Published online Sep 16, 2026. doi: 10.5497/wjp.120862
Revised: May 13, 2026
Accepted: May 26, 2026
Published online: September 16, 2026
Processing time: 185 Days and 11.2 Hours
Gastric mucosal atrophy is widely regarded as a “point of no return” in the Cor
A 45-year-old man with H. pylori-associated CAG presented with abdominal pain rated 4/10, diarrhea occurring 2–3 times daily, and dyspeptic symptoms, inclu
The present clinical case supports a potential role of alpha-glutamyl-tryptophan as adjuvant (or reparative) therapy after H. pylori eradication, with possible effects on gastric mucosal regeneration and reduction of inflammatory activity in H. pylori-associated CAG. Nevertheless, these observations remain preliminary, and further well-designed studies are necessary to confirm efficacy, establish safety, and optimize its use within comprehensive treatment protocols.
Core Tip: The use of alpha-glutamyl-tryptophan as adjuvant reparative therapy following Helicobacter pylori (H. pylori) eradication may represent a promising approach to supporting gastric mucosal recovery and attenuating inflammatory activity in patients with H. pylori-associated chronic atrophic gastritis.
- Citation: Baryshnikova NV, Gulunov ZK, Uspenskiy YP. Alpha-glutamyl-tryptophan as adjuvant reparative therapy after Helicobacter pylori eradication in chronic atrophic gastritis: A case report and literature review. World J Pharmacol 2026; 15(2): 120862
- URL: https://www.wjgnet.com/2220-3192/full/v15/i2/120862.htm
- DOI: https://dx.doi.org/10.5497/wjp.120862
Chronic gastritis is a chronic inflammatory condition of the gastric mucosa characterized by cellular infiltration, impaired physiological regeneration, and subsequent atrophy of the glandular epithelium; intestinal metaplasia; and dysfunction of the stomach’s secretory, motor, and, in some cases, incretory functions[1,2]. As this definition indicates, altered his
Successful H. pylori eradication does not guarantee regression of atrophic and metaplastic changes of the gastric mucosa. In addition, one of the statements of the Maastricht VI consensus postulates that “after successful H. pylori eradication, patients with high-stage (III–IV) gastritis and/or extensive endoscopic atrophy remain at risk for gastric cancer”[7]. Therefore, early detection of gastric atrophy and timely administration of formulations that promote restoration of gastric mucosal structure and function are critically important components of comprehensive therapy for chronic gastritis.
A prominent example of this group of medications is alpha-glutamyl-tryptophan. The regenerative and anti-inflammatory effects of alpha-glutamyl-tryptophan can be explained by two mechanisms of action. First, it activates in
Published data indicate that L-glutamyl-L-tryptophan exerts a modulatory effect on metabolic processes, stimulates the functional activity of immune system cells, has antioxidant properties, promotes tissue regeneration, and accelerates wound healing[12-14]. According to the results of a double-blind, placebo-controlled multicenter study evaluating the efficacy and safety of alpha-glutamyl-tryptophan in the treatment of CAG associated with H. pylori, this agent sig
A 45-year-old man diagnosed with CAG associated with H. pylori infection presented to a gastroenterologist on May 12, 2025. His chief complaints were abdominal pain rated 4 out of 10 on a numeric pain scale, diarrhea occurring 2–3 times per day, and dyspepsia (nausea and bloating). Before all diagnostic procedures, the patient provided written informed consent in accordance with clinical practice guidelines.
The patient’s symptoms began in May 2025 after a dietary indiscretion and remained stable in severity thereafter.
In February 2023, the patient experienced abdominal pain and diarrhea occurring 2–3 times per day, followed by symptoms of dyspepsia, including nausea and bloating, in March 2023. The patient underwent gastroscopy between April and May 2023. Endoscopic assessment revealed hyperemia of the gastric mucosa and a positive rapid urease test for H. pylori. Although eradication therapy was advised, the patient declined treatment. He subsequently received treatment with proton pump inhibitors and bismuth salts, which resulted in a moderate but short-term clinical improvement.
The patient reported maintaining a healthy lifestyle with no significant occupational or social concerns. He denied smoking and both occasional and regular alcohol consumption. No significant genetic disorders or chronic illnesses were reported, and there was no family history of malignant tumors.
At presentation, the patient was in a stable clinical condition, with vital signs as follows: Body temperature, 36.5 °C; blood pressure, 130/80 mmHg; heart rate, 76 beats/min; and respiratory rate, 16 breaths/min. Abdominal examination revealed a soft, non-tender abdomen with no evidence of hepatosplenomegaly or palpable masses.
The patient underwent a comprehensive evaluation before and after treatment to assess gastric mucosal structure and function. The assessment included gastric endoscopy with biopsy, verification of H. pylori infection (rapid urease test, histological examination, and detection of IgG antibodies against H. pylori), morphological and immunohistochemical analysis of gastric mucosal biopsy samples (CXCL-12 and CDX-2), and 24-h intragastric pH monitoring.
Routine laboratory examinations: No clinically significant abnormalities were found in routine blood (clinical and biochemical) or urine analysis.
Specialized laboratory examinations: Before and after treatment, the patient underwent specialized blood testing using the GastroPanel diagnostic system[20-22], with evaluation of the following parameters: PGI: An indicator of the structure and function of the gastric body mucosa and a marker of gastric secretion; normal range, 30–160 μg/L. PGII: An indicator of the structure and function of the gastric mucosa as a whole and a marker of inflammation and atrophy; normal range: 3–15 μg/L. PGI/PGII ratio: A marker of gastric body atrophy that decreases in the presence of gastric body atrophy; normal range > 3. Basal gastrin-17: An indicator of the structure and function of the antral mucosa and a marker of altered gastric acidity; normal range: 1–10 pmol/L. IgG antibodies against H. pylori: A serological marker of H. pylori infection; normal range < 30 U/mL.
Histological method: During the initial endoscopic procedure, chromoendoscopy was performed to delineate areas of gastric mucosal atrophy in accordance with the Updated Sydney and modified Kimura–Takemoto classification systems[23]. Consequently, we performed targeted biopsy mapping, obtaining specimens from five standardized sites: Two from the gastric body, two from the antrum, and one from the incisura angularis. Rigorous site labeling and documentation were maintained throughout the procedure. During the post-treatment examination, serial biopsies were obtained from the identical mucosal sites to ensure comparative accuracy.
Morphometric assessment included the following parameters: Number of glands per 1 mm² of gastric mucosa, depth of gastric glands (non-metaplastic atrophy), number of parietal cells per 100 epithelial cells of the gastric mucosa, and number of goblet cells per 100 epithelial cells (metaplastic atrophy). For each biopsy, at least five fields of view at ×100 magnification were examined. Gland count and depth were measured using a calibrated ocular micrometer. Parietal and goblet cells were counted per 100 epithelial cells in three independent replicates, and the mean value was used for analysis.
Immunohistochemical method: Pre- and post-treatment immunohistologic evaluations were performed, with a focus on proliferative dynamics (stromal cell-derived factor 1, CXCL-12) and the homeobox protein (intestinal differentiation transcription factor, CDX-2). For immunohistochemical staining, 4–6-μm thick serial sections were prepared and mounted on poly-L-lysine–coated slides (Menzel, Germany). Staining was conducted on deparaffinized, rehydrated tissue sections using the avidin–biotin immunoperoxidase technique. To assess marker expression, primary antibodies anti-CDX-2 (EP25, Leica Biosystems, IL, United States) and anti-CXCL-12 (MA5-23759, Thermo Fisher, Waltham, MA, United States) were used. In the gastric mucosal biopsy samples, at least five fields of view at ×40 magnification were examined. The relative expression area (%) of the studied immunohistochemical markers was measured and analyzed via QuPath software, with a positivity threshold set at > 0.25 optical density to calculate % positive area.
In this study, we quantified immunohistochemical expression using the relative positive area percentage. While this approach currently lacks the widespread clinical validation associated with semi-quantitative indices (e.g., H-score or immunoreactive score), it provides a reproducible automated framework that minimizes the interobserver bias typical of subjective visual assessment. Nonetheless, we acknowledge this divergence from standard clinical scoring systems as a methodological limitation.
Endoscopic method: Pre- and post-therapeutic esophagogastroduodenoscopy findings were standardized according to a systematic semiological assessment scale. Evaluated parameters included rugal fold thickness, mucosal erythema and edema, the presence of signs associated with atrophy or intestinal metaplasia, and the topographical severity of erosive lesions. Each criterion was graded on a four-point semi-quantitative scale (0: Absent; 1: Mild; 2: Moderate; 3: Severe). A global composite score was subsequently derived for each patient to facilitate a comparative analysis of therapeutic efficacy. Treatment outcomes were categorized based on the longitudinal evolution of the endoscopic findings as follows: Clinical improvement (regression of inflammatory signs), stable disease (no significant change), or disease progression. Gastric mucosal atrophy was categorized according to its topographical extent using the modified Kimura–Takemoto classification system.
Twenty-four-hour intragastric pH monitoring: Twenty-four-hour pH monitoring was performed using the Gastroscan-24 device and included assessment of the following parameters: Minimum pH value, mean pH value, aggressiveness index, and acidity index. The aggressiveness index reflects the level and fluctuations of basal (spontaneous) gastric acidity over a defined time interval (24 h) without the influence of exogenous factors. The acidity index reflects the duration of specific pH levels of gastric juice throughout the entire recording period (24 h). A decrease in the acidity index is observed in conditions associated with reduced acid-producing function. The integrative nature of the acidity index reflects the full secretory spectrum, encompassing basal acid output as well as responses to postprandial and pharmacological stimulation.
To assess the safety of the intervention, the patient underwent a comprehensive evaluation of the following parameters: Symptoms and medical history, including allergy history, physical examination, measurement of vital signs (respiratory rate, heart rate, blood pressure, and body temperature), quality-of-life assessment using the SF-36 questionnaire, electrocardiography, routine blood and urine tests, and biochemical blood analysis.
A diagnosis of H. pylori-mediated CAG was established at the initial assessment based on standardized endoscopic and histological criteria.
The patient underwent a two-stage treatment regimen (Figure 1), which included the following: (1) A 10-day course of standard triple eradication therapy (omeprazole 20 mg twice daily administered 15–30 min before meals, amoxicillin 1000 mg twice daily, and clarithromycin 500 mg twice daily after meals). (2) A 28-day course of alpha-glutamyl-tryptophan administered as an oral gel prepared from powder (composition per 1 g of powder: Active substance, sodium alpha-glutamyl-tryptophan (calculated as alpha-glutamyl-tryptophan) 0.330 mg; excipients, fructose 713.00 mg, sodium alginate 166.67 mg, sodium carmellose 100.00 mg, colloidal silicon dioxide 20.00 mg). A single dose consisted of 3 g of powder. The medication was administered orally as a freshly prepared gel according to the manufacturer’s instructions, twice daily: In the morning 20–30 min before meals and in the evening before bedtime, at least 1 h after food intake, for a total duration of 28 days. The patient reported full compliance with the prescribed regimen. No concomitant medications, dietary supplements, or lifestyle modifications were introduced during the study period. The patient maintained his usual diet and physical activity level (Figure 1).
Based on the reported outcomes, the patient demonstrated positive changes in laboratory and morphological assessments after treatment (Table 1).
| Parameter | Before treatment | After treatment | Normal values |
| Endoscopic findings | |||
| Hyperemia of gastric mucosa, points | 3 | 1 | 0 |
| Edema of gastric mucosa, points | 2 | 1 | 0 |
| Kimura–Takemoto classification | C1 | C1 | 0 |
| Test for verification of H. pylori infection (rapid urease test) | + | - | - |
| Histological findings | |||
| Number of glands per 1 mm² of the gastric mucosa | 14 | 21 | NA1 (↑)2 |
| Gland depth of gastric mucosa, µm | 155.9 | 192.6 | NA1 (↑)2 |
| H. pylori staining | + | - | - |
| Number of parietal cells per 100 epithelial cells | 0 | 16 | NA1 (+)3 |
| Number of goblet cells per 100 epithelial cells | 3 | 0 | 0 |
| OLGA/OLGIM stage | II/I | I/0 | 0/0 |
| Immunohistochemical findings | |||
| CDX-2 relative expression area (%) | 12.1 | 7 | 0 |
| CXCL-12 relative expression area (%) | 17 | 7.94 | NA1 (↓)4 |
| GastroPanel findings | |||
| Pepsinogen I (μg/L) | 41 | 155 | 30–160 |
| Pepsinogen II (μg/L) | 26 | 8.1 | 3–15 |
| Pepsinogen I/II ratio | 1.6 | 19.1 | > 3 |
| Gastrin-17 (pmol/L) | 41 | 1.7 | 1–10 |
| Anti-H. pylori IgG (U/mL) | 43 | 19 | < 30 |
| 24-h pH monitoring findings | |||
| Mean pH value | 6.8 | 1.2 | 1.0–3.0 |
Endoscopy results: Based on gastroscopy findings, a reduction in gastric mucosal edema (from 2 to 1 point) and hyperemia (from 3 to 1 point) was observed. According to the Kimura–Takemoto classification, C1 atrophy was observed both before and after treatment. This finding does not contradict the overall results, as endoscopic manifestations of atrophy in the antrum may not regress completely during the study period.
Histological findings: Histological examination revealed a reduction in non-metaplastic atrophy, including an increase in the number of glands per 1 mm² (from 14 before treatment to 21 after treatment) and an increase in gland depth (from 155.9 µm to 192.6 µm) in the gastric mucosa (Figure 2). An increase in the number of parietal cells per 100 epithelial cells (from 0 to 16) and a decrease in the number of goblet cells per 100 epithelial cells (from 3 to 0) were also observed, indicating a reduction in metaplastic atrophy of the gastric mucosa (Figure 3). According to the Operative Link for Gastritis Assessment (OLGA)/Operative Link for Gastric Intestinal Metaplasia Assessment (OLGIM) grading, the findings before treatment corresponded to OLGA stage II and OLGIM stage I, and those after treatment corresponded to OLGA stage I and OLGIM stage 0 (Figure 2).
Immunohistochemical findings: Immunohistochemical analysis demonstrated a decrease in the relative expression area (%) of CDX-2 compared with baseline values (from 12.1% to 7%), which indirectly indicates a reduction in gastric mucosal atrophy[24]. A decrease in CXCL-12 expression was also observed, with the relative expression area (%) declining from 17% to 7.94%, suggesting reduced activity of chronic inflammation. This finding is also considered prognostically favorable, as several authors have reported that increased CXCL-12 expression contributes to the progression of gastric cancer[25,26].
GastroPanel results: According to the GastroPanel test, improvements in several parameters were observed after treatment, including an increase in PGI levels (from 41 μg/L to 155 μg/L), a decrease in PG II levels (from 26 μg/L to 8.1 μg/L), a decrease in gastrin-17 levels (from 41 pmol/L to 1.7 pmol/L), and a reduction in IgG antibody titers against H. pylori (from 43 U/mL to 19 U/mL).
Twenty-four-hour pH monitoring findings: Twenty-four-hour intragastric pH monitoring showed a marked shift toward increased acidity, with the mean pH decreasing from 6.8 to 1.2.
No adverse events were reported during the treatment period.
During a three-month follow-up period, the patient exhibited no signs of clinical recurrence. The prognosis remained favorable at the time of this writing, supported by the stability of the post-treatment findings. Future management will prioritize regular surveillance, with a follow-up gastroscopy and biopsy mapping every 3 years in accordance with MAPS III recommendations for endoscopic monitoring[27] to confirm long-term mucosal stability.
Preliminary research on alpha-glutamyl-tryptophan highlights its multifaceted therapeutic potential, specifically through its cytoprotective, anti-inflammatory, and immunomodulatory properties[28-30]. In addition, some studies have substantiated the clinical utility of this compound, highlighting its therapeutic potential to improve outcomes in tuberculosis management[31], discovered its potential inhibitory effects on tumor growth through anti-angiogenic mechanisms[32], indicated a possibility to serve as a source of antioxidant peptides[33], and demonstrated production of measurable changes in anxiety-related indicators and reduced depressive-like behavior by application of this molecule, suggesting its potential as a novel anxiolytic[34]. All these findings may help explain the additional beneficial effects of alpha-glutamyl-tryptophan on regression of gastric mucosal atrophy and inflammation in H. pylori-associated CAG when used in combination with standard eradication therapy.
This clinical case describes the successful management of a 45-year-old man with H. pylori-associated CAG using a two-stage therapeutic approach consisting of a 10-day course of standard eradication therapy followed by a 28-day course of alpha-glutamyl-tryptophan.
Comprehensive pre- and post-treatment evaluation revealed multifaceted improvement in the patient’s gastric mucosal condition. In addition to the successful eradication of H. pylori, marked improvements were observed in histological, serological, and immunohistochemical parameters. These findings suggest that alpha-glutamyl-tryptophan may have contributed to a reduction in mucosal atrophy and inflammation, as well as partial restoration of gastric function, outcomes that extend beyond the expected effects of standard anti-Helicobacter therapy alone. It is important to note that even after successful eradication, atrophic changes and inflammation may persist for a prolonged period. Based on the findings of this clinical case, it can be assumed that, in combination with eradication therapy, alpha-glutamyl-tryptophan may accelerate recovery of the gastric mucosa. Therefore, in some cases, the combination of H. pylori eradication therapy with adjuvant therapy may be justified.
The observed increase in gland number and depth, along with the reemergence of parietal cells, reflects a functional reversal of non-metaplastic atrophic changes. This morphological improvement was accompanied by a decrease in the relative expression area of CDX-2, a transcription factor associated with intestinal metaplasia, suggesting a reduction in metaplastic atrophy. Furthermore, the marked decrease in CXCL-12 expression, a chemokine implicated in chronic inflammation and gastric cancer progression, serves as a cellular correlate of the anti-inflammatory effects observed endoscopically. The reduction in this biomarker is particularly noteworthy, as it aligns with the hypothesis that alpha-glutamyl-tryptophan may modulate the precancerous cascade, potentially offering chemopreventive effects beyond symptomatic improvement.
The functional recovery of the stomach was corroborated by both GastroPanel serology and 24-h intragastric pH monitoring. The substantial increase in PGI levels (from 41 μg/L to 155 μg/L) and the normalization of gastrin-17 levels (from 41 pmol/L to 1.7 pmol/L) are classical indicators of restoration of acid-producing capacity in the gastric body, which is typically impaired in atrophic conditions. This serological profile was mirrored by the shift in mean 24-h intragastric pH from an alkaline value of 6.8 to a strongly acidic value of 1.2. Restoration of the acidic gastric environment is clinically important, as hypochlorhydria not only exacerbates digestive symptoms but also promotes bacterial overgrowth and the formation of potentially carcinogenic N-nitroso compounds. In addition, the decrease in anti-H. pylori IgG titers may be associated with reduced antigenic stimulation from residual bacterial components or modulation of the local immune response.
The observed effects may be mechanistically attributed to the known pharmacological properties of alpha-glutamyl-tryptophan. Its metabotropic activity, mediated through interaction with glutamate receptors, is believed to activate intracellular peptide regulatory cascades that stimulate cellular proliferation and differentiation. At the same time, its modulation of MMPs, including reduction of MMP-1 and MMP-2 activity and modulation of MMP-8 and MMP-9, likely contributes to the resolution of inflammation and restoration of normal extracellular matrix structure, thereby facilitating glandular regeneration. This case provides translational support for these preclinical mechanisms, demonstrating that a 28-day course may result in measurable improvements in both gastric mucosal architecture and function in a patient with established CAG.
The extent to which the observed recovery was driven by alpha-glutamyl-tryptophan, rather than being solely attributable to H. pylori clearance, remains unclear. Evidence suggests that H. pylori clearance can induce partial regressive changes in gastric atrophy, although this response is not observed consistently across all patients. The magnitude of improvement observed in the present case, particularly the restoration of gastric acidity from 6.8 to 1.2 and the increase in the number of parietal cells, is not typically associated with eradication therapy alone.
While this case report provides significant clinical insights, it is subject to the inherent limitations of an N-of-1 design. Specifically, the absence of a control group, blinding, and a washout period precludes definitive differentiation between the effects of H. pylori eradication and the specific contribution of alpha-glutamyl-tryptophan. However, the pronounced improvements observed in mucosal atrophy and function, which are not commonly seen after H. pylori eradication alone, especially in a patient with long-standing untreated infection, suggest a possible synergistic or additive effect of the second-line reparative therapy. While the observed improvements are significant, it is important to acknowledge that spontaneous post-eradication mucosal improvement, though typically modest in long-standing CAG, cannot be entirely excluded, and the 28-day alpha-glutamyl-tryptophan course should be interpreted as an exploratory adjuvant intervention. Our findings are consistent with and extend the results of recent multicenter studies, supporting the potential role of alpha-glutamyl-tryptophan as a component of comprehensive management of CAG. Further research, including larger randomized controlled trials with long-term follow-up, is required to confirm its efficacy in preventing gastric cancer and to establish optimal treatment strategies.
In the present clinical case, post-eradication treatment with alpha-glutamyl-tryptophan was associated with a measurable decrease in gastric mucosal atrophy and inflammation, while simultaneously restoring the stomach’s acid-producing capacity. These findings suggest that alpha-glutamyl-tryptophan may contribute to the partial reversal of key pa
However, because the patient received H. pylori eradication therapy before alpha-glutamyl-tryptophan administration, the observed improvements cannot be unequivocally attributed to this agent alone. These findings should therefore be interpreted as hypothesis-generating rather than as definitive evidence of a causal therapeutic effect. Further controlled studies are necessary to confirm the potential role of alpha-glutamyl-tryptophan in the treatment of atrophic gastritis, including H. pylori-associated cases.
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