Acute Gastritis and Gastropathy

Name: Acute Gastritis and Gastropathy
Creator: MedVellum Editorial Team

1. Clinical Overview

Summary

Acute gastritis and gastropathy represent a spectrum of gastric mucosal injuries ranging from mild inflammation to severe erosions and haemorrhage. [1] It is crucial to distinguish between gastritis (histological evidence of inflammation, typically neutrophils) and gastropathy (mucosal injury with minimal or no inflammation, often chemical or vascular). [2]

The primary aetiologies include Helicobacter pylori infection, Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), alcohol, and severe physiological stress (e.g., in ICU). [3] The Maastricht VI/Florence Consensus (2022) remains the gold standard for H. pylori management, emphasizing 14-day treatment durations and the rising role of bismuth-based quadruple therapy. [4] Management focuses on identifying the cause, acid suppression with Proton Pump Inhibitors (PPIs), and eradication of H. pylori where indicated. [5]

Key Facts

Gastritis vs. Gastropathy: Histology is the differentiator. NSAIDs and alcohol typically cause gastropathy, while H. pylori causes gastritis. [2]
The "2-Week Wait": In the UK (NICE NG12), any patient > 55 years with new-onset unexplained dyspepsia requires urgent endoscopy (2WW) to exclude malignancy. [6]
H. pylori and Cancer: H. pylori is a Class I carcinogen. It triggers the Correa Cascade: Normal → Chronic Gastritis → Atrophic Gastritis → Intestinal Metaplasia → Dysplasia → Adenocarcinoma. [7,8]
P-CABs (Vonoprazan): Potassium-competitive acid blockers (P-CABs) like Vonoprazan are now integrated into guidelines as a potent alternative to PPIs for H. pylori eradication, offering faster and more stable acid inhibition. [9]
HEAT Trial: Demonstrated that H. pylori eradication reduces the risk of peptic ulcer hospitalisation in patients starting long-term aspirin. [10]

Clinical Pearls

The "NSAID+Steroid" Pearl: Corticosteroids alone do not significantly increase the risk of gastritis, but when combined with NSAIDs, they increase the risk of a major GI event by 4 to 15 times. Always use a PPI if both are required. [11]

The "B12 Mystery" Pearl: In a patient with megaloblastic anaemia and autoimmune conditions (e.g., Vitiligo, Thyroiditis), suspect Autoimmune Gastritis (AIG). It causes atrophy of the corpus, leading to loss of parietal cells and intrinsic factor. [12]

The "Testing" Warning: Patients MUST be off PPIs for at least 2 weeks and off antibiotics for 4 weeks before undergoing a Urea Breath Test or Stool Antigen Test to avoid false-negative results. [4]

2. Epidemiology & Risk Factors

Incidence & Distribution

Prevalence: H. pylori colonises approximately 50% of the world's population, though prevalence is declining in developed nations. [13]
NSAID Use: Approximately 25% of chronic NSAID users will develop mucosal injury (gastropathy) on endoscopy. [14]
Stress Gastritis: Occurs in up to 75% of critically ill patients within 24 hours of ICU admission if prophylaxis is not provided. [15]

Risk Factors

Category	Factor	Impact
Infectious	H. pylori	Most common cause of chronic active gastritis globally. [4]
Chemical	NSAIDs/Aspirin	Direct mucosal toxicity + systemic COX-1 inhibition. [10,14]
Lifestyle	Alcohol	Direct irritant; causes erosive "hemorrhagic" gastropathy. [1]
Autoimmune	Anti-parietal antibodies	Leads to corpus-restricted atrophic gastritis and B12 deficiency. [12]
Vascular	Portal Hypertension	Causes "Watermelon Stomach" (GAVE) or Portal Hypertensive Gastropathy.

3. Pathophysiology

1. The Mucosal Barrier

The stomach maintains a balance between "Aggressors" (Acid, Pepsin, Bile) and "Defenders" (Mucus, Bicarbonate, Prostaglandins, Blood Flow).

Prostaglandins (PGE2/PGI2) are the master regulators. They stimulate mucus and bicarbonate secretion and maintain mucosal blood flow. [1]

2. NSAID Injury (Gastropathy)

NSAIDs inhibit the COX-1 enzyme. This reduces prostaglandin synthesis, leading to:

Decreased bicarbonate and mucus production.
Impaired mucosal blood flow.
Direct topical irritation (the "ion-trapping" effect). [14]

3. H. pylori Gastritis

The bacteria produce Urease, which converts urea into ammonia and CO2, creating an alkaline microenvironment. Ammonia is directly toxic to epithelial cells. The resulting chronic inflammation leads to the recruitment of neutrophils (activity) and lymphocytes (chronicity). [7]

Severe physiological stress (burns, sepsis, trauma) causes splanchnic vasoconstriction. The resulting ischaemia reduces the ability of the mucosa to neutralise acid, leading to multiple superficial fundal erosions. [15]

4. Clinical Presentation

Symptoms

Epigastric Pain: Often described as burning or "gnawing."
Dyspepsia: Nausea, bloating, and early satiety.
Vomiting: May be persistent in severe cases.
Asymptomatic: Many patients with H. pylori or early NSAID injury have no symptoms until a complication (e.g., ulcer) occurs. [1,4]

Physical Signs

Epigastric Tenderness: Usually mild. Severe tenderness suggests a complication like perforation.
Pallor: Suggests chronic blood loss (Iron deficiency) or B12 deficiency (Autoimmune gastritis).
Succussion Splash: Rare; suggests gastric outlet obstruction (more common in ulcers or cancer).

Red Flags (NICE NG12)

Haematemesis/Melaena (Acute bleed).
Unexplained weight loss.
Dysphagia (Suspect oesophageal/gastric cancer).
Upper abdominal mass.
Iron deficiency anaemia. [6]

5. Investigations

1. H. pylori Testing (The "Test and Treat" Strategy)

Urea Breath Test (C-13): Gold standard non-invasive test (Sensitivity/Specificity > 95%). [4]
Stool Antigen Test: Excellent alternative.
Serology (IgG): Only indicates exposure; cannot be used to confirm eradication.

2. Endoscopy (OGD)

Indications: Red flags, age > 55 with new symptoms, or failure of medical therapy. [6]
Findings: Erythema, subepithelial haemorrhages (typical of alcohol), or "fluffy" white exudates.
Biopsy: Essential to confirm gastritis (neutrophils) and rule out malignancy or metaplasia.

3. Laboratory Assessment

FBC: Check for microcytic (Iron def) or macrocytic (B12 def) anaemia.
Serum Gastrin: Significantly elevated in Autoimmune Gastritis due to loss of negative feedback from acid. [12]
Anti-Parietal Cell Antibodies: Positive in 85-90% of patients with AIG.

6. Management: The Gastritis Algorithm

Management Flowchart (ASCII)

                  [DYSPEPSIA / SUSPECTED GASTRITIS]
                             |
              +--------------v--------------+
              |    CHECK FOR ALARM SIGNS    |
              | (Bleeding, Weight Loss, Age)|
              +--------------+--------------+
                             |
              /--------------+--------------\
      [ALARM SIGNS PRESENT]           [NO ALARM SIGNS]
      (or Age > 55 new onset)                 |
             |                        +------v------+
      +------v------+                 | TEST & TREAT|
      | URGENT OGD  |                 | (H. pylori) |
      | (2-week wait)                 +------+------+
      +-------------+                        |
                                      /------+------\
                             [POSITIVE]            [NEGATIVE]
                                 |                      |
                        +--------v--------+    +--------v--------+
                        | ERADICATION     |    | 1. STOP NSAIDs  |
                        | (14-day Triple) |    | 2. PPI 4-8 Wks  |
                        +--------+--------+    +-----------------+
                                 |
                        +--------v--------+
                        | TEST OF CURE    |
                        | (UBT @ 4 Weeks) |
                        +-----------------+

1. H. pylori Eradication (Maastricht VI)

Standard 14-day regimens are now preferred over 7-day courses due to rising resistance. [4]

First-line (Standard Triple): PPI (BD) + Amoxicillin (1g BD) + Clarithromycin (500mg BD).
Bismuth Quadruple (If high Clarithromycin resistance): PPI + Bismuth + Metronidazole + Tetracycline.
P-CAB Regimen: Vonoprazan + Amoxicillin + Clarithromycin. [9]

2. Non-H. pylori Management

PPI Therapy: Omeprazole 20mg or Lansoprazole 30mg daily for 4–8 weeks.
NSAID Management: Switch to a COX-2 selective inhibitor (e.g., Celecoxib) + PPI, or ideally, stop NSAIDs entirely. [14]
Stress Ulcer Prophylaxis: IV PPI or H2-receptor antagonists (e.g., Famotidine) in ventilated patients. [15]

7. Complications

Peptic Ulcer Disease (PUD): Progression of erosion to a deep ulcer.
Upper GI Haemorrhage: May be life-threatening.
Gastric Cancer: Specifically associated with chronic H. pylori atrophic gastritis. [8]
Pernicious Anaemia: Secondary to autoimmune atrophic gastritis. [12]
MALT Lymphoma: A low-grade B-cell lymphoma highly associated with H. pylori. [4]

8. Evidence & Landmark Trials

Maastricht VI/Florence Consensus (2022): The definitive international guideline for H. pylori management. [4]
The HEAT Trial (PMID: 36343657): Randomized trial showing H. pylori eradication reduces ulcer bleeding in aspirin users (The H. pylori Eradication Aspirin Trial). [10]
Correa Cascade (1992): Defined the pathological progression from gastritis to gastric cancer. [7]
Cochrane Review (2019): Confirmed that P-CABs (Vonoprazan) are non-inferior (and in some cases superior) to PPIs for H. pylori eradication. [16]

9. Single Best Answer (SBA) Questions

Question 1

A 58-year-old male presents with a 2-month history of epigastric bloating and occasional nausea. He has no weight loss and no change in bowel habits. He takes no regular medications. What is the most appropriate next step according to NICE guidelines?

A) Start Omeprazole 20mg daily for 4 weeks
B) Perform a Urea Breath Test
C) Refer for an urgent (2-week wait) upper GI endoscopy
D) Start triple therapy for H. pylori empirically
E) Check serum gastrin levels
Answer: C. Any patient > 55 years with new-onset unexplained dyspepsia requires a 2-week wait referral for endoscopy.

Question 2

A patient requires H. pylori eradication but is allergic to penicillin. Which of the following is the standard first-line triple therapy for this patient?

A) PPI + Clarithromycin + Amoxicillin
B) PPI + Clarithromycin + Metronidazole
C) PPI + Metronidazole + Tetracycline
D) PPI + Bismuth + Amoxicillin
E) PPI + Vancomycin + Metronidazole
Answer: B. For penicillin-allergic patients, metronidazole is substituted for amoxicillin in the triple therapy regimen.

Question 3

Which histological finding is required to definitively diagnose "gastritis" as opposed to "gastropathy"?

A) Mucosal erythema
B) Presence of subepithelial haemorrhages
C) Infiltration of the mucosa with neutrophils
D) Foveolar hyperplasia
E) Presence of H. pylori on the surface
Answer: C. Gastritis specifically refers to inflammation (neutrophils), whereas gastropathy involves injury/regeneration without significant inflammation.

Question 4

A 45-year-old female with a history of vitiligo presents with fatigue and numbness in her feet. Blood tests show a macrocytic anaemia and low B12. An endoscopy shows thinning of the mucosa in the gastric body and fundus, but a normal antrum. What is the most likely diagnosis?

A) H. pylori pangastritis
B) NSAID-induced gastropathy
C) Autoimmune Gastritis (AIG)
D) Menetrier's disease
E) Zollinger-Ellison Syndrome
Answer: C. AIG is characterized by corpus-restricted atrophy (body/fundus), sparing of the antrum, and association with other autoimmune conditions and B12 deficiency.

Question 5

A patient is planned for a Urea Breath Test to confirm H. pylori eradication. How long should they have stopped their Proton Pump Inhibitor (PPI) before the test?

A) 24 hours
B) 48 hours
C) 1 week
D) 2 weeks
E) 4 weeks
Answer: D. PPIs should be stopped for at least 2 weeks before testing to prevent false negatives.

Question 6

Which trial demonstrated that H. pylori eradication reduces the rate of hospitalisation for peptic ulcer disease in patients taking low-dose aspirin?

A) PLATO
B) HEAT
C) COMPASS
D) AVOID
E) TRITON
Answer: B. The HEAT (H. pylori Eradication Aspirin Trial) showed a significant reduction in ulcer events in the first 2.5 years of follow-up.

Question 7

What is the primary mechanism by which NSAIDs cause gastric mucosal injury?

A) Stimulation of gastrin release
B) Direct inhibition of H+/K+ ATPase
C) Inhibition of COX-1 leading to reduced prostaglandins
D) Activation of the vagus nerve
E) Promotion of H. pylori growth
Answer: C. COX-1 inhibition is the central mechanism of NSAID-induced gastropathy.

Question 8

In the updated Sydney Classification, which term describes the presence of neutrophils on a gastric biopsy?

A) Chronicity
B) Atrophy
C) Metaplasia
D) Activity
E) Dysplasia
Answer: D. "Activity" in the Sydney system refers specifically to the presence of polymorphonuclear leucocytes (neutrophils).

Question 9

A 70-year-old patient on the ICU for sepsis develops coffee-ground vomiting. Endoscopy shows multiple small, shallow erosions throughout the fundus. What is the most likely diagnosis?

A) Dieulafoy lesion
B) Mallory-Weiss tear
C) Stress-related mucosal disease (SRMD)
D) Gastric antral vascular ectasia (GAVE)
E) Peptic ulcer perforation
Answer: C. SRMD typically presents with multiple superficial erosions in the fundus in critically ill patients.

Question 10

Which medication is a Potassium-Competitive Acid Blocker (P-CAB) recently approved for use in H. pylori eradication?

A) Pantoprazole
B) Famotidine
C) Vonoprazan
D) Misoprostol
E) Sucralfate
Answer: C. Vonoprazan is the first-in-class P-CAB used for acid suppression.

10. Patient Explanation

"Gastritis is inflammation of the stomach lining. Imagine the lining of your stomach is like a protective coat that shields the wall from the strong acid used for digestion. If this coat gets damaged—either by a common bacterial infection called H. pylori, certain painkillers (like ibuprofen or aspirin), or too much alcohol—the acid can irritate the stomach wall.

This can cause a burning pain in the top of your tummy, feeling sick, or bloating. The good news is that the stomach lining heals very quickly once we remove the cause. If it's the bacteria, we use a two-week course of antibiotics. If it's a medication, we might ask you to stop it or give you an 'acid-blocker' tablet (like omeprazole) to let the lining rest and heal. It's important to treat it, because if left alone, it can lead to more serious sores called ulcers. If you ever notice very dark stools or vomit that looks like coffee grounds, you should see a doctor immediately."

11. References

Laine L. Gastritis and gastropathy. In: Feldman M, et al. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 2020.
Dixon MF, et al. Classification and grading of gastritis. The updated Sydney System. Am J Surg Pathol. 1996. [PMID: 8827022]
Rugge M, et al. Gastritis: The histology report. Dig Liver Dis. 2011. [PMID: 21239101]
Malfertheiner P, et al. Management of Helicobacter pylori infection-the Maastricht VI/Florence consensus report. Gut. 2022. [PMID: 35948335]
Chey WD, et al. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2017. [PMID: 28141652]
NICE. Suspected cancer: recognition and referral. NG12. 2015 (Updated 2023).
Correa P. Human gastric carcinogenesis: a multistep and multifactorial process. Cancer Res. 1992. [PMID: 1458460]
Wroblewski LE, et al. Helicobacter pylori and gastric cancer: factors that modulate disease risk. Clin Microbiol Rev. 2010. [PMID: 20930075]
Chey WD, et al. Vonoprazan Triple and Dual Therapy for Helicobacter pylori Infection in the United States and Europe. Gastroenterology. 2022. [PMID: 35623453]
Hawkey CJ, et al. Helicobacter pylori eradication for primary prevention of peptic ulcer bleeding in older patients taking aspirin (HEAT): a randomised trial. Lancet. 2022. [PMID: 36343657]
Piper JM, et al. Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs. Ann Intern Med. 1991. [PMID: 2014942]
Lenti MV, et al. Autoimmune gastritis. Nat Rev Dis Primers. 2020. [PMID: 32647111]
Hooi JKY, et al. Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis. Gastroenterology. 2017. [PMID: 28456631]
Sostres C, et al. Adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs, aspirin and coxibs) on upper gastrointestinal tract. Best Pract Res Clin Gastroenterol. 2010. [PMID: 20227718]
Krag M, et al. Pantoprazole in Patients at Risk for Gastrointestinal Bleeding in the ICU. N Engl J Med. 2018. [PMID: 30354950]
Scarpignato C, et al. Vonoprazan for Helicobacter pylori Eradication: A Systematic Review. J Clin Med. 2019. [PMID: 31766620]

Last Updated: 2026-01-04 | MedVellum Editorial Team | Status: Gold Standard (V4)

Clinical board

Urgent signals

Linked comparisons

Editorial and exam context