Antral Gastritis: Types, Symptoms, and Treatment

Antral gastritis is an inflammatory and degenerative change in the antral mucosa of the stomach (the distal 20-30% of the organ adjacent to the pylorus). This is where Helicobacter pylori infection most often begins and "lives," and where chemical damage (bile reflux, alcohol, drugs) also occurs. Therefore, the antrum is often the "first target" for gastritis and gastropathies. The clinical spectrum is broad: from minimal dyspepsia to erosions with bleeding and progression to atrophy with the risk of intestinal metaplasia. Understanding the phenotype (superficial, erosive, atrophic, focal/nodular) determines the treatment strategy. [1]

Today, endoscopists rely on the Kyoto classification of gastritis: a combined "Kyoto score" (0-8) based on key findings (H. pylori-like changes, atrophy, intestinal metaplasia, etc.) helps assess the risk of gastric cancer "at the tip of the endoscope." The diagnosis is then confirmed by histology using the Sydney system with the correct biopsy scheme (antrum × 2, corpus × 2, incisura × 1), and severity is staged according to OLGA/OLGIM, which is important for prognosis. [2]

A distinct phenotype, nodular antral gastritis: "goose bumps" of follicular nodules in young individuals (especially women), is almost always associated with H. pylori and requires eradication; without treatment, some cases are associated with an increased cancer risk. Eradication leads to regression of the nodules and a reduction in risk. [3]

It's important to distinguish between gastritis (inflammation) and gastropathy (chemical/vascular damage with minimal inflammation): for example, "erosive gastritis" in medical reports often reflects erosive gastropathy. For the patient, this isn't just a nitpick, but rather different treatment options: eradication for H. pylori gastritis; elimination of chemical aggression and mucosal protection for gastropathy. [4]

Code according to ICD-10 and ICD-11

In ICD-10-CM, antral gastritis is coded in block K29 "Gastritis and duodenitis." In practice, K29.6x ("other chronic gastritis") is used, specifying "with/without bleeding" (K29.61/K29.60), or K29.0x for acute forms; in the case of bleeding, a complication code is required. There is no specific code for "antral"—location and etiology are indicated in the diagnosis text. [5]

In ICD-11, gastritis is grouped under the heading DA42 with convenient post-coordination: it can record "Helicobacter pylori-induced" (DA42.1), "autoimmune" (DA42.0), "due to duodenogastric reflux" (DA42.5), etc., and also note the complication "with hemorrhage." This approach better aligns with clinical and pathological reality. [6]

If intestinal metaplasia/dysplasia is present, this must be reported separately, as it impacts monitoring according to the European MAPS guidelines (2025 update). If H. pylori is detected, the infection and eradication plan are explicitly stated in the diagnosis. [7]

Table 1. How to formulate a diagnosis (coding logic)

Scenario	ICD-10-CM	ICD-11 (post-coordination idea)
Chronic antral H. pylori gastritis without bleeding	K29.60 + indicate H. pylori in the text	DA42.1 (H. pylori induced)
Erosive gastropathy with bleeding	K29.61	DA42 + “with hemorrhage” + “drug/chemical”
Atrophic antral gastritis	K29.4	DA42 + clarification of etiology/CM

Epidemiology

Antral localization is the classic onset of H. pylori gastritis: in populations with high infection rates, the proportion of antral forms predominates, although with the spread of eradication and a decrease in infection rates, the picture is changing. The nodular antral phenotype is typical for young people, more often women. [8]

Erosive-hemorrhagic lesions (including antral lesions) are a significant cause of hospitalization for upper gastrointestinal bleeding; outcomes have improved thanks to standardized management (early endoscopy, PPIs). In the intensive care unit (ICU), stress injuries remain common, but prophylaxis is indicated only for high-risk patients. [9]

The incidence of atrophy and intestinal metaplasia after uncontrolled antral H. pylori gastritis increases with age; this is reflected in the MAPS III (2025) surveillance protocols, where intervals depend on the extent and type of metaplasia (especially “incomplete”). [10]

In real-life practice, adherence to the Sydney biopsy protocol significantly increases the detection of atrophy/metaplasia and autoimmune gastritis; non-compliance leads to “underestimation” of risk. [11]

Reasons

The main driver of antral gastritis is H. pylori. In the early stages, inflammation is limited to the antrum, but can later spread to the body/fundus, leading to atrophy and intestinal metaplasia. Early eradication reduces the risk of ulcers and gastric cancer. [12]

The second large group is chemical damage: duodenogastric reflux (bile acids/lysolecithin), alcohol, NSAIDs/aspirin, etc. This most often causes erosive gastropathy of the antrum with minimal inflammation, but is clinically dangerous due to bleeding. [13]

The nodular antral phenotype is almost always associated with H. pylori infection and follicular lymphoid hyperplasia; in some series, an association with increased cancer risk has been noted, so eradication is indicated even in cases of mild symptoms. [14]

Less common causes are autoimmune gastritis (usually body-predominant), eosinophilic, lymphocytic gastritis, etc.; they require verification by biopsy and specific management. [15]

Risk factors

Persistent H. pylori infection (familial clusters, residence in endemic regions, childhood infection) is the main modifiable risk factor for antral gastritis and its complications. The longer the infection, the higher the risk of atrophy/metaplasia. [16]

Taking NSAIDs/aspirin, especially in combination with anticoagulants or dual antiplatelet therapy, dramatically increases the risk of antrum erosions/bleeding - gastroprotection with PPIs is important in high-risk groups. [17]

Alcohol, smoking, late, large dinners, and early post-meal horizontalization increase duodenogastric reflux and maintain a "reactive" antral phenotype. Lifestyle modification is a simple and undervalued measure. [18]

Older age and male gender are associated with higher OLGA/OLGIM stages; familial gastric cancer increases the need for MAPS surveillance. [19]

Pathogenesis

H. pylori infection activates inflammation and oxidative stress in the antrum, reduces the bicarbonate barrier, and causes "acid drift" toward the pylorus. The antral mucosa becomes vulnerable to acid, erosions/ulcers develop, and, with prolonged infection, atrophy and metaplasia occur. The Kyoto system captures these endoscopic risk markers. [20]

Chemical trauma (bile acids, NSAIDs, ethanol) disrupts the mucosal-bicarbonate barrier and microcirculation, causing foveolar hyperplasia and superficial erosions with minimal inflammation—a typical "erosive gastropathy." It can bleed even with a "minor" endoscopic picture. [21]

Nodular antral gastritis is a manifestation of follicular lymphoid hyperplasia in the presence of H. pylori; endoscopic "goose bumps" often regress after eradication, confirming a causal relationship. [22]

The transition to atrophy and intestinal metaplasia is the key to oncological risk. The degree of atrophy (OLGA) and metaplasia (OLGIM), as well as the type of metaplasia (incomplete, worse) determine the frequency of surveillance (MAPS III, 2025). [23]

Symptoms

Typical complaints include burning/pain in the epigastrium, heaviness, early satiety, nausea, and bloating; with a biliary component, bitterness in the mouth, worsening after fatty and late meals. Symptoms often correlate weakly with the severity of morphological changes. [24]

The erosive antral phenotype may present with bleeding: melena, coffee ground vomiting, dizziness, weakness - “red flags” requiring emergency care and early endoscopy. [25]

In H. pylori, "functional-like" complaints without obvious endoscopy are possible; this does not exclude the need for a test-and-treat strategy, because eradication reduces the risks of future ulcers/oncopathology. [26]

In the atrophic process, signs of deficiency (iron, B12 in tele-pangastritis) come to the fore, although for “pure” antral atrophy, B12 deficiency is not typical: more often, iron deficiency anemia against the background of microbleeding. [27]

Forms and stages

A distinction is made between: (1) superficial (non-atrophic) antral gastritis, most often H. pylori-associated; (2) erosive/hemorrhagic (often gastropathy); (3) atrophic antral gastritis; (4) focal/nodular phenotype. Endoscopic phenotype + histology determine the route. [28]

Severity is staged according to OLGA (atrophy) and OLGIM (intestinal metaplasia): low stages (I-II) are usually managed individually; high stages (III-IV) are monitored regularly according to MAPS. A Kyoto total score ≥4 indicates an increased oncological risk. [29]

Erosive forms are classified by complications: without bleeding; with occult blood loss (IBL); with acute bleeding (requiring hospitalization and early EGD). This determines the urgency of treatment. [30]

Nodular antral gastritis is considered as an indication for eradication regardless of the severity of symptoms, with monitoring of cure. [31]

Complications and consequences

The main complications of the erosive antral phenotype are bleeding and iron deficiency anemia. Management is standardized: resuscitation, intravenous proton pump inhibitors, early endoscopy with hemostasis, and then secondary prevention. [32]

Long-term H. pylori infection increases the risk of duodenal/gastric ulcer and gastric cancer through the atrophy→metaplasia→dysplasia cascade. Eradication reduces these risks, especially in the early stages. [33]

Atrophic process - risk of nutritional deficiencies and oncopathology; the decision on endoscopic observation is made according to MAPS III, taking into account the extent/type of metaplasia and family history. [34]

Psychosocial consequences include anxiety about "chronic gastritis," dietary restrictions, and antacid overuse. A clear plan (what we're treating and why) increases adherence and reduces risks.

Diagnostics

The starting point is the anamnesis (NSAIDs/aspirin, anticoagulants/antiplatelet agents, alcohol, late dinners), symptoms and “red flags”. Basic tests: complete blood count, ferritin/iron; if blood loss is suspected - a coagulogram; in chronic cases - testing for H. pylori. [35]

The "gold standard" for visualization is high-quality EGD. The endoscopist describes the findings according to the Kyoto standard (atrophy, metaplasia, nodularity, reflux signs) and takes multiple biopsies according to the updated Sydney scheme (antrum × 2, corpus × 2, incisura × 1) + targeted biopsies. This allows for the staging of OLGA/OLGIM and the detection of preneoplastic changes. [36]

H. pylori is diagnosed by a urea breath test or stool antigen (with “windows”: PPI ≥2 weeks, antibiotics/bismuth ≥4 weeks) or biopsy methods (rapid urease, histology). Monitoring of cure is mandatory using the same non-invasive tests. [37]

In case of antrum bleeding, the standard upper GI bleeding management includes early endoscopy (risk assessment for GBS), endoscopic hemostasis (clips/injections/thermocoagulation), and PPIs. Most gastritis/gastropathic bleeding is self-limited, but high risk requires active management. [38]

Table 2. When and what to examine

Situation	What are we doing?	For what
Dyspepsia without "flags"	Test-and-treat H. pylori	Reducing the risk of ulcers/oncocascade
Flags/age/ZhDA	EGD + Sydney biopsies	Rule out preneoplasia/blood source
Suspected reflux chemotherapy	EGD with assessment of bile reflux	Identify gastropathy and adjust treatment tactics
Acute bleeding	I.V. PPI + early EGDS, GBS	Diagnostics + hemostasis/risk stratification

Differential diagnosis

Antral H. pylori gastritis vs. erosive gastropathy: in gastritis, inflammation and H. pylori positivity play a leading role; in gastropathy, chemical injury (bile/NSAIDs) and minimal inflammation. Treatment differs: eradication vs. elimination of aggression + PPIs. [39]

Nodular gastritis vs. hyperplastic polyps: nodularity is a "goose bump" without a stalk; hyperplastic polyps are isolated lesions. The decision is made by high-quality endoscopy, NBI/magnification, and biopsy/removal of suspicious lesions. Eradication of the nodular phenotype is standard. [40]

Antral atrophy vs. chemical "reactive" antritis: in atrophy, there is histological loss of glands and, often, intestinal metaplasia; in the chemical form, there is foveolar hyperplasia and edema without pronounced atrophy. The decision is made by histology with a proper biopsy map. [41]

Eosinophilic/lymphocytic gastritis and Menetrier's disease with "thick folds" are also excluded, but for the antral zone this is rare; biopsy, EUS/CT are helpful when indicated. [42]

Table 3. "Similar, but not the same"

What do we see?	More like…	How to confirm
Multiple punctate erosions of the antrum	Erosive gastropathy	History of NSAIDs/bile, histology
Goosebumps in a young woman	Nodular H. pylori gastritis	H. pylori testing → eradication
Pale thin mucous membrane, areas of CM	Atrophic gastritis	Sydney Biopsies → OLGA/OLGIM
Acute bleeding without ulcer	Erosive phenotype	EGDS + hemostasis if necessary

Treatment

H. pylori-associated antral gastritis. First-line therapy is 14-day optimized bismuth quadruple therapy (PPI bid, tetracycline 500 mg qid, metronidazole 500 mg tid/qid, bismuth qid). The clarithromycin "troika" without susceptibility testing is no longer used. Alternatives in the absence of penicillin allergy are rifabutin—triple or double regimen with PCAB (where available). Monitoring of cure is mandatory. [43]

Erosive/hemorrhagic antral phenotype (often gastropathy). The basis is to eliminate the cause (NSAIDs/alcohol/bile reflux), proton pump inhibitors (PPIs) in healing doses; in case of bleeding, the standard upper gastrointestinal bleeding management is: intravenous PPIs, early EGD with hemostasis (injection/clips/thermotechnics), then transition to oral administration. Most gastritis bleeding is self-limited, but high-risk cases require active endotherapy. [44]

Atrophic antral gastritis. Eradication of H. pylori (if detected), even at the atrophic stage, reduces risks but does not negate monitoring for extensive/incomplete intestinal metaplasia. Intervals are based on MAPS III (2025) with personalization (family history, quality of examination). Symptom control with PPIs is recommended for those who require them, without "indefinite" regimens. [45]

Biliary (reactive) antritis. Behavioral measures (eating small meals, not lying down for 2-3 hours after eating, avoiding late fatty dinners), PPIs in mixed cases, and prokinetics/ursodeoxycholic acid based on symptoms. Regular medication audits (NSAIDs/antiplatelet agents) are essential. [46]

Table 4. Therapy by phenotypes (short plan)

Phenotype	First line	Escalation/Reserve
H. pylori-antrum	14 days of bismuth quadruple therapy + healing monitoring	Rifabutin-triple / PCAB-double
Erosive/hemorrhagic	Canceling the cause + PPI; in case of bleeding - EGDS hemostasis	Repeated hemostasis/angio/surgery as indicated
Atrophic antrum	Eradication (if +) + MAPS monitoring	Individualization of intervals
Biliary (reactive)	Regime + PPI/prokinetics/UDCA	Correction of associated factors

Table 5. “Windows” before H. pylori tests and cure monitoring

Drug/factor	Minimal break
IPP	≥ 2 weeks
Antibiotics/bismuth	≥ 4 weeks
Cure control (UBT/Ag-cal)	≥ 4 weeks after the end of therapy

Table 6. When hospitalization is mandatory

Sign	Why
Melena/hematemesis, hemodynamic instability	Urgent EGD and intensive care are needed.
Rapid fall in Hb/symptomatic IDA	Transfusion/source retrieval, secondary prevention
Antithrombotics + "red flags"	High risk of rebleeding
Elderly + NSAIDs + pain/vomiting	High mortality without early stratification

Prevention

Primary: identify and eradicate H. pylori (test-and-treat strategy), minimize NSAIDs/alcohol, do not combine NSAIDs with anticoagulants/dual antiplatelet agents unless absolutely necessary; in high-gastrointestinal risk groups, gastroprotection with PPIs during the risk period. Correction of diet and avoidance of late dinners reduce biliary reflux and antral symptoms. [47]

Secondary: After bleeding, complete the PPI course, eliminate the cause, and educate the patient about red flags. In case of atrophy/metaplasia, follow-up according to MAPS III (2025) with personalization (familial gastric cancer, type of metaplasia, quality of examination). Review long-term acid suppression, avoiding hyperprescribing. [48]

Forecast

With H. pylori-associated antral gastritis, the prognosis is favorable with successful eradication: inflammation and the nodular phenotype disappear, and the risk of ulcers and cancer is reduced. The key is monitoring the cure using the "window" rules. [49]

Erosive/reactive forms respond well to treatment of the underlying cause and a short course of PPIs; the outcome in cases of bleeding is determined by the speed of routing (early endoscopy reduces mortality). In cases of atrophy, the prognosis depends on the OLGA/OLGIM stage and adherence to MAPS surveillance. [50]

FAQ

• Are antral gastritis and erosive gastritis the same thing?

No. "Antral" is the localization. "Erosive" describes superficial defects and often refers to gastropathy (chemical damage) with minimal inflammation. Tactics vary: eradication of H. pylori versus elimination of aggression and PPIs. [51]

• Is it necessary to treat H. pylori if there are almost no complaints?

Yes. According to ACG-2024/2025, the first line is 14-day bismuth quadruple therapy; the clarithromycin "troika" without susceptibility testing is no longer used. Cure monitoring is mandatory. [52]

• What to do if you need NSAIDs “for life”?

Use the minimum dose/duration, consider alternatives (paracetamol, topical forms), in case of high gastrointestinal risk - PPI for the duration of therapy; avoid combinations with alcohol and unjustified dual antiaggregation. [53]

• Does everyone need biopsies?

No. But for "flags," suspected atrophy/metaplasia, and for OLGA/OLGIM staging, yes, according to the updated Sydney scheme (5 points). This affects prognosis and follow-up. [54]

• Nodular antral gastritis was found in a young woman - is it dangerous?

This is a marker for H. pylori; eradication with cure monitoring is indicated. There is evidence of a link between nodularity and cancer risk, so treatment is important even with mild symptoms. [55]