Subatrophic Gastritis: Symptoms, Forms, and Treatment

The term "subatrophic gastritis" is widely used in Russian-language practice and essentially describes early or moderate manifestations of gastric mucosal atrophy: the glands are partially thinned/lost, but the process is not completely pronounced. International classifications more often use "superficial/non-atrophic gastritis" and "atrophic gastritis," while OLGA/OLGIM staging is used for severity; the concept of "subatrophy" as a separate nosology is not included there. It is more correct to use "early (moderate) atrophy" or "low-stage atrophic gastritis according to OLGA/OLGIM." This is important for an accurate prognosis and monitoring tactics. [1]

Atrophic gastritis is a preneoplastic condition: long-term inflammation (usually caused by Helicobacter pylori or an autoimmune process) leads to loss of glandular epithelium, followed by intestinal metaplasia and an increased risk of gastric cancer. Early stages ("subatrophic") represent a window of opportunity: timely eradication of H. pylori and correction of risk factors slow progression and reduce cancer risks. [2]

Endoscopists are increasingly using the Kyoto score for gastritis, which, based on a combination of features (atrophy, metaplasia, etc.), helps assess the risk of oncopathology and probable H. pylori etiology "at the tip of the endoscope." The diagnosis is then confirmed by histology using the Sydney system, with translation into OLGA/OLGIM staging. [3]

Management tactics depend on the cause (H. pylori, autoimmune gastritis), the stage of atrophy (OLGA/OLGIM), the presence of intestinal metaplasia, and associated deficiencies (iron, vitamin B12). European (MAPS II 2019 and MAPS III update 2025) and American (AGA CPU 2021) guidelines offer clear monitoring pathways, which we adapt below for the "subatrophic" context. [4]

Code according to ICD-10 and ICD-11

In ICD-10-CM, atrophic gastritis is coded in block K29 ("gastritis and duodenitis"), typically as K29.4 (chronic atrophic gastritis) with local clarification ("with/without bleeding"). There is no separate code for the "subatrophic" variant—the clinician specifies "atrophic gastritis" and specifies the degree/etiology in the diagnosis.

In ICD-11, atrophic gastritis is classified under DA42 ("Gastritis or duodenitis") with the possibility of post-coordination: one can add "Helicobacter pylori-induced" (if the etiology is H. pylori) or "autoimmune," as well as concomitant conditions (iron/B12 deficiency anemia) and complications. This approach better reflects the clinical and pathological nature of the process. [5]

If intestinal metaplasia or dysplasia is present, they are recorded as separate items and must be included in the discharge summary—this influences the endoscopic follow-up route according to MAPS. If pernicious anemia is diagnosed, it is listed as a late manifestation of autoimmune gastritis. [6]

Table 1. How to formulate a diagnosis for "subatrophy" (approximate logic)

Situation	How to write on a map
Early antrum atrophy (H. pylori+)	"Chronic atrophic gastritis (OLGA I-II), H. pylori-assoc.; without bleeding"
Early body atrophy (autoimmune)	"Autoimmune atrophic gastritis (OLGA I-II); hyperchlorhydria/achlorhydria, hypergastrinemia"
Atrophy + intestinal metaplasia	"Atrophic gastritis (OLGA/OLGIM stage indicated); incomplete/complete CM"
Pernicious anemia	“Autoimmune gastritis; pernicious anemia (B12 deficiency)" [7]

Epidemiology

The majority of atrophic gastritis worldwide is associated with H. pylori (environmental/metaplastic atrophic gastritis, EMAG). Prevalence varies by region and age cohort: where H. pylori declines, the proportion of EMAG also falls, but autoimmune atrophic gastritis (AIG) remains, more often found in middle-aged/older women and in patients with autoimmune thyroid diseases. [8]

Autoimmune gastritis is relatively rare compared to H. pylori-associated gastritis, but it is of high clinical significance due to deficiencies (iron in the early stages, then B12) and the risk of neurological complications of pernicious anemia. Many cases are recognized late, already at the anemia stage. [9]

Of clinical importance is that "subatrophic" findings are more often recorded in patients with dyspepsia and/or H. pylori carriers; timely eradication at this stage is most effective in halting progression. This is reflected in international guidelines for the management of H. pylori. [10]

The overall cancer risk increases with the transition from non-atrophic inflammation to atrophy and metaplasia. A Kyoto summary score ≥4 and high OLGA/OLGIM stages are associated with an increased risk of gastric cancer and require surveillance. [11]

Reasons

The two main causes are chronic H. pylori infection (antral/pangastritis with subsequent development of atrophy and metaplasia) and autoimmune process with damage to parietal cells (AIG). In both cases, prolonged inflammation leads to glandular loss and mucosal remodeling, but the pathogenesis and profile of deficiencies differ. [12]

In H. pylori, cytokine production and oxidative stress support glandular destruction; eradication at early stages inhibits atrophy and reduces cancer risks (the earlier, the more effective). In AIG, the main driver is autoantibodies to H+/K+-ATPase and intrinsic factor; the result is hypo-/achlorhydria, hypergastrinemia, ECL cell hyperplasia, and micronutrient deficiencies. [13]

Less commonly, atrophy develops with prolonged hypochlorhydria and bile reflux, after partial gastric resections, and with chronic chemical exposures. However, these scenarios are less likely to involve H. pylori and AIG.

Pharmacological acid suppression (PPI) itself does not cause atrophy, but in the case of undetected H. pylori it can mask the activity of the process; therefore, it is recommended to test and treat H. pylori taking into account the “windows” for PPI discontinuation. [14]

Risk factors

A key factor is persistent H. pylori infection (familial clusters, residence in regions of high endemicity, poor socio-hygienic status in childhood). The longer the infection, the higher the risk of transition from non-atrophic inflammation to atrophy. [15]

For AIG, association factors include female gender, other autoimmune diseases (Hashimoto's thyroiditis, vitiligo, T1D), and a family history of autoimmune diseases. These patients require screening for iron and vitamin B12 deficiencies. [16]

Smoking, a diet high in salted/smoked foods, and long-term exposure to nitrosamines are associated with the progression of precancerous lesions, while H. pylori eradication and a diet high in vegetables/fruits are associated with a reduced risk.

Older age and male gender are associated with higher OLGA/OLGIM stages in some cohorts, which is taken into account when choosing observation intervals. [17]

Pathogenesis

In H. pylori, chronic inflammation causes apoptosis and depletion of antrum/body glands, followed by intestinal metaplasia (complete/incomplete). The Kyoto system allows for endoscopic detection of risk factors (atrophy, metaplasia), while histology using the Sydney system confirms and stages the process according to OLGA/OLGIM. [18]

Autoimmune gastritis begins in the body/fundus of the stomach: autoantibodies to parietal cells lead to hypo-/achlorhydria and secondary hypergastrinemia, iron deficiency (an early sign) and, as it progresses, to B12 deficiency (pernicious anemia) and neurological symptoms. Long-term hypergastrinemia is associated with ECL cell hyperplasia. [19]

The transition to intestinal metaplasia (especially the incomplete type) increases the cancer risk: it is at this stage that MAPS surveillance protocols (high-quality endoscopy, targeted biopsies and specific intervals) are relevant. [20]

The physiological consequences of atrophy are a decrease in the secretion of acid/pepsin and Castle's intrinsic factor, which disrupts the absorption of iron and B12, changes the microbiocenosis and potentiates dyspepsia, even with a “minimal” clinical picture. [21]

Symptoms

Common symptoms are mild or nonspecific: epigastric heaviness, early satiety, flatulence, moderate pain/burning. Symptoms correlate weakly with the degree of atrophy: "subatrophy" is often a finding during endoscopy and biopsy performed for dyspepsia.

Signs of deficiency are more important than complaints: fatigue, pallor, brittle nails/hair (iron deficiency), glossitis, paresthesia, unsteadiness of gait (B12 deficiency). AIG is characterized by a combination of iron deficiency in the early stages and B12 deficiency as it progresses. [22]

Some patients experience reflux/heartburn symptoms associated with mixed gastritis; H. pylori-positive patients sometimes present with "function-like" complaints. In any case, the treatment strategy is based on the etiology and stage, not the intensity of symptoms. [23]

“Red flags”: unexplained weight loss, persistent vomiting, dysphagia, unexplained iron/B12 deficiency anemia, familial gastric cancer - indications for expedited endoscopy and targeted biopsies. [24]

Forms and stages

Anatomically, antral-predominant, fundal/body-predominant (typical for AIG), and pangastritis are distinguished. For communication with the oncorisk center and monitoring planning, OLGA (atrophy) and OLGIM (intestinal metaplasia) are used: stages 0-IV. Low stages (I-II) often correspond to what is commonly referred to as "subatrophy." [25]

The Kyoto score (0-8) is used endoscopically: total scores ≥2 indicate H. pylori gastritis, ≥4 indicate an increased risk of gastric cancer; findings of "atrophy" and "metaplasia" are particularly significant. This helps stratify patients already during examination. [26]

By etiology - H. pylori-associated gastritis (H. pylori-associated gastritis (H. pylori-associated gastritis) and autoimmune gastritis (AIG); sometimes - mixed forms (previous infection + autoimmunity). The profile of deficiencies and monitoring depend on the form. [27]

The presence of intestinal metaplasia (complete/incomplete) and dysplasia are identified separately - these findings transfer the patient to MAPS observation protocols at specific intervals. [28]

Complications and consequences

The main ones are nutritional deficiencies (iron, B12) with anemia, neurological manifestations (with B12 deficiency) and decreased quality of life. Correction should be etiotropic (eradication/management of AIG) and pathogenetic (iron, B12). [29]

The cancer risk increases with increasing OLGA/OLGIM stages and with incomplete intestinal metaplasia. Timely eradication of H. pylori reduces this risk, but does not eliminate it once severe atrophy/metaplasia has already developed; this is where surveillance protocols come into play. [30]

In AIG, prolonged hypergastrinemia leads to ECL cell hyperplasia; the risk of type 1 neuroendocrine neoplasms (usually inert but requiring monitoring) is discussed. This is another argument in favor of regular mucosal assessment. [31]

Social consequences include fatigue, cognitive decline (B12), and anxiety due to "precancer." Patient education about the real risks and the role of eradication/surveillance reduces anxiety and improves adherence.

Diagnostics

The baseline is high-quality EGD with multiple biopsies according to the Sydney protocol (lesser curvature of the antrum and body, greater curvature of the antrum and body, incisura) + targeting of suspicious areas. Histology provides Sydney scores and the OLGA stage; in the presence of metaplasia, the OLGIM stage. The endoscopist records findings according to the Kyoto protocol (atrophy/CM, etc.). [32]

H. pylori - mandatory testing and treatment: urea breath test or stool antigen (with PPI discontinuation windows of ≥2 weeks and antibiotics/bismuth ≥4 weeks), or rapid urea/histology during EGD. Cure monitoring is performed using the same noninvasive tests. [33]

Serum markers useful for AIG include parietal cell/intrinsic factor antibodies, gastrin-17 (often elevated), pepsinogen I, and the PGI/PGII ratio (a decrease indicates body atrophy). Ferritin/serum iron and vitamin B12 are also tested. [34]

The decision on observation is made according to MAPS (2019, updated 2025): the extent of metaplasia, type (incomplete/complete), OLGA/OLGIM stage, family history of GC and the quality of endoscopy are taken into account. [35]

Table 2. What and when to submit/do

Task	Tool	Comment
Confirm atrophy/CM	EGD + Sydney biopsies → OLGA/OLGIM	Basic step of risk stratification
Find/Exclude H. pylori	UBT/fecal antigen or biopsy tests	Observe the PPI/AB withdrawal windows
Rate AIG	AT to parietal cells/HF, gastrin, PGI/PGII	+ ferritin, vitamin B12
Decide about observation	MAPS II/III (ESGE), AGA CPU 2021	Intervals depend on stage/CM [36]

Differential diagnosis

We differentiate H. pylori gastritis without atrophy ("non-atrophic") from early atrophy: biopsies and serum markers (PGI/PGII) are decisive. In AIG, the body/fundus is primarily affected, whereas in H. pylori, the antrum is affected. [37]

We exclude chemical (reactive) gastritis (bile reflux/NSAIDs): histologically, there is little inflammation, foveolar hyperplasia; it is not equivalent to atrophy and is treated by eliminating aggression.

It is necessary to remember the rare granulomatous and eosinophilic gastritis, as well as Menetrier's disease (giant folds, protein loss) - their phenotypes and morphology are different.

In pernicious anemia, we always confirm AIG and exclude concomitant neoplasms (ECL-cell NET1, adenocarcinoma) according to the observation protocol. [38]

Table 3. "Similar, but not the same"

State	Tips	How to confirm
Non-atrophic H. pylori gastritis	Active inflammation, without loss of glands	Biopsies; UBT/Ag-cal
Reactive (chemical) gastritis	Bile reflux/NSAIDs, foveolar hyperplasia	Histology, anamnesis
Autoimmune gastritis	Atrophy of the body/fundus, AT+, hypergastrinemia	Serology + biopsies
Ménétrier/infiltration	Giant folds, protein-losing gastropathy	EUS/CT + targeted biopsy [39]

Treatment

1) Etiotropic therapy for H. pylori. The current standard is 14-day optimized bismuth quadruple therapy as an empirical first-line therapy. The clarithromycin "troika" without susceptibility testing is no longer used. Alternatives (when available/indicated) include rifabutin—a triple or double regimen with PCAB. Monitoring of cure is mandatory. Eradication at early stages slows/stops the progression of atrophy. [40]

2) Management of autoimmune gastritis. There is no therapeutic eradication here (if H. pylori is absent), so the emphasis is on correcting deficiencies (iron orally/intravenously; vitamin B12 - most often parenterally), monitoring gastrin/PGI and endoscopic observation according to MAPS/AGA in the presence of CM/dysplasia. In pernicious anemia - lifelong B12 replacement therapy. [41]

3) Symptom control and mucosal protection. PPI/β-blockers are used to control dyspepsia and reflux symptoms, but long-term acid suppression is avoided unless indicated (regularly review). Dietary measures (moderating salt/smoked foods, increasing vegetable/fruit intake) and smoking cessation have long-term benefits.

4) Surveillance (endoscopic intervals). According to MAPS II (2019) and the MAPS III update (2025), the intervals depend on the extent and type of CM, the OLGA/OLGIM stage, family history, and the quality of the examination. Simply put: for extensive incomplete CM and/or high stages, monitoring is more frequent (e.g., every ~3 years); for limited low stages, monitoring is individualized or without routine screening. The AGA CPU 2021 emphasizes personalization and quality of biopsies. [42]

Table 4. Anti-H. pylori regimens (2024–2025 targets)

Situation	Mode	Notes
First line (empirically)	14-day bismuth quadruple therapy	Preferred for unknown sensitivity
If BQT was already there	Rifabutin-triple (14 days)	An alternative to "salvation"
PCAB-double	By availability/indications	Not available everywhere
Cure control	UBT/Ag-cal, PPI “windows” ≥2 weeks, AB/bismuth ≥4 weeks.	Mandatory for all patients [43]

Table 5. AIG Management (Workshop)

Task	What to do
Iron deficiency	Oral or IV iron; look for blood loss
B12 deficiency	Subcutaneous or intramuscular circuits (download → support)
Markers	Gastrin, PGI/PGII, antibodies to PC/VF
Observation	EGDS according to MAPS/AGA in CM/high stages of OLGA/OLGIM [44]

Table 6. When and for whom is MAPS monitoring appropriate (diagram-hint)

Profile	Interval (approximately)
High stages OLGA/OLGIM and/or extensive incomplete CM	~every 3 years (personalize)
Limited CM, low stages, no familial GC	Individually/interval >3-5 years or without routine
AIG without CM/dysplasia	Personalized; monitor for shortages
Familial GC + CM/atrophy	More often, by multidisciplinary decision [45]

Prevention

Primary: identify and eradicate H. pylori (familial clusters, risk groups), quit smoking, reduce salt/pickled/smoked foods, and increase vegetable/fruit intake. For dyspepsia, perform a high-quality EGD if any red flags are present. Kyoto assessment and competent biopsies allow for early detection. [46]

Secondary: if atrophy is established, follow monitoring charts, achieve sustained eradication, treat deficiencies (iron, B12), reconsider long-term acid suppression, and educate the patient about signs requiring unscheduled EGD. [47]

Forecast

At the “subatrophic” stage, the prognosis is good with etiotropic correction: eradication of H. pylori slows/stops progression, reduces cancer risk; with AIG, high-quality management of deficiencies restores work capacity and prevents neurological complications. [48]

The risk of gastric cancer is determined not by the name ("subatrophic"), but by the objective OLGA/OLGIM stages and the presence of intestinal metaplasia. Therefore, it is the histological stage and the quality of MAPS/AGA follow-up that determine long-term outcomes. [49]

FAQ

• Is "subatrophic gastritis" a separate diagnosis?

In international practice, no. This is essentially early/moderate atrophy (OLGA I-II). For tactics, the OLGA/OLGIM stage and etiology (H. pylori or AIG) are more important than the term. [50]

• Is it possible to “cure” atrophy?

H. pylori eradication often halts progression and is sometimes partially reversible in the early stages. In cases of advanced atrophy/metaplasia, the focus should be on monitoring and risk control. [51]

• What is the current main treatment regimen for H. pylori?

14-day optimized bismuth quadruple therapy is preferred; the "clarithromycin triple" without susceptibility testing is no longer used. Monitoring of cure is mandatory. [52]

• How is autoimmune gastritis different from H. pylori gastritis?

In AIG, the body/fundus is affected, there are antibodies to parietal cells/intrinsic factor, hypergastrinemia, and iron deficiencies→B12. In H. pylori, the antrum is more often the starting point; the key is eradication. [53]

• Does everyone need endoscopic monitoring?

No. The intervals and the need itself depend on OLGA/OLGIM, the presence/type of intestinal metaplasia, family history and the quality of the examination - see MAPS II/III and AGA CPU. [54]