Gastroenterology & Family Medicine & Internal Medicine
Gastritis
Gastritis refers to an inflammation of the stomach lining, histologically confirmed by the presence of an inflammatory infiltrate in a gastric biopsy. It is distinguished from functional dyspepsia—a clinical syndrome of epigastric pain without identifiable mucosal lesions—and gastropathy, a term describing mucosal lesions without significant inflammatory infiltrate (such as NSAID-induced or hypertensive gastropathy). Gastritis is classified according to its evolution (acute or chronic), topography (antral, fundic, or pangastritis), histological appearance (superficial, atrophic, metaplastic), and etiology. Helicobacter pylori remains the most frequent cause of chronic gastritis worldwide—responsible for over 90% of active chronic gastritis—and its eradication is one of the most cost-effective treatments in medicine. Atrophic chronic gastritis, whether secondary to H. pylori or autoimmune in origin (type A gastritis – Biermer's disease), represents a recognized precancerous state that can progress to intestinal metaplasia, dysplasia, and then gastric adenocarcinoma in the Correa cascade.
Classification, etiologies, and clinical presentation
- Histological classification of gastritis — revised Sydney System: the Sydney System (revised in 1994 – Houston) is the reference classification for gastritis — it integrates topography + histology + etiology; topography: antral gastritis (predominant in the antrum — gastritis with H. pylori classic) + fundic gastritis (predominantly in the fundus/body - autoimmune gastritis) + pangastritis (involvement of the entire mucosa - advanced stage of gastritis) H. pylori or diffuse chemical gastritis); histological parameters graded (0 to 3 — 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 — goblet cells) + presence of H. pylori ; score OLGIM (Operative Link on Gastric Intestinal Metaplasia): staging of gastric cancer risk according to the extent and severity of intestinal metaplasia — stages 0 to IV — stages III–IV → high risk → intensified endoscopic surveillance; Correa cascade (intestinal-type gastric carcinogenesis): normal mucosa → superficial gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → gastric adenocarcinoma — each stage is influenced by H. pylori + tobacco + salty food + lack of fruits and vegetables
- Main etiologies of gastritis: gastritis Helicobacter pylori (type B — antral predominant): most frequent cause globally (50 % of the world's population infected - variable prevalence: <30 % dans les pays développés + 70–90 à bas revenus) — au québec : prévalence estimée 20–35 (population générale) → plus élevée communautés autochtones immigrants de première génération transmission oro-fécale ou oro-orale (enfance surtout conditions socioéconomiques promiscuité eau non traitée) H. pyloriem Microaerophilic spiral Gram-negative bacillus - colonizes gastric mucosa (superficial mucus layer) - virulence factors: urease (neutralizes local acidity) + CagA (oncoprotein - cagA+ strains → 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 → reduced synthesis of gastroprotective prostaglandins → altered mucus + reduced mucosal blood flow) + bile reflux (partial gastrectomy + gastric bypass + incompetent pylorus) + alcohol (direct caustic effect) + corticoids (potentiate effect of NSAIDs - alone → low risk of gastritis); autoimmune gastritis (type A - fundic): anti-parietal cell + antiintrinsic factor antibodies → destruction of fundus parietal cells → achlorhydria + intrinsic factor deficiency → vitamin B12 malabsorption → 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 : H. pylori (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 (*H. heilmannii* + 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 + H. pylori)
- Clinical presentation and peculiarities: gastritis H. pylori : often asymptomatic (70–80 % of carriers) — when symptomatic: dyspepsia (epigastric pain or discomfort + early satiety + bloating + nausea) — gastritis H. pylori does not systematically cause symptoms — but to eradicate H. pylori in dyspeptic patients, it improves symptoms in an additional 10–15 % of cases compared to placebo (modest but real effect — «test and treat» recommended for uninvestigated dyspepsia) <60 ans sans signes d'alarme au québec) ; gastrite érosive aiguë aux ains : souvent asymptomatique — symptômes si présents épigastralgies + nausées vomissements risque de complications (ulcère hémorragie digestive haute) précurseurs (paradoxe des → analgésiques masquent la douleur) surveillance et prévention importantes chez les patients à auto-immune biermer insidieuse carence b12 asthénie progressive pâleur glossite (langue rouge vernissée dépapillée) neurologiques (paresthésies ataxie signe lhermitte syndrome dégénérescence combinée subaiguë moelle) achlorhydrie (perte l'acidité gastrique dyspepsie diarrhée malabsorption fer calcium) devant une nécessitant endoscopie urgente (règles «alarm»): anémie lésion palpable (masse abdominale) amaigrissement inexpliqué (>5 % weight loss in 3-6 months) + Persistent regurgitation + Melena / hematemesis → Urgent EGD ((Less than 2 weeks) regardless of age
Diagnosis, treatment, and monitoring
| Clinical situation | Diagnosis | Treatment and follow-up |
|---|---|---|
| Gastritis H. pylori Screening — eradication — control |
Diagnostic Methods for Infection H. pylori : non-invasive tests (recommended as a first-line treatment in the absence of an indication for EGD): ¹³C-labeled urea breath test (UBT): 95% sensitivity % + 96% specificity % — mechanism: ingestion of labeled urea → urease from H. pylori → Labeled CO2 expired → detection by infrared spectroscopy — conditions: PPIs stopped for ≥2 weeks + antibiotics stopped for ≥4 weeks (false negatives) → non-invasive gold standard test for post-eradication control + fecal antigen test (fecal Ag — monoclonal ELISA): sensitivity 94 % + specificity 97 % — as effective as UBT — same conditions (stop PPIs + antibiotics) — practical + inexpensive — recommended by several Quebec algorithms (INESSS) as first-line diagnosis in uninvestigated dyspepsia in <60 ans sans signes d'alarme + sérologie H. pyloriem (IgG) : moins recommandée en pratique courante — sensibilité 80–90 % + spécificité 75–90 % — IgG restent positives des années après éradication (pas utile pour le contrôle post-traitement) — utile si IPP impossible à arrêter ou en épidémiologie ; tests invasifs (biopsies lors de la FOGD) : test rapide à l'uréase (CLO test) : résultat en 1–24h + sensibilité 90–95 % (réduite si IPP ou antibiotiques récents) — histologie + coloration spéciale (Giemsa + Warthin-Starry + immunohistochimie) : sensibilité 90–95 % + référence pour évaluer la gastrite (atrophie + métaplasie + grade OLGIM) — culture + antibiogramme : indispensable si suspicion de résistance ou échec de 2e ligne (disponible au LSPQ + laboratoires spécialisés) — PCR sur biopsie : détection + résistances (clarithromycine + lévofloxacine) en une seule analyse — disponibilité croissante au Québec | Eradication treatment of H. pylori — Canadian Recommendations (CAG 2022 + INESSS Québec): «Test and Treat» Strategy: In patients <60 years with uninvestigated dyspepsia + without alarm signs + without ATCD of ulcer → test (UBT or fecal Ag) → if positive: treat without prior FOGD → if symptoms persist after eradication → FOGD; 1st-line regimens: bismuth quadritherapy × 14 days (now 1st-line recommended in Canada due to increasing resistance to clarithromycin): bismuth subsalicylate (Pepto-Bismol 2 tablets × 4/d) + tetracycline 500 mg × 4/d + metronidazole 500 mg × 3/d + PPI × 2/d → eradication rate: 85-95 % + standard triple therapy × 14 days (if low resistance to clarithromycin documented locally - <15 %): PPI × 2/d + amoxicillin 1 g × 2/d + clarithromycin 500 mg × 2/d → eradication rate: 70-85 % (declining in Canada) + sequential or concomitant therapy (OCAP): omeprazole + clarithromycin + amoxicillin + metronidazole × 10-14 days → limited Canadian data + not recommended in 1st line by all experts; 2nd line regimens (if 1st line fails): bismuth quadritherapy if triple therapy used in 1st line - or levofloxacin-based triple therapy (PPI + amoxicillin + levofloxacin 500 mg × 2/d × 14 days) - or culture + antibiogram guiding 3rd-line treatment + post-eradication control: mandatory 4-8 weeks after end of treatment (PPI stopped ≥2 weeks before) → UBT or fecal Ag - do not use serology for control |
| NSAID-induced gastritis and drug-induced gastropathy Prevention - PUD - COXIBs |
NSAIDs are the most common cause of drug-induced gastroduodenal lesions outside of H. pylori - their use is widespread in Quebec (OTC analgesics + prescription); mechanisms of NSAID gastro-toxicity : inhibition of COX-1 (ubiquitous) → reduction in gastroprotective prostaglandins (PGE2 + PGI2) → alteration of gastric mucus (reduction in its viscosity + production) + reduction in submucosal blood flow + increased epithelial permeability → mucosal lesions + ulcers + bleeding - direct topical effect (lipophilic acid NSAIDs → accumulation in epithelial cells → direct lesion) - coxibs (selective COX-2 inhibitors : celecoxib - Celebrex + etoricoxib) spare COX-1 → less gastric toxicity (50 % reduction in endoscopic ulcers vs. non-selective NSAIDs) but do not protect completely + increased cardiovascular risk; risk factors for gastroduodenal complications on NSAIDs: age >65 years + history of peptic ulcer or upper GI bleeding + concomitant use of aspirin + corticosteroids + anticoagulants + antiplatelet agents + infection with H. pylori 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 | Prévention et traitement des gastropathies aux AINS : gastroprotection systématique recommandée si ≥1 facteur de risque : IPP en 1re ligne : oméprazole 20 mg/j + pantoprazole 40 mg/j + rabéprazole 20 mg/j + ésoméprazole 20–40 mg/j + lansoprazole 30 mg/j → réduction de 80 % des ulcères gastriques + 70 % des ulcères duodénaux liés aux AINS — commencer l'IPP en même temps que l'AINS (pas après l'apparition des symptômes) + misoprostol (Cytotec — analogue des prostaglandines) : 200 µg × 2–4/j → efficace mais mal toléré (diarrhées + crampes abdominales) → réservé aux patientes enceintes (propriétés utérotoniques) ou si CI aux IPP ; stratégie si AINS indispensable malgré risque élevé : préférer un coxib (célécoxib) + IPP associé → protection maximale — éliminer et éradiquer H. pylori Before starting long-term NSAIDs (ulcer risk reduction); long-term PPIs – adverse effects to consider: hypomagnesemia + hyponatremia + bone fractures (reduced calcium absorption) + intestinal infectionsC. difficile + pneumonias) + B12 deficiency + interaction with clopidogrel (debate - avoid omeprazole + prefer pantoprazole if combination necessary) → 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 → no gastroprotection needed → to be preferred for local pain + osteoarthritis of small joints |
| Autoimmune gastritis (Biermer's disease) Anti-Intrinsic Factor — Vitamin B12 — Carcinoid Surveillance |
Autoimmune gastritis (GAA - type A - fundic) is a chronic progressive disease characterized by autoimmune destruction of gastric fundus parietal cells by IgG anti-parietal cell (ACP) and anti-intrinsic factor (AFI) antibodies; pathogenesis: anti-ATPase H+/K+ autoantibodies (target on parietal cells) + antiintrinsic factor autoantibodies (type I = blocking + type II = precipitating) → destruction of parietal cells → progressive fundus atrophy → achlorhydria (loss of acid secretion) + intrinsic factor deficiency (IF - required for B12 absorption in the terminal ileum) → vitamin B12 malabsorption → Biermer's anemia ; diagnostic work-up for autoimmune gastritis: anti-parietal cell antibodies (ACP): present in 80-90 % of GAA + low specificity (positive in 10-15 % of asymptomatic elderly general population) + antiintrinsic factor antibodies (AFI - type I blocking): specificity 98-100 % but sensitivity only 50-60 % → positive = GAA almost certain → negative = cannot exclude + serum gastrin (reactive hypergastrinemia - >100 pg/mL - often >500 pg/mL): achlorhydria lifts the brake on gastrin secretion → hypergastrinemia → stimulates ECL cells → hyperplasia → risk of gastric carcinoids (type 1 - good prognosis) + serum chromogranin A (CgA): marker of gastric endocrine cells - elevated if ECL hyperplasia + carcinoids + pepsinogen I (low in GAA - indirect marker of fundus atrophy) + low pepsinogen I/II ratio (<3) → sign of fundus atrophy; FOGD with multiple biopsies (Sydney protocol): antral (2 antrales) + fundic (2 funduses) + angular incisure biopsies - histology: fundic atrophy + pseudopyloric metaplasia + ECL cell hyperplasia ± type 1 carcinoids ± intestinal metaplasia - absence of H. pylori (excluding co-infection) — dysplasia search | Treatment and monitoring of autoimmune gastritis: vitamin B12 substitution: same regimen as for Biermer's anemia (see Red Blood Cells / Macrocytic Anemia fact sheet) - IM or high-dose oral route depending on preference and severity: cyanocobalamin 1,000 µg IM/month for life (or 1,000-2,000 µg/d PO if oral route chosen) + hematological monitoring: CBC + B12 + homocysteine + MMA (methylmalonic acid) at 1-3 months then annually + correct associated deficiencies: iron (frequent - achlorhydria → reduced absorption of non-haem iron) + folate + zinc + calcium (achlorhydria → reduced calcium absorption); endoscopic surveillance of autoimmune gastritis: risk of gastric cancer × 2-3 + risk of type 1 gastric carcinoids (associated with hypergastrinemia) → surveillance FOGD: initial FOGD for staging (protokole Sydney biopsies + OLGIM evaluation) → if OLGIM stage 0-II and no carcinoid → FOGD every 3-5 years (MAPS II consensus - European Society of Gastroenterology 2019) → if OLGIM stage III-IV or carcinoids (>1 cm or multiple) → annual surveillance + gastroenterology opinion + echoendoscopy if visible carcinoid; type 1 gastric carcinoids (associated with GAA): small fundic polyps (<1-2 cm) + multiple + good prognosis (rare metastases <5 %) + treatment: endoscopic resection if <2 cm + monitoring + octreotide (somatostatin analogues) if multiple + invasive → gastroenterology opinion; assessment of associated autoimmune diseases: TSH + TPO + anti-thyroglobulin antibodies (Hashimoto's thyroiditis associated in 30 % of GAAs) + glycemia + HbA1c (type 1 diabetes associated in 5-10 %) + CBC + skin assessment (vitiligo) |
| Atrophic gastritis and gastric cancer prevention Intestinal metaplasia — OLGIM — Correa cascade |
Atrophic gastritis with intestinal metaplasia (MI) constitutes a gastric precancerous condition requiring structured endoscopic surveillance; definitions: gastric atrophy: loss of specialized glands (fundic or antral) with replacement by fibrous or metaplastic tissue → reduction in functional mucosal surface area - intestinal metaplasia (MI): replacement of gastric epithelium by intestinal-type epithelium (absorptive cells + neutral or sulfated mucin-producing caliciform cells) → complete MI (type I - enteric - neutral mucins - low risk) + incomplete MI (types II-III - gastric and sulfated - higher risk of malignant transformation); staging by OLGIM and OLGA : OLGA (Operative Link for Gastritis Assessment): atrophy score (0-IV) → stages III-IV = high risk - OLGIM (Operative Link on Gastric IM Assessment): IM score (0-IV) → stages III-IV = high cancer risk (OR 10-15 vs. stage 0) → preferred to OLGA in practice (better inter-observer reproducibility) + high-definition chromoendoscopy (NBI - narrow band imaging): improves detection of intestinal metaplasia + dysplasia lesions compared to standard white light → recommended for surveillance in specialized centers; factors aggravating the risk of gastric cancer in the context of MI: extensive MI (pangastric) + incomplete-type MI + OLGIM III-IV stage + family history of gastric cancer in the 1st degree + infection with H. pylori 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) | Management of atrophic gastritis with intestinal metaplasia: eradication of H. pylori (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) → 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) ± perioperative chemotherapy (FLOT - fluorouracil + leucovorin + oxaliplatin + docetaxel); aspirin and gastric chemoprevention: observational data suggest a protective effect of aspirin on gastric cancer → no formal recommendation for aspirin chemoprevention in IM - statins: favorable observational data - prospective studies in progress |
| Stress gastritis and critical care gastritis PPI Prevention — acute mucosal lesions |
Stress gastritis (acute damage to the gastroduodenal mucosa - ADGPL) is a frequent complication in critical care patients - potentially fatal in the event of massive digestive hemorrhage; pathophysiology of ADGPL in intensive care: ischemia of the gastric mucosa (splanchnic vasoconstriction during shock + hypoperfusion) + stress acid hypersecretion (sympathetic + vagal stimulation) + impaired mucosal defense mechanisms (mucus + prostaglandins + bicarbonates) + bile reflux in case of gastrostasis → superficial erosions → bleeding ulcers; risk factors for clinically significant LAMGD (hemorrhage requiring transfusion or intervention): mechanical ventilation ≥48h (risk × 15 - major risk factor) + coagulopathy (TP <50 % or platelets 35 % body surface area - Curling ulcer - mucosal ischemia) + shock + severe sepsis + acute hepatic or renal failure + high-dose corticoids + anticoagulants ; incidence of clinically significant GI bleeding in intensive care (with prophylaxis) : 2-4 % - without prophylaxis: 5-10 %; diagnosis: emergency upper GI endoscopy if hemorrhage suspected - FOGD: multiple superficial erosions + fundic or antral ulcers → Forrest classification (assessment of risk of hemorrhagic recurrence + endoscopic therapeutic decision) | Prophylaxis of LAMGD in intensive care: IV PPI : reference drug for LAMGD prophylaxis in intensive care - pantoprazole 40 mg IV × 1-2/d (most widely used) + esomeprazole 40 mg IV × 1/d + omeprazole 40 mg IV × 1/d → superiority over anti-H2 demonstrated (meta-analysis PLOS ONE 2013) + reduction in risk of clinically significant bleeding by 50-60 %; anti-H2 (famotidine + ranitidine withdrawn from the market): alternative to PPIs if available or allergic - less effective on LAMGD prophylaxis; sucralfate (Sulcrate): mucosal protector (aluminum complex + sucrose sulfate - adheres to ulcers + stimulates PGE2 + mucus) → alternative to PPIs in certain protocols (theoretical advantage: no pH elevation - preservation of flora) → recent meta-analyses: less effective than PPIs for prophylaxis - similar risk of healthcare-associated pneumonia with both approaches (PEPTIC 2020 studies - NEJM); early enteral nutrition: reduces risk of LAMGD by maintaining mucosal blood flow + buffering acidity → recommended within 24-48h if possible (prevention of LAMGD + overall nutritional benefit) - early enteral nutrition can sometimes suffice as prophylaxis if started within 24h + low-risk patient; curative treatment of bleeding on LAMGD: PPI IV bolus → continuous infusion (80 mg IV bolus then 8 mg/h × 72h) if active hemorrhage - endoscopic hemostasis (adrenaline injection + clip or thermal coagulation) if lesion accessible - interventional radiology (embolization) if massive hemorrhage not controlled endoscopically → surgery as last resort (gastrectomy + vagotomy) if other approaches fail |
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H. pylori — Test and treat for uninvestigated dyspepsia: In a patient under 60 years old with dyspepsia and no alarm signs (no weight loss, no bleeding, no dysphagia, no anemia), the «test and treat» strategy—testing for H. pylori by breath test or fecal antigen and treat if positive without prior EGD — 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).
Situations requiring urgent medical assessment
Hematemesis (vomiting blood) or melena (tarry black stools) with hemodynamic instability high gastrointestinal bleeding from erosive gastritis or ulcer → emergency → emergency EGD + resuscitation + IV PPI bolus + continuous infusion.
Epigastric pain + alarm signs (weight loss >5 % + dysphagia + anemia + palpable mass) → Urgent FOGD(Less than 2 weeks) regardless of age → rule out gastric cancer.
Patient on NSAIDs + epigastric pain + iron deficiency anemia or melena → immediate cessation of NSAIDs + urgent EGD + IV PPI + search for H. pylori on biopsies.
Refractory dyspepsia + achlorhydria + macrocytic anemia + paresthesias in a patient with known autoimmune diseases Autoimmune gastritis of Biermer → B12 dosage + anti-Intrinsic Factor antibodies + parietal cell antibodies + upper endoscopy + urgent B12 replacement if neurological symptoms.
Consult at Clinique Omicron
The doctors at Clinique Omicron manage dyspepsia and gastritis as part of the «test and treat» strategy recommended in Quebec — prescribing the urea breath test or fecal antigen test, initiating eradication therapy H. pylori, 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 cliniqueomicron.ca.
The content of this page is provided for informational purposes only and does not replace the advice of a doctor or gastroenterologist. Any persistent digestive symptoms or those accompanied by warning signs should be rapidly evaluated by a healthcare professional.
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