ECL cells by reactive hypergastrinemia) + frequent association with other autoimmune diseases (Hashimoto's thyroiditis + type 1 diabetes + vitiligo + lupus); acute gastritis : <em>H. pylori<\/em> (acute phase - transient - often unrecognized) + NSAIDs\/alcohol (acute erosive gastritis) + stress (stress gastritis - ICU patients + burn victims + trauma patients - mucosal ischemia + stress acid hypersecretion) + viral infections (CMV + EBV + HSV - in immunocompromised patients) + other bacteria (<em>*H. heilmannii*<\/em> + gastric phlegmon - rare but serious); rare causes: Crohn's disease (Crohn's granulomatous gastritis) + gastric sarcoidosis + eosinophilic gastritis + collagenous gastritis + lymphocytic gastritis (associated with celiac disease + <em>H. pylori<\/em>)<\/li>\n <li><strong>Pr\u00e9sentation clinique et particularit\u00e9s :<\/strong> gastritis <em>H. pylori<\/em> : often asymptomatic (70\u201380 % of carriers) \u2014 when symptomatic: dyspepsia (epigastric pain or discomfort + early satiety + bloating + nausea) \u2014 gastritis <em>H. pylori<\/em> does not systematically cause symptoms \u2014 but to eradicate <em>H. pylori<\/em> chez les dyspeptiques am\u00e9liore les sympt\u00f4mes dans 10\u201315 % des cas suppl\u00e9mentaires vs placebo (effet modeste mais r\u00e9el \u2014 \u00ab test and treat \u00bb recommand\u00e9 en dyspepsie non investigu\u00e9e <60 ans sans signes d'alarme au Qu\u00e9bec) ; gastrite \u00e9rosive aigu\u00eb aux AINS : souvent asymptomatique \u2014 sympt\u00f4mes si pr\u00e9sents : \u00e9pigastralgies + naus\u00e9es + vomissements \u2014 risque de complications (ulc\u00e8re + h\u00e9morragie digestive haute) souvent sans sympt\u00f4mes pr\u00e9curseurs (paradoxe des AINS \u2192 analg\u00e9siques \u2192 masquent la douleur) \u2192 surveillance et pr\u00e9vention importantes chez les patients \u00e0 risque ; gastrite auto-immune de Biermer : insidieuse \u2014 sympt\u00f4mes de la carence B12 : asth\u00e9nie progressive + p\u00e2leur + glossite (langue rouge verniss\u00e9e + d\u00e9papill\u00e9e) + signes neurologiques (paresth\u00e9sies + ataxie + signe de Lhermitte \u2014 syndrome de d\u00e9g\u00e9n\u00e9rescence combin\u00e9e subaigu\u00eb de la moelle) + achlorhydrie (perte de l'acidit\u00e9 gastrique \u2192 dyspepsie + diarrh\u00e9e + malabsorption de fer et de calcium) ; signes d'alarme devant une dyspepsie n\u00e9cessitant une endoscopie urgente (r\u00e8gles \u00abALARM\u00bb): An\u00e9mie + L\u00e9sion palpable (masse abdominale) + Amaigrissement inexpliqu\u00e9 (>5 % du poids en 3\u20136 mois) + R\u00e9gurgitations persistantes + M\u00e9l\u00e9na \/ h\u00e9mat\u00e9m\u00e8se \u2192 FOGD urgente (<2 semaines) quel que soit l'\u00e2ge<\/li>\n <\/ul>\n\n <h2>Diagnosis, treatment, and monitoring<\/h2>\n <table class=\"co-table\">\n <colgroup><col style=\"width:200px;\"><col style=\"width:42%;\"><col><\/colgroup>\n <thead>\n <tr><th>Clinical situation<\/th><th>Diagnosis<\/th><th>Treatment and follow-up<\/th><\/tr>\n <\/thead>\n <tbody>\n <tr>\n <td>Gastrite \u00e0 <em>H. pylori<\/em><br><small style=\"font-weight:400;color:#7a8fa0;\">D\u00e9pistage \u2014 \u00e9radication \u2014 contr\u00f4le<\/small><\/td>\n <td>M\u00e9thodes diagnostiques de l'infection \u00e0 <em>H. pylori<\/em> : non-invasive tests (recommended as a first-line treatment in the absence of an indication for EGD): \u00b9\u00b3C-labeled urea breath test (UBT): 95% sensitivity % + 96% specificity % \u2014 mechanism: ingestion of labeled urea \u2192 urease from <em>H. pylori<\/em> \u2192 CO2 marqu\u00e9 expir\u00e9 \u2192 d\u00e9tection par spectroscopie infrarouge \u2014 conditions : arr\u00eat des IPP depuis \u22652 semaines + arr\u00eat des antibiotiques depuis \u22654 semaines (faux n\u00e9gatifs) \u2192 test de r\u00e9f\u00e9rence non invasif pour le contr\u00f4le post-\u00e9radication + test antig\u00e9nique f\u00e9cal (Ag f\u00e9cal \u2014 ELISA monoclonal) : sensibilit\u00e9 94 % + sp\u00e9cificit\u00e9 97 % \u2014 aussi performant que l'UBT \u2014 conditions identiques (arr\u00eat IPP + antibiotiques) \u2014 pratique + peu co\u00fbteux \u2014 recommand\u00e9 par plusieurs algorithmes qu\u00e9b\u00e9cois (INESSS) comme 1re ligne diagnostic en dyspepsie non investigu\u00e9e chez <60 ans sans signes d'alarme + s\u00e9rologie <em>H. pylori<\/em> (IgG) : moins recommand\u00e9e en pratique courante \u2014 sensibilit\u00e9 80\u201390 % + sp\u00e9cificit\u00e9 75\u201390 % \u2014 IgG restent positives des ann\u00e9es apr\u00e8s \u00e9radication (pas utile pour le contr\u00f4le post-traitement) \u2014 utile si IPP impossible \u00e0 arr\u00eater ou en \u00e9pid\u00e9miologie ; tests invasifs (biopsies lors de la FOGD) : test rapide \u00e0 l'ur\u00e9ase (CLO test) : r\u00e9sultat en 1\u201324h + sensibilit\u00e9 90\u201395 % (r\u00e9duite si IPP ou antibiotiques r\u00e9cents) \u2014 histologie + coloration sp\u00e9ciale (Giemsa + Warthin-Starry + immunohistochimie) : sensibilit\u00e9 90\u201395 % + r\u00e9f\u00e9rence pour \u00e9valuer la gastrite (atrophie + m\u00e9taplasie + grade OLGIM) \u2014 culture + antibiogramme : indispensable si suspicion de r\u00e9sistance ou \u00e9chec de 2e ligne (disponible au LSPQ + laboratoires sp\u00e9cialis\u00e9s) \u2014 PCR sur biopsie : d\u00e9tection + r\u00e9sistances (clarithromycine + l\u00e9vofloxacine) en une seule analyse \u2014 disponibilit\u00e9 croissante au Qu\u00e9bec<\/td>\n <td>Traitement d'\u00e9radication de <em>H. pylori<\/em> \u2014 recommandations canadiennes (CAG 2022 + INESSS Qu\u00e9bec) : strat\u00e9gie \u00ab test and treat \u00bb : chez le patient <60 ans avec dyspepsie non investigu\u00e9e + sans signes d'alarme + sans ATCD d'ulc\u00e8re \u2192 tester (UBT ou Ag f\u00e9cal) \u2192 si positif : traiter sans FOGD pr\u00e9alable \u2192 si sympt\u00f4mes persistent apr\u00e8s \u00e9radication \u2192 FOGD ; sch\u00e9mas de 1re ligne : quadrith\u00e9rapie bismuth\u00e9e \u00d7 14 jours (devenue 1re ligne recommand\u00e9e au Canada en raison de la r\u00e9sistance croissante \u00e0 la clarithromycine) : bismuth subsalicylate (Pepto-Bismol 2 comprim\u00e9s \u00d7 4\/j) + t\u00e9tracycline 500 mg \u00d7 4\/j + m\u00e9tronidazole 500 mg \u00d7 3\/j + IPP \u00d7 2\/j \u2192 taux d'\u00e9radication : 85\u201395 % + trith\u00e9rapie standard \u00d7 14 jours (si r\u00e9sistance faible \u00e0 la clarithromycine document\u00e9e localement \u2014 <15 %) : IPP \u00d7 2\/j + amoxicilline 1 g \u00d7 2\/j + clarithromycine 500 mg \u00d7 2\/j \u2192 taux d'\u00e9radication : 70\u201385 % (en baisse au Canada) + th\u00e9rapie s\u00e9quentielle ou concomitante (OCAP) : om\u00e9prazole + clarithromycine + amoxicilline + m\u00e9tronidazole \u00d7 10\u201314 jours \u2192 donn\u00e9es canadiennes limit\u00e9es + non recommand\u00e9e en 1re ligne par tous les experts ; sch\u00e9mas de 2e ligne (si \u00e9chec de 1re ligne) : quadrith\u00e9rapie bismuth\u00e9e si trith\u00e9rapie utilis\u00e9e en 1re ligne \u2014 ou trith\u00e9rapie \u00e0 base de l\u00e9vofloxacine (IPP + amoxicilline + l\u00e9vofloxacine 500 mg \u00d7 2\/j \u00d7 14 jours) \u2014 ou culture + antibiogramme guidant le traitement de 3e ligne + contr\u00f4le post-\u00e9radication : obligatoire 4\u20138 semaines apr\u00e8s la fin du traitement (arr\u00eat IPP \u22652 semaines avant) \u2192 UBT ou Ag f\u00e9cal \u2014 ne pas utiliser la s\u00e9rologie pour le contr\u00f4le<\/td>\n <\/tr>\n <tr>\n <td>Gastrite \u00e0 AINS et gastropathie m\u00e9dicamenteuse<br><small style=\"font-weight:400;color:#7a8fa0;\">Pr\u00e9vention \u2014 IPP \u2014 coxibs<\/small><\/td>\n <td>Les AINS sont la cause la plus fr\u00e9quente de l\u00e9sions gastroduod\u00e9nales m\u00e9dicamenteuses en dehors de <em>H. pylori<\/em> \u2014 leur utilisation est tr\u00e8s r\u00e9pandue au Qu\u00e9bec (analg\u00e9siques OTC + prescription) ; m\u00e9canismes de la gastro-toxicit\u00e9 des AINS : inhibition de la COX-1 (ubiquitaire) \u2192 r\u00e9duction des prostaglandines gastroprotectrices (PGE2 + PGI2) \u2192 alt\u00e9ration du mucus gastrique (r\u00e9duction de sa viscosit\u00e9 + de sa production) + r\u00e9duction du flux sanguin sous-muqueux + augmentation de la perm\u00e9abilit\u00e9 \u00e9pith\u00e9liale \u2192 l\u00e9sions muqueuses + ulc\u00e8res + h\u00e9morragie \u2014 effet topique direct (AINS acides lipophiles \u2192 accumulation dans les cellules \u00e9pith\u00e9liales \u2192 l\u00e9sion directe) \u2014 les coxibs (inhibiteurs s\u00e9lectifs de la COX-2 : c\u00e9l\u00e9coxib \u2014 Celebrex + \u00e9toricoxib) \u00e9pargnent la COX-1 \u2192 moins de toxicit\u00e9 gastrique (r\u00e9duction de 50 % des ulc\u00e8res endoscopiques vs AINS non s\u00e9lectifs) mais ne prot\u00e8gent pas compl\u00e8tement + risque cardiovasculaire accru ; facteurs de risque de complications gastroduod\u00e9nales sous AINS : \u00e2ge >65 ans + ATCD d'ulc\u00e8re gastroduod\u00e9nal ou d'h\u00e9morragie digestive haute + utilisation concomitante d'aspirine + cortico\u00efdes + anticoagulants + antiplaquettaires + infection \u00e0 <em>H. pylori<\/em> Coexistence with high dose NSAIDs, prolonged duration, heart or kidney failure; endoscopic evaluation of NSAID-induced lesions: erythema, erosions, ulcers - Lanza score (0 to 4) - indication for EGD: gastrointestinal bleeding (melena, hematemesis), unexplained iron deficiency anemia, alarm signs, epigastric pain persistent despite treatment<\/td>\n <td>Pr\u00e9vention et traitement des gastropathies aux AINS : gastroprotection syst\u00e9matique recommand\u00e9e si \u22651 facteur de risque : IPP en 1re ligne : om\u00e9prazole 20 mg\/j + pantoprazole 40 mg\/j + rab\u00e9prazole 20 mg\/j + \u00e9som\u00e9prazole 20\u201340 mg\/j + lansoprazole 30 mg\/j \u2192 r\u00e9duction de 80 % des ulc\u00e8res gastriques + 70 % des ulc\u00e8res duod\u00e9naux li\u00e9s aux AINS \u2014 commencer l'IPP en m\u00eame temps que l'AINS (pas apr\u00e8s l'apparition des sympt\u00f4mes) + misoprostol (Cytotec \u2014 analogue des prostaglandines) : 200 \u00b5g \u00d7 2\u20134\/j \u2192 efficace mais mal tol\u00e9r\u00e9 (diarrh\u00e9es + crampes abdominales) \u2192 r\u00e9serv\u00e9 aux patientes enceintes (propri\u00e9t\u00e9s ut\u00e9rotoniques) ou si CI aux IPP ; strat\u00e9gie si AINS indispensable malgr\u00e9 risque \u00e9lev\u00e9 : pr\u00e9f\u00e9rer un coxib (c\u00e9l\u00e9coxib) + IPP associ\u00e9 \u2192 protection maximale \u2014 \u00e9liminer et \u00e9radiquer <em>H. pylori<\/em> Before starting long-term NSAIDs (ulcer risk reduction); long-term PPIs \u2013 adverse effects to consider: hypomagnesemia + hyponatremia + bone fractures (reduced calcium absorption) + intestinal infections<em>C. difficile<\/em> + pneumonias) + B12 deficiency + interaction with clopidogrel (debate - avoid omeprazole + prefer pantoprazole if combination necessary) \u2192 re-evaluate PPI indication every 6-12 months + gradual discontinuation (withdrawal) if no longer necessary (acid rebound with abrupt stop); topical NSAIDs (diclofenac gel + patch): no significant systemic absorption \u2192 no gastroprotection needed \u2192 to be preferred for local pain + osteoarthritis of small joints<\/td>\n <\/tr>\n <tr>\n <td>Autoimmune gastritis (Biermer's disease)<br><small style=\"font-weight:400;color:#7a8fa0;\">Anti-FI \u2014 vitamine B12 \u2014 surveillance carcino\u00efdes<\/small><\/td>\n <td>La gastrite auto-immune (GAA \u2014 type A \u2014 fundique) est une maladie chronique progressive caract\u00e9ris\u00e9e par la destruction auto-immune des cellules pari\u00e9tales du fundus gastrique par des anticorps IgG anti-cellules pari\u00e9tales (ACP) et anti-facteur intrins\u00e8que (AFI) ; pathogen\u00e8se : auto-anticorps anti-ATPase H+\/K+ (cible sur les cellules pari\u00e9tales) + auto-anticorps anti-facteur intrins\u00e8que (type I = bloquants + type II = pr\u00e9cipitants) \u2192 destruction des cellules pari\u00e9tales \u2192 atrophie progressive du fundus \u2192 achlorhydrie (perte de la s\u00e9cr\u00e9tion acide) + carence en facteur intrins\u00e8que (FI \u2014 n\u00e9cessaire \u00e0 l'absorption de la B12 dans l'il\u00e9on terminal) \u2192 malabsorption de la vitamine B12 \u2192 an\u00e9mie de Biermer ; bilan diagnostique de la gastrite auto-immune : anticorps anti-cellules pari\u00e9tales (ACP) : pr\u00e9sents dans 80\u201390 % des GAA + faible sp\u00e9cificit\u00e9 (positifs dans 10\u201315 % de la population g\u00e9n\u00e9rale asymptomatique \u00e2g\u00e9e) + anticorps anti-facteur intrins\u00e8que (AFI \u2014 type I bloquant) : sp\u00e9cificit\u00e9 98\u2013100 % mais sensibilit\u00e9 seulement 50\u201360 % \u2192 positif = GAA quasi certain \u2192 n\u00e9gatif = ne permet pas d'exclure + gastrine s\u00e9rique (hypergastrin\u00e9mie r\u00e9actionnelle \u2014 >100 pg\/mL \u2014 souvent >500 pg\/mL) : l'achlorhydrie l\u00e8ve le frein sur la s\u00e9cr\u00e9tion de gastrine \u2192 hypergastrin\u00e9mie \u2192 stimule les cellules ECL \u2192 hyperplasie \u2192 risque de carcino\u00efdes gastriques (type 1 \u2014 de bon pronostic) + chromogranine A (CgA) s\u00e9rique : marqueur des cellules endocrines gastriques \u2014 \u00e9lev\u00e9e si hyperplasie ECL + carcino\u00efdes + pepsinog\u00e8ne I (bas dans la GAA \u2014 marqueur indirect de l'atrophie du fundus) + ratio pepsinog\u00e8ne I\/II bas (<3) \u2192 signe d'atrophie fundique ; FOGD avec biopsies multiples (protocole Sydney) : biopsies antrale (2 antre) + fundique (2 fundus) + incisure angulaire \u2014 histologie : atrophie fundique + m\u00e9taplasie pseudopylorique + hyperplasie des cellules ECL \u00b1 carcino\u00efdes de type 1 \u00b1 m\u00e9taplasie intestinale \u2014 absence de <em>H. pylori<\/em> (excluding co-infection) \u2014 dysplasia search<\/td>\n <td>Traitement et surveillance de la gastrite auto-immune : substitution en vitamine B12 : m\u00eame sch\u00e9ma que l'an\u00e9mie de Biermer (voir fiche Globules rouges \/ An\u00e9mie macrocytaire) \u2014 voie IM ou voie orale haute dose selon les pr\u00e9f\u00e9rences et la s\u00e9v\u00e9rit\u00e9 : cyanocobalamine 1 000 \u00b5g IM\/mois \u00e0 vie (ou 1 000\u20132 000 \u00b5g\/j PO si voie orale choisie) + surveillance h\u00e9matologique : NFS + B12 + homocyst\u00e9ine + MMA (acide m\u00e9thylmalonique) \u00e0 1\u20133 mois puis annuellement + corriger les carences associ\u00e9es : fer (fr\u00e9quent \u2014 achlorhydrie \u2192 r\u00e9duction de l'absorption du fer non h\u00e9minique) + folates + zinc + calcium (achlorhydrie \u2192 r\u00e9duction de l'absorption calcique) ; surveillance endoscopique de la gastrite auto-immune : risque de cancer gastrique \u00d7 2\u20133 + risque de carcino\u00efdes gastriques de type 1 (associ\u00e9s \u00e0 l'hypergastrin\u00e9mie) \u2192 FOGD de surveillance : FOGD initiale pour stadification (biopsies protokole Sydney + \u00e9valuation OLGIM) \u2192 si stade OLGIM 0\u2013II et pas de carcino\u00efde \u2192 FOGD tous les 3\u20135 ans (consensus MAPS II \u2014 European Society of Gastroenterology 2019) \u2192 si stade OLGIM III\u2013IV ou carcino\u00efdes (>1 cm ou multiples) \u2192 surveillance annuelle + avis gastroent\u00e9rologie + \u00e9choendoscopie si carcino\u00efde visible ; carcino\u00efdes gastriques de type 1 (associ\u00e9s \u00e0 la GAA) : petits polypes fundiques (<1\u20132 cm) + multiples + de bon pronostic (m\u00e9tastases rares <5 %) + traitement : r\u00e9section endoscopique si <2 cm + surveillance + octr\u00e9otide (analogues de la somatostatine) si multiples + envahissants \u2192 avis gastroent\u00e9rologie ; bilan des maladies auto-immunes associ\u00e9es : TSH + TPO + anticorps anti-thyroglobuline (thyro\u00efdite de Hashimoto associ\u00e9e dans 30 % des GAA) + glyc\u00e9mie + HbA1c (diab\u00e8te de type 1 associ\u00e9 dans 5\u201310 %) + NFS + bilan cutan\u00e9 (vitiligo)<\/td>\n <\/tr>\n <tr>\n <td>Gastrite atrophique et pr\u00e9vention du cancer gastrique<br><small style=\"font-weight:400;color:#7a8fa0;\">M\u00e9taplasie intestinale \u2014 OLGIM \u2014 cascade de Correa<\/small><\/td>\n <td>La gastrite atrophique avec m\u00e9taplasie intestinale (MI) constitue un \u00e9tat pr\u00e9canc\u00e9reux gastrique n\u00e9cessitant une surveillance endoscopique structur\u00e9e ; d\u00e9finitions : atrophie gastrique : perte des glandes sp\u00e9cialis\u00e9es (fundiques ou antrales) avec remplacement par du tissu fibreux ou m\u00e9taplasique \u2192 r\u00e9duction de la surface fonctionnelle muqueuse \u2014 m\u00e9taplasie intestinale (MI) : remplacement de l'\u00e9pith\u00e9lium gastrique par un \u00e9pith\u00e9lium de type intestinal (cellules absorbantes + cellules caliciformes productrices de mucines neutres ou sulfat\u00e9es) \u2192 MI compl\u00e8te (type I \u2014 ent\u00e9rique \u2014 mucines neutres \u2014 faible risque) + MI incompl\u00e8te (types II\u2013III \u2014 gastriques et sulfat\u00e9es \u2014 risque plus \u00e9lev\u00e9 de transformation maligne) ; stadification par OLGIM et OLGA : OLGA (Operative Link for Gastritis Assessment) : score d'atrophie (0\u2013IV) \u2192 stades III\u2013IV = risque \u00e9lev\u00e9 \u2014 OLGIM (Operative Link on Gastric IM Assessment) : score de MI (0\u2013IV) \u2192 stades III\u2013IV = risque cancer \u00e9lev\u00e9 (OR 10\u201315 vs stade 0) \u2192 pr\u00e9f\u00e9r\u00e9 \u00e0 l'OLGA en pratique (meilleure reproductibilit\u00e9 inter-observateurs) + chromoendoscopie haute d\u00e9finition (NBI \u2014 narrow band imaging) : am\u00e9liore la d\u00e9tection des l\u00e9sions de m\u00e9taplasie intestinale + dysplasie par rapport \u00e0 la lumi\u00e8re blanche standard \u2192 recommand\u00e9e pour la surveillance dans les centres sp\u00e9cialis\u00e9s ; facteurs aggravants le risque de cancer gastrique en contexte de MI : MI \u00e9tendue (pangastrique) + MI de type incompl\u00e8te + stade OLGIM III\u2013IV + ATCD familial de cancer gastrique au 1er degr\u00e9 + infection \u00e0 <em>H. pylori<\/em> untreated + active smoking + diet rich in salt and cured meats + antioxidant deficiency (fruits + vegetables + vitamins C + E) + residence or origin from a high-incidence country (Japan + Korea + Latin America + Eastern Europe)<\/td>\n <td>Prise en charge de la gastrite atrophique avec m\u00e9taplasie intestinale : \u00e9radication de <em>H. pylori<\/em> (if not yet done): reduced risk of gastric cancer by 30-40 % if eradication before establishment of intestinal metaplasia - lesser but real benefit even after establishment of IM + lifestyle modification: stop smoking + reduce salty and processed foods + increase fruits and vegetables (antioxidants - vitamins C + E + beta-carotene) + reduce alcohol; endoscopic surveillance - MAPS II recommendations (European Society of Gastrointestinal Endoscopy - ESGE 2019) + Quebec adaptation (CAG): OLGIM stage 0-II with no family risk factors: no systematic surveillance recommended (or FOGD every 3-5 years if MI limited to the antrum) + OLGIM stage III-IV OR extensive MI (pangastric) OR family history of 1st-degree gastric cancer + MI: FOGD every 1-2 years with chromoendoscopy (NBI) + multiple biopsies according to Sydney protocol + low-grade dysplasia (LGD): confirmatory FOGD at 6 months (eliminate missed high-grade lesion) \u2192 then annual FOGD with NBI + biopsies + endoscopic resection if visible lesion + high-grade dysplasia (HGD) or early adenocarcinoma: endoscopic resection (mucosectomy - EMR or submucosal dissection - ESD) or surgery according to Curie criteria - outside early stages : surgery (subtotal or total gastrectomy depending on location) \u00b1 perioperative chemotherapy (FLOT - fluorouracil + leucovorin + oxaliplatin + docetaxel); aspirin and gastric chemoprevention: observational data suggest a protective effect of aspirin on gastric cancer \u2192 no formal recommendation for aspirin chemoprevention in IM - statins: favorable observational data - prospective studies in progress<\/td>\n <\/tr>\n <tr>\n <td>Gastrite de stress et gastrite en r\u00e9animation<br><small style=\"font-weight:400;color:#7a8fa0;\">Pr\u00e9vention IPP \u2014 l\u00e9sions aigu\u00ebs de la muqueuse<\/small><\/td>\n <td>La gastrite de stress (l\u00e9sions aigu\u00ebs de la muqueuse gastroduod\u00e9nale \u2014 LAMGD) est une complication fr\u00e9quente chez les patients en soins critiques \u2014 potentiellement mortelle en cas d'h\u00e9morragie digestive massive ; physiopathologie des LAMGD en r\u00e9animation : isch\u00e9mie de la muqueuse gastrique (vasoconstriction splanchnique lors du choc + hypoperfusion) + hypers\u00e9cr\u00e9tion acide de stress (stimulation sympathique + vagale) + alt\u00e9ration des m\u00e9canismes de d\u00e9fense muqueux (mucus + prostaglandines + bicarbonates) + reflux biliaire en cas de gastrostase \u2192 \u00e9rosions superficielles \u2192 ulc\u00e8res h\u00e9morragiques ; facteurs de risque de LAMGD cliniquement significative (h\u00e9morragie n\u00e9cessitant une transfusion ou une intervention) : ventilation m\u00e9canique \u226548h (risque \u00d7 15 \u2014 facteur de risque majeur) + coagulopathie (TP <50 % ou plaquettes <50 G\/L) + ATCD d'ulc\u00e8re ou d'h\u00e9morragie digestive haute + traumatisme cr\u00e2nien grave (ulc\u00e8re de Cushing \u2014 hypers\u00e9cr\u00e9tion acide neurog\u00e8ne) + br\u00fblures \u00e9tendues (>35 % de la surface corporelle \u2014 ulc\u00e8re de Curling \u2014 isch\u00e9mie muqueuse) + choc + sepsis grave + insuffisance h\u00e9patique ou r\u00e9nale aigu\u00eb + cortico\u00efdes \u00e0 fortes doses + anticoagulants ; incidence de l'h\u00e9morragie digestive cliniquement significative en r\u00e9animation (avec prophylaxie) : 2\u20134 % \u2014 sans prophylaxie : 5\u201310 % ; diagnostic : endoscopie digestive haute en urgence si h\u00e9morragie suspect\u00e9e \u2014 FOGD : \u00e9rosions superficielles multiples + ulc\u00e8res fundiques ou antraux \u2192 classification de Forrest (\u00e9valuation du risque de r\u00e9cidive h\u00e9morragique + d\u00e9cision th\u00e9rapeutique endoscopique)<\/td>\n <td>Prophylaxie des LAMGD en r\u00e9animation : IPP IV : m\u00e9dicament de r\u00e9f\u00e9rence pour la prophylaxie des LAMGD en r\u00e9animation \u2014 pantoprazole 40 mg IV \u00d7 1\u20132\/j (le plus utilis\u00e9) + \u00e9som\u00e9prazole 40 mg IV \u00d7 1\/j + om\u00e9prazole 40 mg IV \u00d7 1\/j \u2192 sup\u00e9riorit\u00e9 sur les anti-H2 d\u00e9montr\u00e9e (m\u00e9ta-analyse PLOS ONE 2013) + r\u00e9duction du risque d'h\u00e9morragie cliniquement significative de 50\u201360 % ; anti-H2 (famotidine + ranitidine retir\u00e9 du march\u00e9) : alternative aux IPP si disponibilit\u00e9 ou allergie \u2014 efficacit\u00e9 moindre sur la prophylaxie des LAMGD ; sucralfate (Sulcrate) : protecteur muqueux (complexe aluminium + sulfate de saccharose \u2014 adh\u00e8re aux ulc\u00e8res + stimule PGE2 + mucus) \u2192 alternative aux IPP dans certains protocoles (avantage th\u00e9orique : pas d'\u00e9l\u00e9vation du pH \u2014 pr\u00e9servation de la flore) \u2192 m\u00e9ta-analyses r\u00e9centes : moins efficace que les IPP pour la prophylaxie \u2014 risque de pneumonie associ\u00e9e aux soins similaire avec les deux approches (\u00e9tudes PEPTIC 2020 \u2014 NEJM) ; nutrition ent\u00e9rale pr\u00e9coce : r\u00e9duit le risque de LAMGD en maintenant le flux sanguin muqueux + en tamponant l'acidit\u00e9 \u2192 recommand\u00e9e dans les 24\u201348h si possible (pr\u00e9vention des LAMGD + b\u00e9n\u00e9fice nutritionnel global) \u2014 la nutrition ent\u00e9rale pr\u00e9coce peut parfois suffire comme prophylaxie si d\u00e9but\u00e9e dans les 24h + patient \u00e0 faible risque ; traitement curatif de l'h\u00e9morragie sur LAMGD : IPP en bolus IV \u2192 perfusion continue (80 mg IV en bolus puis 8 mg\/h \u00d7 72h) si h\u00e9morragie active \u2014 h\u00e9mostase endoscopique (injection d'adr\u00e9naline + clip ou coagulation thermique) si l\u00e9sion accessible \u2014 radiologie interventionnelle (embolisation) si h\u00e9morragie massive non contr\u00f4l\u00e9e endoscopiquement \u2192 chirurgie en dernier recours (gastrectomie + vagotomie) si \u00e9chec des autres approches<\/td>\n <\/tr>\n <\/tbody>\n <\/table>\n\n <div class=\"co-infobox\">\n <span class=\"ico\">\u2139\ufe0f<\/span>\n <span><strong><em>H. pylori<\/em> \u2014 Test and treat for uninvestigated dyspepsia:<\/strong> In a patient under 60 years old with dyspepsia and no alarm signs (no weight loss, no bleeding, no dysphagia, no anemia), the \u00abtest and treat\u00bb strategy\u2014testing for <em>H. pylori<\/em> by breath test or fecal antigen and treat if positive without prior EGD \u2014 is recommended by Canadian and Quebec guidelines (CAG + INESSS). This approach is cost-effective and avoids unnecessary endoscopies. EGD is only indicated upfront in the presence of alarm signs or in patients aged 60 years and older (increased risk of gastric cancer).<\/span>\n <\/div>\n\n <div class=\"co-urgence\">\n <div class=\"co-urgence-titre\">Situations requiring urgent medical assessment<\/div>\n <p><strong>H\u00e9mat\u00e9m\u00e8se (vomissements de sang) ou m\u00e9l\u00e9na (selles noires goudronneuses) avec instabilit\u00e9 h\u00e9modynamique<\/strong> high gastrointestinal bleeding from erosive gastritis or ulcer \u2192 emergency \u2192 emergency EGD + resuscitation + IV PPI bolus + continuous infusion.<\/p>\n <p><strong>\u00c9pigastralgies + signes d'alarme (amaigrissement >5 % + dysphagie + an\u00e9mie + masse palpable)<\/strong> \u2192 FOGD urgente (<2 semaines) quel que soit l'\u00e2ge \u2192 \u00e9liminer un cancer gastrique.<\/p>\n <p><strong>Patient sous AINS + douleurs \u00e9pigastriques + an\u00e9mie ferriprive ou m\u00e9l\u00e9na<\/strong> \u2192 immediate cessation of NSAIDs + urgent EGD + IV PPI + search for <em>H. pylori<\/em> on biopsies.<\/p>\n <p><strong>Dyspepsie r\u00e9fractaire + achlorhydrie + an\u00e9mie macrocytaire + paresth\u00e9sies chez un patient avec maladies auto-immunes connues<\/strong> Autoimmune gastritis of Biermer \u2192 B12 dosage + anti-Intrinsic Factor antibodies + parietal cell antibodies + upper endoscopy + urgent B12 replacement if neurological symptoms.<\/p>\n <\/div>\n\n <h2>Consult at Clinique Omicron<\/h2>\n <p>Les m\u00e9decins de Clinique Omicron prennent en charge les dyspepsies et les gastrites dans le cadre de la strat\u00e9gie \u00ab test and treat \u00bb recommand\u00e9e au Qu\u00e9bec \u2014 prescription du test respiratoire \u00e0 l'ur\u00e9e ou de l'antig\u00e8ne f\u00e9cal, initiation du traitement d'\u00e9radication de <em>H. pylori<\/em>, adjustment of gastroprotection in patients on NSAIDs, and referral to gastroenterology for atrophic forms requiring endoscopic monitoring. These services are available at several service points in Quebec and through telemedicine. To make an appointment, visit <a href=\"https:\/\/cliniqueomicron.ca\">cliniqueomicron.ca<\/a>.<\/p>\n\n <p class=\"co-disclaimer\">Le contenu de cette page est fourni \u00e0 titre informatif uniquement et ne remplace pas l'avis d'un m\u00e9decin ou d'un gastroent\u00e9rologue. Tout sympt\u00f4me digestif persistant ou accompagn\u00e9 de signes d'alarme doit \u00eatre \u00e9valu\u00e9 rapidement par un professionnel de sant\u00e9.<\/p>\n<\/div>\n<\/body>\n<\/html>\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t\t\t<\/div>","protected":false},"excerpt":{"rendered":"<p> Gastroent\u00e9rologie & M\u00e9decine de famille & M\u00e9decine interne Gastrite La gastrite d\u00e9signe une inflammation de la muqueuse de l’estomac, confirm\u00e9e histologiquement par la pr\u00e9sence d’un infiltrat inflammatoire \u00e0 la biopsie gastrique. Elle se distingue de la dyspepsie fonctionnelle \u2014 syndrome clinique de douleurs \u00e9pigastriques sans l\u00e9sion muqueuse identifiable \u2014 et de la gastropathie, terme… <a href=\"https:\/\/cliniqueomicron.ca\/en\/gastrite\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">Gastrite : sympt\u00f4mes, causes et traitement | Clinique Omicron<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"om_disable_all_campaigns":false,"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"off","neve_meta_content_width":100,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","_themeisle_gutenberg_block_has_review":false,"_metasync_otto_title":"Gastrite : causes, sympt\u00f4mes, | Brossard | Clinique Omicron","_metasync_otto_description":"La gastrite est une inflammation de la muqueuse gastrique. Helicobacter pylori, AINS, gastrite auto-immune, traitement par IPP et prise en charge au Qu\u00e9bec.","_metasync_otto_keywords":"","_metasync_otto_og_title":"Gastrite : causes, sympt\u00f4mes, | Brossard | Clinique Omicron","_metasync_otto_og_description":"","_metasync_otto_twitter_title":"Gastrite : causes, sympt\u00f4mes, | Brossard | Clinique Omicron","_metasync_otto_twitter_description":"La gastrite est une inflammation de la muqueuse gastrique. Helicobacter pylori, AINS, gastrite auto-immune, traitement par IPP et prise en charge au Qu\u00e9bec.","rank_math_title":"","rank_math_description":"","_yoast_wpseo_title":"","_yoast_wpseo_metadesc":"","_aioseo_title":null,"_aioseo_description":"Reconnaissez et traitez la gastrite : douleurs, causes et options th\u00e9rapeutiques \u2014 consultez un m\u00e9decin en priv\u00e9 ou RAMQ dans nos points de service au Qu\u00e9bec.","_metasync_seo_title":"","_metasync_seo_desc":"","_metasync_breadcrumb_title":"","_metasync_primary_category":0,"_metasync_primary_product_cat":0,"_metasync_otto_disabled":"","_metasync_hreflang":"","_metasync_plugin_sync_ts":"{\"aioseo\":\"2026-06-21T17:17:36+00:00\"}","_metasync_robots_advanced":"","footnotes":""},"class_list":["post-24598","page","type-page","status-publish","hentry"],"aioseo_notices":[],"aioseo_head":"\n\t\t\n\t<meta name=\"description\" content=\"La gastrite est une inflammation de la muqueuse gastrique. 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