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Collagenous Gastritis in Children: Exploring the Link With Iron Deficiency Anemia

Case Studies 3 min 11

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Created On: 30/10/2026

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Poster abstract

Collagenous gastritis (CG) is a rare disorder in which collagen deposits form beneath the gastric epithelium, accompanied by chronic mucosal inflammation. In this pediatric case series, 7 patients aged 3–14 years were identified with CG. All patients depicted gastric nodularity on esophagogastroduodenoscopy (EGD), with prominent subepithelial collagen deposition on gastric biopsy confirming the diagnosis. Abdominal pain, fatigue, dizziness or syncope, and vomiting were among the presenting complaints. Six patients had iron deficiency, whereas 1 had normocytic anemia with vitamin B12 deficiency. Four patients required packed red blood cell (PRBC) transfusion, and all received oral iron supplementation; two patients with recurrent severe anemia also received intravenous (IV) iron.

Antisecretory therapy was used in five patients. Four patients received a 6–8-week course of oral budesonide, without documented endoscopic or histologic improvement. Although symptoms resolved, follow-up endoscopy depicted persistent histologic abnormalities. Duodenal bulb involvement developed in some patients, indicating that pediatric disease may extend beyond the stomach. Long-term iron supplementation was associated with improvement and maintenance of hemoglobin (Hb) levels. These findings highlight the importance of recognizing CG as a potential cause of unexplained pediatric anemia.

Complaints

Seven pediatric patients aged 3–14 years (median age, 12 ± 4.9 years) presented with:
- Abdominal pain: 4/7 patients (57%)
- Fatigue: 3/7 patients (43%)
- Dizziness or syncope: 3/7 patients (43%)
- Vomiting: 3/7 patients (43%)
Other complaints were pallor, nausea, weight loss, constipation, dark stools, and pica.

Anamnesis

CG is marked by an abnormally prominent subepithelial collagen band within the gastric mucosa together with inflammatory changes. The underlying mechanism remains poorly defined, although immune-mediated or autoimmune processes have been proposed. Pediatric CG differs in clinical distribution from the disease described in adults. Pediatric disease generally remains confined to the stomach, whereas adult disease can involve the stomach, duodenum, and colon.

Abdominal pain, vomiting, and anemia are commonly reported clinical manifestations in children. There is currently no definitive treatment or established management guideline for pediatric CG, and treatment is generally supportive. The present case series was clinically relevant because of the association between gastric nodularity and significant anemia, as well as the limited information regarding treatment response and the potential involvement of the duodenal bulb in pediatric patients.

Medical history

No prior autoimmune or inflammatory gastrointestinal (GI) diagnosis was reported.
No relevant obstetric history was reported or applicable in the patients.
No disease-specific medications were used before diagnosis.
One patient followed a predominantly pescatarian diet, considered relevant to the observed vitamin B12 deficiency; one patient underwent a trial of a gluten-free diet.
No gastric atrophy or associated autoimmune comorbidity was identified.

Examination

a) Laboratory investigations

Hb levels: Ranged from 2.2 to 11.1 g/dL across all patients, indicating moderate to severe anemia.
Iron studies: 6 out of 7 patients were iron deficient.
Vitamin B12: 1 out of 7 patients had a normocytic anemia with vitamin B12 deficiency and normal iron studies.
Stool testing: Fecal occult blood test was positive in 57% (4 out of 7) of cases.

(b) EGD findings

Stomach: All subjects (100%) illustrated localized or diffuse nodularity in the stomach (specifically in the gastric body, fundus, or cardia), along with erythema, friability, edema, erosions, pseudopolyps, or plaque-like appearance.
Duodenum: 2 patients featured visible nodularity in the duodenal bulb on initial EGD.

(c) Histopathological findings

A thickened subepithelial collagen band was identified in the gastric body of all 7 patients.
Chronic gastritis was commonly noted, while increased lamina propria eosinophils were identified in 2 patients.
Duodenal bulb histology was abnormal in 2 patients despite a normal endoscopic appearance, with subtle collagen increase in one patient and focal foveolar metaplasia in the other.
Notably, the 2 patients with visibly nodular duodenal bulbs had normal duodenal histology, demonstrating a gross–histologic mismatch.
Colonoscopy and colonic biopsies were normal in all 7 patients.

Working diagnosis: The findings supported a diagnosis of pediatric-onset CG associated with iron deficiency anemia (IDA), attributed to chronic occult GI blood loss. One patient had concurrent vitamin B12 deficiency, while duodenal bulb involvement consistent with CG was identified in a subset of patients.

Treatment

(a) Hematologic & resuscitation interventions

Blood transfusion: 4 patients received PRBC transfusions for severe anemia.
Iron supplementation: All 7 patients received oral iron supplementation. 2 patients with recurrent severe anemia received IV iron.
Vitamin B12 supplementation: The 1 patient with vitamin B12 deficiency received B12 supplementation (for 2 months).

(b) Antisecretory medications

5 patients received antisecretory therapy (4 treated with proton pump inhibitors [PPIs] and 1 with histamine [H2] receptor antagonists).

(c) Corticosteroids & dietary trials

Budesonide: 4 patients completed a 6–8 week course of oral budesonide (or topical budesonide).
Gluten-free diet: 1 patient trialed a gluten-free diet.

Results

(a) Symptomatic outcome: All 7 patients (100%) attained complete resolution of clinical symptoms. Antisecretory medications appeared to aid in the resolution of abdominal pain.

(b) Hematologic outcome: Hb levels improved over time in all patients following long-term iron use. The B12-deficient patient's vitamin B12 levels normalized after 2 months of supplementation.

(c) Endoscopic and histologic outcomes

No histological improvement: None of the patients illustrated histologic or gross endoscopic improvements on follow-up EGDs (carried out between 4 months and 3 years post-diagnosis).
Budesonide non-response: Oral/topical budesonide treatment did not result in gross or histological improvement in any of the patients who received it.
Gluten-free diet non-response: The gluten-free diet trial did not improve symptoms or biopsy findings.
Disease progression: In 1 patient assessed 1–3 years post-diagnosis, disease progressed into the duodenal bulb with new nodularity, erythema, and duodenal biopsies showing inflammation with increased subepithelial collagen.

Key learnings

Pediatric-onset CG presents primarily with recurrent abdominal pain, upper GI distress (nausea/vomiting), and moderate-to-severe anemia.
While most pediatric cases feature severe IDA driven by occult GI bleeding, CG can also present as normocytic anemia with co-existing vitamin B12 deficiency.
Disease extension beyond the stomach into the duodenal bulb can occur, presenting as duodenal nodularity, duodenitis, or subepithelial collagen deposition on initial or follow-up biopsies.
Long-term iron/B12 repletion and acid suppression successfully resolve clinical symptoms and normalize Hb levels. However, mucosal nodularity and collagen deposition persist on follow-up endoscopies.
Oral or topical budesonide trials fails to yield any gross endoscopic or histological improvement, highlighting the requisition for targeted trials to identify effective therapies.