Gastritis medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Aravind Reddy Kothagadi M.B.B.S[3]

Overview

Gastritis encompasses a heterogeneous group of conditions, and treatment is directed by the underlying etiology. Offending agents (particularly NSAIDs and alcohol) should be discontinued. Proton pump inhibitors (PPIs) form the backbone of acid suppression across most subtypes but should be prescribed only when a valid indication exists and deprescribed promptly thereafter.

For Helicobacter pylori gastritis — the most common form worldwide — the 2024 American College of Gastroenterology (ACG) guideline and the 2022 Maastricht VI/Florence Consensus Report establish optimized bismuth quadruple therapy (BQT) as the preferred empiric first-line regimen, replacing clarithromycin-based triple therapy which is no longer recommended empirically due to rising global resistance rates. Vonoprazan-based dual or triple therapy and rifabutin-based triple therapy are recognized alternative first-line regimens. All eradication regimens must be given for 14 days, followed by mandatory test of cure.

For other subtypes: autoimmune gastritis requires lifelong parenteral vitamin B12 and iron replacement, with endoscopic surveillance for gastric cancer and neuroendocrine tumors; NSAID-associated gastropathy is managed with risk-stratified PPI co-therapy or COX-2 selective inhibitors; stress-related mucosal disease in the ICU is treated with PPI or H2RA while qualifying risk factors persist, then discontinued at ICU discharge per the 2024 SCCM/ASHP guideline; eosinophilic gastritis is treated with dietary elimination and corticosteroids, with dupilumab as an emerging option; CMV gastritis requires IV ganciclovir in immunocompromised hosts; and bile reflux gastropathy is managed with ursodeoxycholic acid and sucralfate. Rational PPI deprescribing and gastroprotection in patients on antiplatelet or anticoagulant therapy must also be kept in consideration.

Classification

Gastritis Subtype	Etiology
Alcohol-related Gastritis	Chemical/toxic mucosal injury
Autoimmune Gastritis	Anti-parietal cell antibodies; intrinsic factor deficiency
Bile Reflux Gastropathy	Duodenogastric reflux of bile acids / pancreatic enzymes
CMV Gastritis	Cytomegalovirus (viral, immunocompromised host)
Eosinophilic Gastritis	Immune-mediated / allergic (IL-4/IL-13 pathway)
Fungal Gastritis	Candida, Histoplasma, Aspergillus (immunocompromised)
Granulomatous Gastritis	Crohn's disease, sarcoidosis, TB, fungal, idiopathic
Helicobacter pylori Gastritis	Chronic bacterial infection (H. pylori)
Lymphocytic Gastritis	H. pylori, celiac disease, idiopathic
NSAID-associated Gastropathy	Prostaglandin depletion (COX-1 inhibition)
Phlegmonous/Suppurative Gastritis	Bacterial submucosa infection (Streptococcus pyogenes, gram-negatives)
Radiation Gastritis	Ionizing radiation injury (acute and chronic)
Stress-related Mucosal Disease (SRMD)	Ischemia in critical illness

Alcohol-Related Gastritis

Acute alcoholic gastropathy manifests as subepithelial hemorrhage, erosions, and edema visible on endoscopy. Chronic alcohol use leads to progressive gastric mucosal atrophy and may impair mucosal defense mechanisms independently of acid.

Acute Alcoholic Gastropathy

• Alcohol cessation is the primary intervention and is often sufficient for resolution of acute injury.
• Proton pump inhibitors (e.g., omeprazole 20–40 mg orally once or twice daily) suppress acid, promote mucosal healing, and control epigastric pain.
• Sucralfate 1 g orally four times daily may provide additional mucosal protection and is particularly useful in patients with erosive disease.
• H2 receptor antagonists (e.g., famotidine 20–40 mg orally twice daily) are an acceptable alternative to PPIs when cost or drug interactions are a concern.
• Patients with alcohol use disorder should be assessed for thiamine deficiency and treated prophylactically with thiamine 100 mg intravenously or intramuscularly before any glucose administration to prevent Wernicke's encephalopathy.
• Helicobacter pylori testing should be performed and eradication offered if positive.

Chronic Alcohol-Related Gastric Changes

• Repeat endoscopy is recommended if symptoms persist despite abstinence and PPI therapy, to exclude chronic atrophic gastritis or other structural pathology.
• Alcohol cessation counseling and referral to addiction services are essential for long-term management.

Autoimmune Gastritis

Autoimmune gastritis results from immune-mediated destruction of parietal cells, leading to achlorhydria, loss of intrinsic factor, and vitamin B12 deficiency (pernicious anemia). There is no disease-modifying therapy currently available. Autoimmune gastritis is the pathological substrate of pernicious anemia, and the two conditions represent a continuum; type I gastric neuroendocrine tumors arise from hypergastrinemia-driven enterochromaffin-like cell proliferation. Risk of gastric adenocarcinoma is increased approximately 3-fold above the general population.

Recommended diagnostic workup:

• Serum anti-parietal cell antibodies (sensitivity ~90% but poor specificity) and anti-intrinsic factor antibodies (specificity ~99%, sensitivity ~50–70%)
• Fasting serum gastrin (markedly elevated due to hypochlorhydria-driven antral G-cell stimulation)
• Pepsinogen I and pepsinogen I/II ratio (pepsinogen I <25 µg/L and pepsinogen I/II ratio <3 suggest severe corpus atrophy)
• Serum vitamin B12, iron, ferritin, transferrin saturation, and complete blood count
• Thyroid function tests and anti-thyroid peroxidase antibodies (autoimmune thyroid disease co-occurs in up to one-third of patients with autoimmune gastritis)
• Upper endoscopy with gastric mapping biopsies (Sydney protocol: minimum 5 biopsies from antrum, incisura angularis, and corpus) at the time of diagnosis

Medical Treatment

• Vitamin B12 replacement: Parenteral hydroxocobalamin 1 mg intramuscularly every 2–3 months is the conventional lifelong replacement therapy when intrinsic factor deficiency is established. This dosing schedule has limited evidence; the 2024 NICE guideline NG239 on vitamin B12 deficiency acknowledges that many patients may require more frequent injections for adequate symptom control. High-dose oral cyanocobalamin (1000–2000 mcg daily) achieves adequate serum levels via passive intestinal absorption in patients who decline injections, but parenteral routes remain preferred.
• Iron deficiency anemia should be treated with oral or intravenous iron supplementation. Oral iron (e.g., ferrous sulfate 325 mg one to three times daily) is first-line; however, hypochlorhydria impairs absorption, and IV iron (e.g., ferric carboxymaltose, iron sucrose) is preferred when oral formulations are ineffective or not tolerated.
• PPI therapy in autoimmune gastritis should be avoided unless there is a separate specific indication, as these patients already have markedly reduced acid secretion and long-term PPI use may promote hypergastrinemia and increase the risk of type I gastric carcinoid tumors.
• H. pylori eradication therapy should be offered if concurrent infection is identified, as it may modulate the autoimmune process.

Endoscopic Surveillance

• Regular endoscopic surveillance with gastric mapping biopsies is recommended given the increased risk of gastric cancer and gastric neuroendocrine tumors.
• Current guidelines recommend upper endoscopy at diagnosis and subsequent surveillance every 3–5 years depending on degree of atrophy; annual monitoring of vitamin B12, ferritin, and CBC.
• Autoimmune thyroid disease screening (TSH, anti-thyroid peroxidase antibodies) should be performed at diagnosis and periodically thereafter.
• Type I gastric neuroendocrine tumors >1–2 cm, rapidly increasing in number, or with invasion require endoscopic resection or specialist referral for consideration of somatostatin analogue therapy.

Bile Reflux Gastropathy

Bile reflux gastropathy occurs primarily in post-surgical patients (e.g., following Billroth II gastrectomy, total or subtotal gastrectomy, or Roux-en-Y gastric bypass) and is characterized by bile acid–induced mucosal injury manifesting as diffuse erythema, erosions, and foveolar hyperplasia on endoscopy. Lifestyle modifications (small meals, avoidance of fatty foods, avoiding recumbency after meals) are first-line non-pharmacological measures.

Sucralfate

Sucralfate (1 g orally four times daily, 30 minutes before meals) forms a protective barrier over the gastric mucosa and may chelate bile acids within the gastric lumen; it is a first-line pharmacological agent for bile reflux gastropathy.

Ursodeoxycholic Acid (UDCA)

Ursodeoxycholic acid (250–500 mg orally twice daily) reduces the cytotoxicity of the bile acid pool and has been shown to reduce symptoms and mucosal injury; it is considered a primary pharmacological agent.

Prokinetics

Prokinetic agents (e.g., metoclopramide 10 mg orally three times daily, or domperidone where available) enhance gastric emptying and reduce duodenogastric reflux; they may be particularly useful in patients with concurrent gastroparesis.

Cholestyramine

Cholestyramine (4 g orally one to four times daily) binds bile acids within the lumen, reducing mucosal contact; however, tolerability is often limited by constipation and GI side effects.

Surgical Therapy

Surgical revision (e.g., conversion to Roux-en-Y anatomy with a Roux limb of ≥40–60 cm) may be considered in patients with refractory symptoms and documented bile reflux, particularly after initial medical therapy failure.

CMV Gastritis

Cytomegalovirus (CMV) gastritis occurs almost exclusively in immunocompromised patients (HIV/AIDS, solid organ or hematopoietic stem cell transplant recipients, patients receiving high-dose immunosuppressive therapy). Diagnosis requires endoscopic biopsy demonstrating characteristic CMV inclusion bodies (confirmed by CMV immunohistochemistry or in situ hybridization), supported by peripheral blood CMV PCR viral load.

IV Ganciclovir (Preferred for Severe Disease)

Ganciclovir 5 mg/kg intravenously every 12 hours for 2–3 weeks is the standard induction regimen for tissue-invasive CMV disease, including CMV gastritis with severe ulceration, obstruction, or significant bleeding. Dose adjustment is required for renal impairment.

Oral Valganciclovir (Mild-Moderate Disease or Step-Down)

Valganciclovir 900 mg orally twice daily is acceptable for mild to moderate CMV gastritis or step-down after initial IV induction. Maintenance/secondary prophylaxis with valganciclovir 900 mg once daily for ≥12 weeks after induction is recommended in patients at high risk for relapse (low CD4+ count in HIV, transplant recipients on high-dose immunosuppression).

Foscarnet

Foscarnet (60 mg/kg IV every 8 hours or 90 mg/kg IV every 12 hours) is reserved for ganciclovir-resistant CMV disease; careful monitoring for nephrotoxicity and electrolyte disturbances is required.

Post-Treatment Assessment

Confirm CMV eradication with repeat endoscopic biopsy and serum CMV PCR after completing therapy. Optimize immune reconstitution: initiate or optimize antiretroviral therapy in HIV patients; consider reduction of immunosuppression where feasible in transplant recipients.

Eosinophilic Gastritis

Eosinophilic gastritis (EoG) is an immune-mediated disorder defined histologically by eosinophilic infiltration of the gastric wall (generally accepted threshold: >30 eosinophils per high-power field) in the setting of compatible symptoms (nausea, vomiting, abdominal pain, early satiety, weight loss) and exclusion of secondary causes. It is frequently associated with atopic conditions including eosinophilic esophagitis, allergic rhinitis, asthma, and atopic dermatitis. Treatment options remain limited, and evidence consists predominantly of case series and small cohort studies.

Dietary Elimination Therapy

• Identification and elimination of dietary triggers (six-food elimination diet targeting milk, wheat, egg, soy, nuts, and seafood) is recommended as a first-line measure, particularly in patients with identifiable food allergens or concurrent atopic disease.
• Allergen testing (skin prick test, specific IgE panels) should be performed to identify potential dietary triggers.
• Elemental diet (amino acid-based formula) may be considered in refractory cases.

PPI Trial

• A 6–8 week trial of high-dose PPI (e.g., omeprazole 40 mg twice daily or esomeprazole 40 mg once to twice daily) is recommended, as a subset of patients with eosinophilic esophagitis and eosinophilic gastrointestinal disorders respond to acid suppression with reduction in eosinophilic inflammation.

Corticosteroids

• Prednisone 20–40 mg orally daily (or weight-based 1 mg/kg/day to a maximum of 40 mg) with gradual taper over 6–8 weeks is the most reliably effective induction treatment for significant or refractory EoG. Systemic steroids are typically reserved for severe, symptomatic, or refractory cases.
• Budesonide (oral 9 mg daily, or compounded oral suspension 2 mg/10 mL) is preferred over systemic prednisone for long-term maintenance therapy due to its significantly lower systemic bioavailability (first-pass hepatic metabolism >90%), reducing the risk of adrenal suppression, osteoporosis, and other corticosteroid adverse effects.

Dupilumab (Emerging Biologic Therapy)

Dupilumab, a human monoclonal antibody targeting the IL-4 receptor α subunit (blocking both IL-4 and IL-13 signaling), has demonstrated clinical and histological improvement in retrospective case series of EoG. A 2024 retrospective case series reported that all patients with EoG treated with dupilumab experienced improvement of at least one symptom, and histological peak eosinophil counts decreased significantly; no patients had worsening symptoms. A randomized, double-blind, placebo-controlled trial (NCT03678545) evaluating dupilumab for EoG was completed in 2024; peer-reviewed results are pending. Dupilumab remains investigational for EoG pending regulatory approval for this indication.

Leukotriene Receptor Antagonists and Mast Cell Stabilizers

• Montelukast 10 mg orally daily has been used as a steroid-sparing agent in EoG based on limited case series.
• Cromolyn sodium 200 mg orally four times daily may reduce mast cell–mediated eosinophil recruitment; evidence is limited to case reports and small series.

Monitoring

• Repeat upper endoscopy with biopsy at 8–12 weeks after initiating therapy to confirm histological remission.
• In steroid-dependent patients, biologic therapy (e.g., dupilumab) should be considered.
• In remission, endoscopic surveillance every 1–2 years or with symptom recurrence.

Fungal Gastritis

Fungal gastritis is rare and occurs predominantly in immunocompromised patients. The most common organisms are Candida albicans, Histoplasma capsulatum, and Aspergillus species. Diagnosis requires endoscopic biopsy with culture, histopathology, and special stains (GMS, PAS).

• For Candida gastritis: Fluconazole 400 mg loading dose then 200–400 mg daily orally or IV (fluconazole-susceptible species); micafungin 100 mg IV daily or anidulafungin for fluconazole-resistant species.
• For Histoplasma gastritis: Liposomal amphotericin B 3 mg/kg IV daily for severe/life-threatening disease, followed by oral itraconazole 200 mg twice daily for at least 12 months.

Granulomatous Gastritis

Granulomatous gastritis is defined by the presence of granulomas on gastric biopsy and may be caused by Crohn's disease (most common in Western populations), sarcoidosis, infectious organisms (Mycobacterium tuberculosis, Histoplasma capsulatum, Treponema pallidum), vasculitis, foreign body reaction, or may be idiopathic. Extensive workup to establish the underlying etiology is required before initiating targeted therapy.

Recommended workup:

• Angiotensin-converting enzyme (ACE) level and chest imaging (sarcoidosis)
• Tuberculin skin test or interferon-gamma release assay (IGRA) and sputum/gastric biopsy acid-fast bacilli culture (tuberculosis)
• Serologies: syphilis (RPR/VDRL, confirmatory FTA-ABS), Histoplasma urine antigen
• Stool calprotectin and ileocolonoscopy if Crohn's disease is suspected
• Special stains on gastric biopsy: Ziehl-Neelsen (AFB), GMS and PAS (fungi)

Medical Treatment

Crohn's-Associated Granulomatous Gastritis

Treatment targets systemic Crohn's disease. Options include budesonide 9 mg daily for induction; azathioprine or 6-mercaptopurine for maintenance; and biologic therapy with anti-TNF agents (e.g., infliximab, adalimumab) or other biologics for moderate-to-severe disease per current IBD guidelines.

Sarcoid Granulomatous Gastritis

Systemic corticosteroids (prednisone 20–40 mg daily, tapered over several months) are the mainstay of treatment for symptomatic gastric sarcoidosis.

Infectious Granulomatous Gastritis

Treat the underlying pathogen: anti-tuberculosis regimen for tuberculosis; liposomal amphotericin B followed by itraconazole for histoplasmosis; penicillin G for gastric syphilis.

Idiopathic Granulomatous Gastritis

A trial of corticosteroids may be considered after exclusion of infectious and systemic causes. Symptomatic relief with PPI therapy while workup is pending.

H. pylori Gastritis

Indications for H. pylori eradication treatment include:

• Past or present duodenal and/or gastric ulcer, with or without complications
• Following resection of gastric cancer
• Gastric mucosa-associated lymphoid tissue (MALT) lymphoma
• Atrophic gastritis
• Dyspepsia
• Patients with first-degree relatives with gastric cancer
• Patients at increased risk for gastric adenocarcinoma (including those with autoimmune gastritis or gastric intestinal metaplasia)
• Household contacts of patients with confirmed H. pylori (non-serologic test)
• Patient's wishes

General Principles of H. pylori Eradication

Maintenance of adequate intragastric acid suppression is critical for successful H. pylori eradication, as elevated intragastric pH promotes active bacterial replication and enhances antibiotic bactericidal activity. H2-receptor antagonists are not adequate for this purpose and are not recommended as the acid-suppressive backbone for any eradication regimen. All eradication regimens should be administered for 14 days; shorter durations are associated with meaningfully lower eradication rates.

Antibiotic stewardship principles must guide regimen selection. Clarithromycin resistance has risen to 17–27% globally and levofloxacin resistance is increasing rapidly in many regions, rendering empiric use of clarithromycin-based triple therapy and empiric levofloxacin-based therapy no longer appropriate as standard first-line approaches. Where molecular or culture-based antibiotic susceptibility testing (AST) is available, susceptibility-guided therapy is the preferred strategy per the 2022 Maastricht VI consensus.

First-Line Regimens for Treatment-Naïve Patients

Key 2024 ACG guideline change: Clarithromycin-based PPI triple therapy (PPI + clarithromycin + amoxicillin or metronidazole) is no longer recommended as empiric first-line therapy. It should only be used if antibiotic susceptibility testing has confirmed clarithromycin sensitivity. Eradication rates with PPI-clarithromycin triple therapy drop to approximately 30% in clarithromycin-resistant H. pylori strains. Concomitant therapy (PPI + amoxicillin + clarithromycin + metronidazole simultaneously) has also been removed as a first-line recommendation by the 2024 ACG guideline, though it retains a role in some international guidelines in regions with low dual clarithromycin and metronidazole resistance.

Regimen	Medications and Dosing	Duration	ACG 2024 Recommendation (GRADE)	Comments
Optimized Bismuth Quadruple Therapy (BQT) (Preferred first-line)	PPI b.i.d. + tetracycline 500 mg q.i.d. + metronidazole 500 mg t.i.d.–q.i.d. + bismuth subcitrate or bismuth subsalicylate q.i.d.	14 days	Strong recommendation; moderate quality evidence	Doxycycline must NOT be substituted for tetracycline (10–17% lower eradication rate). Metronidazole 500 mg preferred over 250 mg. All components must be dosed at full frequency and dose.
Rifabutin-Based Triple Therapy (Alternative first-line; RHB-105/Talicia®)	Omeprazole 40 mg + amoxicillin 1000 mg + rifabutin 50 mg; all three dosed every 8 hours (t.i.d.)	14 days	Conditional recommendation; low quality evidence	Phase 3 ERADICATE Hp2 trial: eradication rate 83.8% (95% CI 78.4–88.0%) vs. 57.7% comparator (P<0.001). Efficacy not significantly impacted by clarithromycin, amoxicillin or multi-drug resistance. Monitor CBC for myelosuppression.
PCAB (Vonoprazan)–Amoxicillin Dual Therapy (Alternative first-line)	Vonoprazan 20 mg b.i.d. + amoxicillin 1 g t.i.d.	14 days	Conditional recommendation; moderate quality evidence	Superior to lansoprazole triple therapy overall (77.2% vs. 68.5%; P=0.013) and markedly superior in clarithromycin-resistant strains (69.6% vs. 31.9%). FDA approved in US (Voquezna® Dual Pak).
PCAB (Vonoprazan)–Amoxicillin–Clarithromycin Triple Therapy (Alternative first-line)	Vonoprazan 20 mg b.i.d. + amoxicillin 1 g b.i.d. + clarithromycin 500 mg b.i.d.	14 days	Conditional recommendation; moderate quality evidence	Eradication 80.8% overall and 65.8% in clarithromycin-resistant infections vs. 31.9% with lansoprazole triple (superior; P<0.001). FDA approved in US (Voquezna® Triple Pak).
PPI-clarithromycin triple therapy (Only if susceptibility-confirmed)	Standard dose PPI b.i.d. + clarithromycin 500 mg b.i.d. + amoxicillin 1 g b.i.d. (or metronidazole 500 mg b.i.d. if penicillin allergy)	14 days	Not recommended empirically (Key Concept, expert consensus)	Use only when AST confirms clarithromycin sensitivity. No longer first-line per ACG 2024 or Maastricht VI 2022 for empiric use.
PPI = proton pump inhibitor; PCAB = potassium-competitive acid blocker; b.i.d. = twice daily; t.i.d. = three times daily; q.i.d. = four times daily; AST = antibiotic susceptibility testing; CBC = complete blood count. Standard PPI doses: lansoprazole 30 mg, omeprazole 20 mg, pantoprazole 40 mg, rabeprazole 20 mg, esomeprazole 40 mg.

Vonoprazan-Based Therapy

Vonoprazan (a potassium-competitive acid blocker) provides more potent and sustained intragastric acid suppression than conventional PPIs, independent of CYP2C19 genotype. In the pivotal phase 3 VOCAL trial (n=1,046 treatment-naïve patients), vonoprazan triple therapy (20 mg b.i.d. + amoxicillin 1 g b.i.d. + clarithromycin 500 mg b.i.d. × 14 days) achieved eradication rates of 84.7% vs. 78.8% with lansoprazole triple therapy in non-resistant strains (non-inferior; difference 5.9%, 95% CI −0.8 to 12.6; P<0.001). In clarithromycin-resistant infections, vonoprazan triple therapy achieved 65.8% eradication compared to 31.9% with lansoprazole triple (difference 33.9%, 95% CI 17.7–48.1; P<0.001). Vonoprazan dual therapy achieved 69.6% eradication in clarithromycin-resistant strains vs. 31.9% with lansoprazole triple (difference 37.7%, 95% CI 20.5–52.6; P<0.001). A systematic meta-analysis of 13 RCTs (n=4,023) confirmed vonoprazan–amoxicillin high-dose dual therapy ITT eradication rate of 88.81% and per-protocol rate of 93.56%, with significantly fewer adverse events (14.56% vs. 26.00%; RR=0.57, 95% CI 0.48–0.67; P<0.0001).

Rifabutin-Based Triple Therapy

The combination product RHB-105 (Talicia®) containing omeprazole 40 mg, amoxicillin 1000 mg, and rifabutin 50 mg administered every 8 hours for 14 days achieved H. pylori eradication of 83.8% (95% CI 78.4–88.0%; P<0.001) in the phase 3 ERADICATE Hp2 double-blind trial (n=455 treatment-naïve US patients). Efficacy was not significantly affected by clarithromycin, amoxicillin, or multi-drug resistance. Adverse effects include diarrhea (12.7%), headache (11.9%), and chromaturia (9.3%). Rifabutin has potential for myelosuppression and ocular toxicity; complete blood count monitoring is recommended. As a second-line antituberculous agent, its use for H. pylori requires careful consideration in settings with endemic tuberculosis to minimize the risk of promoting rifamycin resistance.

Predictors of H. pylori Treatment Outcome

Predictors of treatment failure include:

• Poor compliance with the regimen
• Antibiotic resistance (the key factor in eradication failure), particularly to clarithromycin, levofloxacin, and metronidazole
• Bacterial factors: CagA-negative strains are at increased risk of treatment failure compared with CagA-positive strains
• CYP2C19 polymorphisms may influence treatment outcomes when PPIs are used (this effect is largely overcome by vonoprazan, which is not CYP2C19-dependent)
• Smoking and heavy alcohol use are associated with lower eradication rates
• High bacterial load before treatment

For more details, please read the main article Helicobacter pylori infection medical therapy.

Lymphocytic Gastritis

Lymphocytic gastritis is defined histologically by intraepithelial lymphocytosis exceeding 25 lymphocytes per 100 surface epithelial cells. It is most commonly associated with Helicobacter pylori infection, celiac disease (particularly the "celiac variant" presenting as varioliform gastritis), and use of immune checkpoint inhibitors; it may also be idiopathic.

• If Helicobacter pylori is identified, eradication therapy (see above) is the primary treatment and typically results in histological improvement.
• If celiac disease is the underlying etiology, strict adherence to a gluten-free diet leads to histological resolution in most patients. Celiac serologies (anti-tissue transglutaminase IgA, total IgA) should be checked in all patients with lymphocytic gastritis without a confirmed cause.
• For idiopathic or refractory lymphocytic gastritis, budesonide (9 mg orally daily for 8 weeks, then tapered) has been used in small series with some benefit.
• Bismuth subsalicylate and PPIs may provide symptomatic relief.

NSAID-Associated Gastropathy

Risk Stratification

Non-steroidal anti-inflammatory drug (NSAID)-associated gastropathy arises from prostaglandin depletion secondary to COX-1 inhibition, impairing mucus and bicarbonate secretion, reducing mucosal blood flow, and promoting epithelial injury. Risk factors determine the appropriate gastroprotective strategy:

GI Risk Category	Risk Factors Present	Recommended Strategy
Low	Age <65, no prior GI event, no anticoagulant/antiplatelet/corticosteroid use, no H. pylori	NSAID alone (lowest effective dose, shortest duration)
Moderate (1–2 risk factors)	Age ≥65; high-dose NSAID; prior uncomplicated ulcer; concurrent low-dose ASA; concurrent corticosteroid use	NSAID + PPI once daily; OR COX-2 selective inhibitor (coxib) alone
High (>2 risk factors or prior complicated ulcer or concurrent anticoagulant therapy)	Prior complicated GI event (bleeding, perforation); multiple risk factors; concurrent anticoagulant use	COX-2 selective inhibitor + PPI once daily; or consider discontinuation of NSAID and alternative analgesic strategy

H. pylori testing before initiating chronic NSAID therapy is recommended; eradication should be performed if the test is positive, as concurrent infection synergistically increases ulcer risk.

Gastroprotection Strategies

Proton Pump Inhibitors (Preferred)

PPIs (e.g., omeprazole 20 mg, esomeprazole 20 mg, pantoprazole 40 mg orally once daily) reduce the risk of NSAID-induced gastric and duodenal ulcers and are superior to standard-dose H2 receptor antagonists. A Cochrane meta-analysis confirmed that PPIs significantly reduced the risk of endoscopic gastric ulcers (relative risk 0.40; 95% CI: 0.32–0.51) and duodenal ulcers in NSAID users.

COX-2 Selective Inhibitors (Coxibs)

Celecoxib and other selective COX-2 inhibitors reduce NSAID-associated gastroduodenal injury by sparing COX-1-mediated prostaglandin synthesis in the gastric mucosa. In high GI-risk patients, the combination of a COX-2 inhibitor + PPI is the most effective gastroprotective strategy. Cardiovascular risk must be assessed; COX-2 inhibitors are relatively contraindicated in patients with established cardiovascular disease or high cardiovascular risk.

Misoprostol

Misoprostol (200 mcg orally four times daily, or 400 mcg twice daily) is a prostaglandin E1 analogue that is the only agent proven to reduce clinically significant ulcer complications (not only endoscopic ulcers) in NSAID users. Misoprostol 800 mcg/day was superior to 400 mcg/day for prevention of endoscopic gastric ulcers (RR 0.17 vs RR 0.39, respectively; P=0.0055); however, gastrointestinal side effects (diarrhea, cramping) at full dose significantly limit use.

H2 Receptor Antagonists

Standard-dose H2 receptor antagonists (e.g., famotidine 20 mg twice daily) reduce the risk of endoscopic duodenal ulcers (RR 0.36; 95% CI: 0.18–0.74) but are not effective for prevention of endoscopic gastric ulcers (RR 0.73; 95% CI: 0.50–1.08) at standard doses. Double-dose H2 receptor antagonists are effective for both gastric and duodenal ulcer prevention.

Healing Timelines for NSAID-Associated Ulcers

• If NSAID is discontinued: duodenal ulcer healing >90% at 4 weeks with standard-dose PPI; gastric ulcer healing >80% at 8 weeks.
• If NSAID must continue: healing rates are approximately 10–20% lower; PPI remains required for the duration of NSAID use.
• H. pylori eradication should be confirmed separately; healing of ulcer on PPI does not confirm eradication.

Phlegmonous (Suppurative) Gastritis

Phlegmonous gastritis is a rare, rapidly progressive bacterial infection of the gastric submucosa, predominantly caused by Streptococcus pyogenes (most common), gram-negative organisms, and mixed flora. Mortality remains 17–33% despite antibiotics. Early diagnosis and prompt institution of antibiotics can prevent mortality and defer the need for surgical intervention.

• Empiric broad-spectrum IV antibiotics should be initiated immediately upon clinical or radiological suspicion: e.g., piperacillin-tazobactam 3.375 g IV every 6 hours, or vancomycin + meropenem (for high-risk or complex flora).
• Adjust antibiotics based on gastric biopsy culture results and organism susceptibilities; infectious disease specialist consultation is strongly recommended.
• Surgical consultation is mandatory; gastrectomy is indicated for perforation, gastric necrosis, or failure to respond to antibiotics within 48–72 hours.
• PPI therapy and supportive care (IV fluids, nutritional support) should be provided alongside antibiotics.

Radiation Gastritis

Acute Radiation Gastritis

Acute radiation gastritis develops during or shortly after radiotherapy for abdominal or thoracic malignancies, manifesting with edema, hemorrhagic erosions, nausea, and epigastric discomfort.

• Proton pump inhibitors (e.g., omeprazole 20–40 mg orally or IV twice daily) are the cornerstone of symptomatic management.
• Sucralfate 1 g four times daily provides additional mucosal protection.
• Antiemetics (e.g., ondansetron, metoclopramide) for nausea and vomiting.
• IV hydration and nutritional support as required.

Chronic Radiation Gastritis and Radiation-Induced Vascular Ectasia

Chronic radiation injury (occurring months to years after radiation) involves mucosal atrophy, fibrosis, vascular ectasias, and ulceration with risk of recurrent GI bleeding.

• Argon plasma coagulation (APC) delivered endoscopically is the preferred treatment for radiation-induced gastric antral vascular ectasia (GAVE) and diffuse gastric telangiectasias causing recurrent or active bleeding; multiple sessions may be required.
• Sucralfate suspension (1 g/10 mL orally four times daily) has been used as a mucosal protectant with modest evidence of benefit.
• Hyperbaric oxygen therapy has been evaluated in small series for chronic radiation gastropathy; it may promote angiogenesis and mucosal healing in selected centers.
• Coordinate care with radiation oncology; modify concurrent anticoagulant or antiplatelet therapy where clinically safe.

Stress-Related Mucosal Disease and Stress Ulcer Prophylaxis

Stress-related mucosal disease (SRMD), also referred to as stress ulcer syndrome or stress gastritis, encompasses diffuse superficial gastric erosions and ulcerations occurring in critically ill patients secondary to mucosal ischemia, reperfusion injury, and disruption of cytoprotective mechanisms. Clinically important gastrointestinal bleeding (CIGIB) from SRMD carries a 90-day mortality exceeding 50% in the ICU. The 2024 Society of Critical Care Medicine (SCCM) and American Society of Health-System Pharmacists (ASHP) Guideline for the Prevention of Stress-Related Gastrointestinal Bleeding in Critically Ill Adults (Crit Care Med. 2024;52(8):e421–e430) is the current reference standard.

ICU Indications for Stress Ulcer Prophylaxis

The 2024 SCCM/ASHP guideline recommends pharmacological stress ulcer prophylaxis (SUP) in critically ill patients with the following conditions:

Indication	Strength of Recommendation	Notes
Coagulopathy (INR >1.5, aPTT >2× normal, or platelets <50 × 10⁹/L)	Conditional (moderate certainty)	Consistently identified as a major risk factor across all major guidelines
Shock (septic, cardiogenic, hemorrhagic, or vasopressor-dependent)	Conditional (moderate certainty)	Mucosal ischemia is the primary pathophysiological driver of SRMD
Chronic liver disease (cirrhosis)	Conditional (moderate certainty)	Portal hypertension and coagulopathy synergistically increase CIGIB risk
High-risk neurocritical care patients (severe TBI, acute spinal cord injury, subarachnoid hemorrhage)	Conditional (low certainty)	Evidence less robust than for coagulopathy and shock
Enterally-fed high-risk patients	Conditional (very low certainty)	SUP suggested even with enteral nutrition in high-risk patients; EN alone is insufficient in high-risk settings

• The 2024 SCCM/ASHP guideline does not specifically recommend routine SUP in mechanically ventilated patients without other qualifying risk factors, representing a nuanced departure from older guidelines. This remains clinically controversial given the REVISE trial results (see below).

Pharmacological Agents: PPI vs H2RA

The 2024 SCCM/ASHP guideline states no preference between PPIs and H2 receptor antagonists (H2RAs) as SUP agents, given that landmark randomized controlled trials did not demonstrate a consistent mortality benefit favoring either class. Both intravenous and oral/enteral routes are acceptable when the patient has reliable enteral access.

Drug	IV Dose	Enteral Dose
Pantoprazole (PPI)	40 mg IV once or twice daily	40 mg orally once or twice daily
Esomeprazole (PPI)	40 mg IV once daily	40 mg orally once daily
Famotidine (H2RA)	20 mg IV every 12 hours	20–40 mg orally twice daily

Landmark Trials Informing SUP Practice

Trial	n	Design	Key Finding
SUP-ICU (2018)	3,298	RCT, pantoprazole vs. placebo, ICU patients with ≥1 risk factor	No significant difference in 90-day mortality (primary outcome); pantoprazole reduced clinically important GI bleeding but was associated with a numerically higher rate of pneumonia and C. difficile infection
PEPTIC (2020)	26,774	Cluster-randomized crossover, PPI vs. H2RA, mechanically ventilated ICU patients	No significant difference in in-hospital mortality (PPI 18.3% vs. H2RA 17.5%); PPI group had a non-significant trend toward lower GI bleeding but numerically higher C. difficile rate
REVISE (2024)	Multicenter RCT	IV pantoprazole vs. placebo, invasively ventilated ICU patients	Pantoprazole significantly reduced clinically important upper GI bleeding vs. placebo (1.0% vs. 3.5%; 95% CI 1.6 to 3.3%); no significant difference in 90-day mortality or ventilator-associated pneumonia

Duration and Deprescribing of SUP

• SUP should be continued until the risk factor(s) that prompted initiation have resolved, or until the patient is transferred from the ICU.
• SUP must be discontinued at ICU discharge unless there is an independently documented outpatient indication for ongoing acid suppression therapy (e.g., active peptic ulcer, GERD with erosive esophagitis, chronic NSAID use with GI risk factors).
• Pharmacist-led and protocol-driven deprescribing initiatives are effective in reducing inappropriate continuation of ICU-initiated PPI therapy on ward transfer and at discharge.

Acid Suppression in Non-H. pylori Gastritis

For patients with reactive gastropathy or chemical gastropathy related to NSAIDs, bile reflux, or other injury, discontinuation of the offending agent plus PPI therapy is the primary approach. Standard-dose PPI therapy once daily for 4–8 weeks is effective for symptom relief and mucosal healing. For NSAID-associated peptic ulcer, standard PPI therapy provides healing rates above 90% for duodenal ulcer in 4 weeks and gastric ulcer in 8 weeks. Long-term PPI therapy should be deprescribed if no ongoing indication exists, given associations with Clostridioides difficile infection, hypomagnesemia, bone fracture, and potential small absolute increase in gastric cancer risk in patients with preexisting atrophic gastritis.

PPI Deprescribing

PPIs are among the most frequently prescribed medications worldwide, yet studies estimate that up to 82% of PPI prescriptions lack an evidence-based indication or are continued beyond the recommended duration. The 2022 American Gastroenterological Association (AGA) Clinical Practice Update on De-Prescribing of PPIs provides evidence-based guidance on appropriate indications and deprescribing strategies.

Conditions That Support Long-Term PPI Use

Long-term PPI therapy is appropriate in the following settings (deprescribing is NOT appropriate):

• Gastroesophageal reflux disease (GERD) with documented erosive esophagitis (Los Angeles grade C or D) or confirmed Barrett's esophagus
• Chronic NSAID use in patients at moderate-to-high GI risk (see NSAID section above)
• Maintenance therapy for peptic ulcer disease in patients with persistent H. pylori eradication failure or ongoing NSAID use
• Zollinger-Ellison syndrome
• Eosinophilic esophagitis managed with PPI therapy
• Chronic anticoagulant therapy combined with prior GI bleeding history

Conditions That Do Not Support Long-Term PPI Use

• Non-erosive GERD (step-down to on-demand H2RA or PPI is appropriate)
• Functional dyspepsia not responding to an adequate PPI trial
• Stress ulcer prophylaxis after ICU discharge without independent outpatient indication
• H. pylori eradication therapy (short-course only; deprescribe after test of cure)
• Prophylactic use in low-to-moderate-risk NSAID users without GI risk factors

Deprescribing Approaches

Per the AGA 2022 Best Practice Advice:

1. Review indication: All patients taking a PPI should have a regular review by their primary care provider of the ongoing indication, with documentation.
2. Assess appropriateness: Determine whether the indication is valid and whether long-term use is necessary.
3. Three deprescribing strategies (once the patient qualifies):

• Reduce to the lowest effective dose
• Switch to on-demand (as-needed) therapy
• Complete discontinuation

1. Step-down: Tapering from PPI to H2 receptor antagonist before complete discontinuation may reduce rebound acid hypersecretion symptoms, particularly in patients on long-term therapy.
2. Counsel on rebound acid hypersecretion: Patients should be informed that rebound symptoms (epigastric burning, dyspepsia) may occur for 2–4 weeks after PPI discontinuation, representing physiological rebound rather than disease recurrence; this should not automatically prompt re-prescribing.

Clinical Situation	Recommended Deprescribing Action
Short-term use (<8 weeks) for uncomplicated dyspepsia or non-erosive GERD	Discontinue; use on-demand PPI or H2RA as needed for symptom recurrence
Moderate-risk GERD without erosive esophagitis or Barrett's esophagus	Step-down to lowest effective dose; trial of on-demand therapy
Long-term NSAID use with prior cessation of NSAID	Discontinue PPI; reassess if NSAID restarted
SUP initiated in ICU, no outpatient indication identified	Discontinue at ICU discharge
Barrett's esophagus, erosive esophagitis LA grade C or D	Continue long-term; deprescribing is NOT appropriate
Documented Zollinger-Ellison syndrome	Continue indefinitely; deprescribing is NOT appropriate

Adverse Effects of Long-Term PPI Use

Clinicians should weigh confirmed risks when evaluating long-term PPI use:

• Clostridioides difficile infection (FDA safety communication; risk increases with prolonged use)
• Hypomagnesemia (risk increases significantly with >1 year of use)
• Vitamin B12 and iron malabsorption (relevant in patients with borderline stores)
• Bone density reduction and increased fracture risk (modest association; most relevant in high-risk patients)
• Potential increased risk of community-acquired pneumonia
• Potential small absolute increase in gastric cancer risk in patients with preexisting atrophic gastritis and untreated H. pylori

Gastroprotection in Antiplatelet and Anticoagulant Therapy

Patients receiving antiplatelet and/or anticoagulant therapy are at significantly increased risk for upper gastrointestinal bleeding (UGIB). This risk is multiplied in patients receiving dual antiplatelet therapy (DAPT), combined antiplatelet and anticoagulant therapy, or those with concurrent NSAID use, H. pylori infection, age >65 years, or prior GI bleeding. The ACG and Canadian Association of Gastroenterology published a Clinical Practice Guideline on the management of antithrombotic therapy in acute GI bleeding in 2022.

Gastroprotection Indications

Clinical Scenario	Gastroprotective Recommendation
Low-dose aspirin (cardioprotective) without additional GI risk factors	PPI only if additional GI risk factors present (age >65, concurrent NSAID, prior peptic ulcer, H. pylori)
Dual antiplatelet therapy (DAPT) post-percutaneous coronary intervention (PCI)	PPI recommended for duration of DAPT (typically 6–12 months); reassess after DAPT completion
Warfarin or direct oral anticoagulants (DOACs) alone, without additional GI risk factors	PPI only if additional GI risk factors present
Combined antiplatelet + anticoagulant therapy (any combination)	PPI strongly recommended for all patients; H. pylori testing and eradication recommended
High-dose NSAID + antiplatelet or anticoagulant	Avoid combination if possible; if unavoidable: PPI + COX-2 selective inhibitor; H. pylori eradication mandatory

Management of Active GI Bleeding on Antithrombotic Therapy (ACG/CAG 2022)

• Aspirin for secondary prevention: The ACG/CAG 2022 guideline suggests continuing aspirin during GI bleeding in patients receiving it for secondary cardiovascular prevention, as stopping aspirin does not improve bleeding outcomes and may increase mortality. Aspirin should be resumed on the day hemostasis is endoscopically confirmed in patients in whom it was held.
• P2Y12 inhibitors (clopidogrel, ticagrelor, prasugrel): Stopping the P2Y12 inhibitor does not consistently reduce active bleeding; risk of stent thrombosis with interruption >4–5 days must be weighed. Multidisciplinary (gastroenterology + cardiology) shared decision-making is recommended.
• Warfarin: Suggests against routine fresh frozen plasma (FFP) administration for warfarin reversal in acute GI bleeding; prothrombin complex concentrate (PCC) may be preferred over FFP when reversal is clinically indicated.
• Direct oral anticoagulants (DOACs): Prothrombin complex concentrates appear to have limited benefit for DOAC-related GI bleeding. Andexanet alfa (anti-factor Xa reversal agent) sequesters apixaban and rivaroxaban and is available for severe life-threatening bleeding.
• Platelet transfusions: The guideline suggests against platelet transfusions in patients with GI bleeding taking antiplatelet agents, as evidence suggests they may increase mortality.

PPI–Clopidogrel Interaction

Concomitant use of PPIs with clopidogrel is associated with a pharmacokinetic interaction: omeprazole and esomeprazole are potent inhibitors of CYP2C19 and reduce clopidogrel bioactivation to its active thiol metabolite. The MHRA and European Medicines Agency (EMA) advise against concurrent use of clopidogrel with omeprazole or esomeprazole based on pharmacokinetic data. The 2023 ESC guidelines for acute coronary syndromes acknowledge this interaction but note that no strong clinical evidence demonstrates a significantly increased risk of major adverse cardiovascular events or stent thrombosis in clinical trials and propensity score-matched studies.

The increasing order of CYP2C19 interaction strength of different PPIs, from lowest to highest, is: rabeprazole, pantoprazole, lansoprazole, esomeprazole, omeprazole. When PPI co-administration with clopidogrel is required, pantoprazole or rabeprazole are preferred based on their lower CYP2C19 inhibitory activity; omeprazole and esomeprazole should be avoided.

• No clinically meaningful interaction has been observed between PPIs and aspirin, prasugrel, or ticagrelor.
• For patients taking dabigatran (direct thrombin inhibitor), concomitant PPI use has been reported to slightly reduce dabigatran bioavailability; the clinical significance is generally considered modest.

H. pylori Eradication in Patients on Antithrombotic Therapy

All patients with peptic ulcers who are taking antithrombotic therapy should be tested for Helicobacter pylori and receive eradication therapy if positive, as the combination of H. pylori infection and antithrombotic therapy synergistically increases ulcer and bleeding risk.

Treatment Algorithm for Clinicians

The following algorithm routes clinicians from the presentation of confirmed or suspected gastritis through etiology-specific treatment pathways:

Step	Clinical Decision	Action
1. Identify etiology	Upper endoscopy with biopsies ± non-invasive H. pylori testing	Classify gastritis subtype (see Classification table above)
2a. H. pylori confirmed	All treatment-naïve patients with unknown susceptibility	Optimized BQT × 14 days (preferred); or vonoprazan dual/triple therapy × 14 days; or rifabutin triple therapy × 14 days. Test of cure ≥4 weeks post-antibiotics.
2b. NSAID-associated	Risk stratification (low/moderate/high)	Low risk: NSAID + lowest dose. Moderate: NSAID + PPI or COX-2. High: COX-2 + PPI; consider NSAID discontinuation. Test and treat H. pylori.
2c. Autoimmune gastritis	Anti-PCA/anti-IF Ab, B12, iron, pepsinogen I/II, gastrin	IM hydroxocobalamin lifelong; IV/oral iron; surveillance endoscopy q3–5y; thyroid screening; avoid unnecessary PPI.
2d. Stress (ICU)	2024 SCCM/ASHP criteria: coagulopathy, shock, liver disease, high-risk neuro	IV/enteral PPI or H2RA while risk factors persist. Deprescribe at ICU discharge if no outpatient indication.
2e. Eosinophilic	Allergen testing; endoscopy + biopsy (>30 eos/HPF)	Elimination diet; high-dose PPI trial × 6–8 weeks; budesonide 9 mg/day; prednisone for severe disease; dupilumab if steroid-dependent (investigational).
2f. CMV (immunocompromised)	CMV IHC biopsy + serum PCR	IV ganciclovir 5 mg/kg q12h × 2–3 weeks; step-down valganciclovir. Maintenance 12 weeks. Optimize immune reconstitution.
2g. Bile reflux	Endoscopy (diffuse erythema, bile pooling); pH-impedance if uncertain	UDCA; sucralfate; prokinetics. Refractory post-surgical: Roux-en-Y revision.
2h. Granulomatous	Systemic workup (ACE, IGRA, serology, colonoscopy)	Treat underlying cause: corticosteroids (Crohn's/sarcoid); anti-TB; antifungal. Symptomatic PPI.
2i. Radiation	Clinical history; endoscopy	Acute: PPI + sucralfate + antiemetics. Chronic: APC endoscopy ± hyperbaric oxygen.
2j. Phlegmonous	CT abdomen; blood cultures; endoscopic biopsies for culture	IV broad-spectrum antibiotics immediately; surgical consultation; adjust per culture results.
3. PPI prescribed?	Review indication at every visit	Deprescribe if no ongoing indication (see Deprescribing section)
4. On antithrombotic therapy?	DAPT, anticoagulant, or combined therapy	Add PPI if GI risk factors present; prefer pantoprazole/rabeprazole over omeprazole/esomeprazole with clopidogrel; test and treat H. pylori.

Summary Comparison Table

Gastritis Subtype	Key Diagnostic Features	First-Line Treatment	Monitoring / Follow-Up
Alcohol-related Gastritis	Alcohol history; subepithelial hemorrhage, erosions on endoscopy	Alcohol cessation; PPI or H2RA; sucralfate; thiamine if alcohol use disorder	Abstinence monitoring; repeat endoscopy if symptoms persist
Autoimmune Gastritis	Anti-PCA and anti-IF antibodies; elevated fasting gastrin; low pepsinogen I/II ratio; corpus-predominant atrophy	IM hydroxocobalamin 1 mg q2–3mo lifelong; oral or IV iron; avoid PPIs unless separately indicated	Endoscopy + mapping biopsies at diagnosis and q3–5 years; annual B12/ferritin/CBC; thyroid screening
Bile reflux Gastropathy	Post-surgical; bile pooling on endoscopy; foveolar hyperplasia on biopsy	Sucralfate; UDCA; prokinetics; cholestyramine (second-line); Roux-en-Y for refractory cases	Symptom review; repeat endoscopy if refractory
CMV Gastritis	Immunocompromised; CMV inclusion bodies on biopsy; positive CMV PCR	IV ganciclovir 5 mg/kg q12h × 2–3 weeks → step-down to oral valganciclovir 900 mg b.i.d.; maintenance × 12 weeks	CMV PCR monitoring; repeat endoscopy; immune reconstitution
Eosinophilic Gastritis	>30 eos/HPF on gastric biopsy; atopic history; normal H. pylori serology	Elimination diet; high-dose PPI trial; oral budesonide 9 mg/day; prednisone for severe disease; dupilumab (investigational)	Repeat endoscopy + biopsy at 8–12 weeks; annual surveillance in remission
Fungal Gastritis	Immunocompromised; fungal hyphae/yeasts on GMS/PAS stain; positive culture	Fluconazole (Candida); liposomal amphotericin B → itraconazole (Histoplasma); optimize immune status	Antifungal susceptibility testing; endoscopic follow-up
Granulomatous Gastritis	Granulomas on biopsy; systemic workup required (Crohn's, sarcoid, TB, fungal)	Treat underlying cause: corticosteroids (Crohn's/sarcoid); anti-TB (TB); antifungal; symptomatic PPI	Per underlying disease protocol; regular endoscopy
H. pylori Gastritis	UBT or stool antigen positive; antral predominant histology; CLO test positive	Optimized BQT × 14 days (preferred 2024 ACG); vonoprazan dual/triple or rifabutin triple as alternatives	Test of cure (UBT or FAT) ≥4 weeks post-treatment, after 2-week PPI hold; endoscopy for alarm features; gastric cancer surveillance if atrophy
Lymphocytic Gastritis	>25 IEL/100 epithelial cells; association with H. pylori, celiac disease	H. pylori eradication if positive; gluten-free diet if celiac; budesonide for refractory idiopathic cases	Repeat biopsy to confirm resolution; celiac serology if relevant
NSAID Gastropathy	NSAID use history; erosions or ulcers on endoscopy; often asymptomatic	PPI once daily (standard dose); NSAID discontinuation if possible; H. pylori test-and-treat; COX-2 + PPI for high GI risk	Symptom reassessment at 4–8 weeks; endoscopy if alarm features; reassess need for gastroprotection at every visit
Phlegmonous Gastritis	Sepsis + gastric wall thickening on CT; purulent endoscopic findings; bacterial culture from biopsy	IV broad-spectrum antibiotics (piperacillin-tazobactam or vancomycin + meropenem); surgical consultation	Blood cultures; repeat CT/endoscopy to assess response; surgery for non-response or perforation
Radiation Gastritis	Radiation history; telangiectasias/erosions on endoscopy; recurrent bleeding	Acute: PPI + sucralfate + antiemetics. Chronic: APC endoscopy (preferred for vascular ectasia bleeding); hyperbaric oxygen (select centers)	Endoscopy as clinically indicated; multidisciplinary coordination
Stress-related Mucosal Disease	Critically ill; ICU risk factors (coagulopathy, shock, liver disease); diffuse superficial erosions	IV/enteral PPI or H2RA while risk factors persist (no agent superiority per PEPTIC/REVISE)	Daily reassessment; deprescribe at ICU discharge; REVISE (2024): pantoprazole reduced CIGIB vs. placebo in ventilated patients