INTRODUCTION
First reported in 1989, collagenous gastritis (CoG) is a rare disorder defined by at least 10 µm of subepithelial collagen deposition in the gastric mucosa.1,2 The prevalence of CoG has been estimated to be around 13 cases per 100,000 endoscopies.2,3 Previous literature has noted a bimodal distribution for age of diagnosis with 1 peak occurring in young adults and a second occurring in those 60 years and older.3 Despite its rarity, it has been repeatedly observed that CoG falls under 2 main phenotypes: pediatric and adult. Pediatric patients tend to have predominantly foregut involvement and present with abdominal pain, nausea, vomiting, and anemia. In contrast, adults tend to have concomitant midgut and hindgut involvement and accordingly present with diarrhea, abdominal pain, and anemia.1,4 Gastric mucosal nodularity and friability are seen endoscopically with collagen deposition and inflammatory infiltrates on histology.4–7 Although the overall pathophysiology of CoG remains unclear, it has been proposed that an environmental trigger in a susceptible host leads to chronic eosinophilic inflammation and later, collagen deposition.4,8–10 CoG therapy includes proton pump inhibitors, corticosteroids, elimination diets, and even off-label biologics such as dupilumab and vedolizumab for refractory cases.3,4,6,11,12
We report a case of CoG manifesting as recurrent isolated postprandial nausea and vomiting, thus adding to the limited number of adult cases present in the literature, in hopes of establishing CoG's clinical course and aid in the future development of diagnostic and therapeutic guidelines.
CASE REPORT
A 33-year-old woman with a medical history of chronic low back pain and obesity presented to a tertiary academic center gastroenterology clinic with an 8-month history of episodic postprandial nausea and vomiting. These episodes were described as nausea occurring 1 hour after meals, followed by mild epigastric pain, and then a few occurrences of emesis of undigested food. Symptoms resolved immediately after vomiting and did not vary with food portion sizes.
These episodes were frequent, although irregular (occurring daily to weekly), however, symptomology remained the same. The patient denied specific triggers (ie, spicy, fatty, high FODMAPs foods). Review of symptoms was negative for weight loss or overt gastroenterology bleeding.
Before presentation, the patient had trialed famotidine calcium carbonate, and various proton pump inhibitor trials without lasting benefit. Ondansetron did not provide relief despite escalating doses. The patient denied any preceding viral or bacterial gastroenteritis, antibiotic exposure, sick contacts, or travel.
In the months leading up to her symptoms, she had a flare of her low back pain requiring frequent use of nonsteroidal anti-inflammatories (NSAIDs).
Laboratory test results revealed a normal complete blood count and chemistry panel. Quantitative immunoglobulin testing was notable for mildly low immunoglobulin A (IgA) on 2 separate tests, 7 months apart (52 mg/dL, normal range 76–426 mg/dL). Celiac serology, including IgG-based, was normal.
Helicobacter pylori (H. pylori) breath test was negative. A gastric emptying study was normal with a 5% residual at 4 h (normal <10%). The patient underwent an upper endoscopy and was noted to have a 1 cm hiatal hernia graded as Hill grade 2, American Foregut Society 2 (no axial hernia, flap valve intact).
She was also noted to have normal gastroduodenal mucosa. However, gastric body biopsies revealed glandular atrophy of the oxyntic mucosa without intestinal metaplasia (Figure 1) consistent with CoG. Helicobacter pylori staining was negative.
The patient was subsequently started on oral budesonide 9 mg daily, open capsule protocol. Repeat endoscopy 3 months after the index endoscopy appeared normal, with pathology showing CoG involving only 1 of 5 biopsies (with 4 additional gastric biopsies showing minimal lamina propria lymphoplasmacytic infiltrates). At a follow-up visit, the patient noted significant symptom improvement with budesonide; she was recommended to monitor for symptom recurrence and scheduled for close follow-up.
DISCUSSION
To our knowledge, this is the first case report of an otherwise healthy, young adult patient found to have CoG presenting with isolated postprandial nausea and vomiting with concomitant NSAID use. Previous literature has emphasized nausea and vomiting in the presentation of CoG in pediatric patients (less frequently in adults).1 Given the CoG diagnosis is based on histopathologic evaluation of gastric biopsies, it is possible that other patients with persistent nausea and vomiting may have undiagnosed CoG as the etiology when accounting for biopsy variability during endoscopic workups. To increase the histologic probability of yielding a diagnosis of CoG when performing endoscopy, 1 may consider taking 3–6 biopsies from the antrum, 3–6 biopsies from the gastric body, and 2–3 biopsies from the fundus.
A previous case report postulated that CoG inflammatory infiltrates at the lower esophageal or pyloric sphincter may contribute to decreased sphincter distensibility and thus lead to nausea and vomiting.13
Similar to other reported cases of CoG, our patient was found to have IgA insufficiency, highlighting the possible association of CoG with immune dysregulation.14,15 Further research is needed to investigate what role decreased IgA levels may play in the development of CoG. Interestingly, patients with IgA deficiency are more likely to develop celiac disease compared to the general population.14,16 Previous literature suggests that there may be a progression of eosinophilic gastritis to CoG and, as a result, typical eosinophilic gastritis elimination diets have been shown to be helpful for symptom improvement in these cases.4,8 Similarly, for patients with CoG who have concurrent IgA deficiency or celiac disease, it may also be beneficial to follow a gluten-free diet and monitor for symptomatic improvement.4,17
This case reiterates the importance of conducting an accurate medication reconciliation to determine reversable causes of CoG. Our patient was taking NSAIDs frequently for her back pain, which is a previously reported drug trigger for CoG.18,19 Part of her management included patient education and subsequent reduction of NSAID use given previous studies for CoG have noted symptomatic improvement on doing so.4,16,19,20
This case underscores the indolent nature of CoG. CoG should be considered in functional or undifferentiated nausea and vomiting. Moreover, this case corroborates previously documented associations between CoG, NSAID use, and isolated IgA deficiency.
It also highlights the chronic nature of CoG and how histopathologic collagen deposition may remain present despite symptomatic improvement. Treatment may prevent progression but not lead to complete histological remission. Long-term endoscopic monitoring should be considered for this unique patient population to evaluate for appropriate and sustained treatment response.
DISCLOSURES
Author contributions: B. Shahrvini: Performed literature review, analyzed and interpreted clinical data, wrote case report. AC Greb: Assisted with literature review, assisted with analyzing and interpreting clinical data.
HL Wang: Obtained and analyzed relevant histopathology for the case report, helped revise case report. PV Tripathi: Assisted with analyzing and interpreting clinical data, helped revise case report. GA Weiss: Assisted with analyzing and interpreting clinical data, helped revise case report.
A. Myint: Identified the patient case, obtained patient consent, assisted with analyzing and interpreting clinical data, helped revise case report. A.
Myint is the article guarantor.
Financial disclosure: None to report.
Informed consent was obtained for this case report.