|Year : 2018 | Volume
| Issue : 2 | Page : 285-287
Collagenous gastritis: A case report and literature review
Prabin Sharma1, Andrea Barbieri2, Amir Masoud3
1 Department of Internal Medicine, Yale New Haven Health, Bridgeport Hospital, Bridgeport, USA
2 Department of Pathology, Yale New Haven Hospital, New Haven, CT, USA
3 Department of Section of Digestive Diseases, Yale New Haven Hospital, New Haven, CT, USA
|Date of Web Publication||20-Jun-2018|
Department of Internal Medicine, Yale New Haven Health, Bridgeport Hospital, 267 Grant Street, Bridgeport, CT 06610
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Collagenous gastritis (CG) is a rare disease, which is characterized by subepithelial deposition of collagen in the gastric mucosa, surface epithelial injury, and a lamina propria inflammatory infiltrate. Approximately 100 cases of CG have been reported in the literature. We report another case of a young girl who presented to us with severe anemia and chronic diarrhea and was diagnosed with CG based on clinical features and endoscopic and pathologic findings. She was successfully managed with oral iron, sucralfate, and proton pump inhibitor therapy.
Keywords: Anemia, collagenous colitis, collagenous gastritis, diarrhea
|How to cite this article:|
Sharma P, Barbieri A, Masoud A. Collagenous gastritis: A case report and literature review. J Nat Sc Biol Med 2018;9:285-7
|How to cite this URL:|
Sharma P, Barbieri A, Masoud A. Collagenous gastritis: A case report and literature review. J Nat Sc Biol Med [serial online] 2018 [cited 2020 Jun 4];9:285-7. Available from: http://www.jnsbm.org/text.asp?2018/9/2/285/234705
| Introduction|| |
Collagenous gastritis (CG), collagenous sprue, and collagenous colitis are rare form of collagenous gastroenteritides with characteristic features of subepithelial collagen deposition along with inflammatory infiltrate in the lamina propria.,, Among them, the most common variant is collagenous colitis, with annual incidence rates between 1.1 and 5.2 cases per 100,000 population., First described in 1989, CG is characterized by subepithelial deposition of collagen in the gastric mucosa, surface epithelial injury, and a lamina propria inflammatory infiltrate.,,,,, Due to the limited number of cases reported, it remains a poorly understood condition in terms of pathogenesis, diagnosis, and management.
We report another case of a young girl who presented with severe anemia and chronic diarrhea that was diagnosed with CG based on clinical features and endoscopic and pathologic findings. She was successfully managed with oral iron, sucralfate, and proton pump inhibitor (PPI) therapy.
| Case Report|| |
A 19-year-old female with diarrhea-predominant irritable bowel syndrome (IBS) presented to the emergency department for evaluation of progressive shortness of breath for a week. Prior to this, she had presented to an outside hospital with complaints of intermittent loose black stools ongoing for about a year where esophagogastroduodenoscopy (EGD) and colonoscopy with biopsies were reported negative for any pathology. Workup for celiac disease with serum tissue transglutaminase antibodies and Helicobacter pylori testing was also reported negative. She denied epigastric pain, nausea, vomiting, heartburn, bloating, and difficulty or pain in swallowing. She had no history of change in appetite, weight gain or weight loss, hematemesis, hematochezia, or abnormal menstruation. She had no personal or family history of autoimmune disease. She was not taking any medications and did not have a history of taking nonsteroidal anti-inflammatory drugs, steroids, olmesartan, or venlafaxine. She endorsed compliance to IBS-FODMAP (Fermentable Oligo-, Di-, Monosaccharides And Polyols) diet.
Vitals were stable with blood pressure of 136/85 mmHg, heart rate of 74 beats/min, temperature of 36.8°C, and respiratory rate of 18/min. She was saturating 100% in room air. She had pallor on examination. Abdominal examination was unremarkable with no abdominal tenderness or palpable hepatosplenomegaly. Blood work was suggestive of severe microcytic iron deficiency anemia: hemoglobin of 5.6 g/dL (reference range: 12–18 g/dL), hematocrit of 20.4% (reference range: 37.0–52.0%), and mean corpuscular volume of 69.9 fl (reference range: 80–100 fl). Iron studies showed iron of 20 μg/dL (50–170 μg/dL), iron saturation of 6% (15–50%), total iron-binding capacity of 321 μg/dL (250–450 μg/dL), and ferritin of 2 ng/mL (6–67 ng/mL). The rest of the blood work including basic metabolic panel, liver function panel, and coagulation studies were all normal. Computed tomography of the abdomen and pelvis did not show any acute abnormal findings. She was treated in the hospital with blood transfusion and intravenous PPIs. We repeated the EGD, which showed normal-appearing gastric mucosa but with increased friability which bled easily to touch [Figure 1]. Histologic examination revealed patchy mild-to-marked thickening of subepithelial collagen, most prominent in the antral mucosa suggestive of CG [Figure 2]a and [Figure 2]b. Video capsule endoscopy did not reveal any other source of gastrointestinal bleeding. She was discharged on sucralfate (1 g per oral four times daily), iron (ferrous sulfate 325 mg per oral three times daily with meals), and oral PPI (pantoprazole 40 mg per oral very 12 h). On a follow-up at 6 months, she reported significant improvement of her symptoms and her blood counts.
|Figure 1: Upper endoscopy showing normal-appearing gastric mucosa with increased friability that bled easily on touch|
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|Figure 2: (a) Hematoxylin and eosin stain showed irregular subepithelial collagen thickening, most prominent in the antral mucosa (shown) with associated mild-to-moderate chronic inactive lamina propria inflammation composed of lymphocytes, plasma cells, and scattered eosinophils. The subepithelial collagen was further highlighted by trichrome stain (inset). (b) At higher power, the band of subepithelial collagen showed entrapped small vessels, occasional fibroblasts, and few inflammatory cells. Intestinal metaplasia was also appreciated focally within the antrum (arrow)|
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| Discussion|| |
Early literature described distinct differences in the presentations of CG and diseases associated with CG in children (≤18 years) and adults (>18 years).,, Two clinicopathologic types were described: a presentation of severe anemia and nodular gastric mucosa in the younger age group and presentation with chronic diarrhea in association with diffuse collagenous involvement of the gastrointestinal tract in the older age group.,, More recent literature, however, suggests that there are more similarities between these two groups in terms of presentation and endoscopic findings, with anemia, diarrhea, and gastric nodularity being the most common findings in both., This overlap of the clinicopathologic features was also seen in our patient who was 19 years old and had features of severe anemia as well as chronic diarrhea.
CG seems to have a female preponderance and may affect all age groups but primarily affects young adults., The etiology of CG is unknown. Stancu et al. outlined that three pathogenic mechanisms may lead to collagen deposition in cases of CG: (1) chronic inflammation, (2) fibroblast sheath abnormality, and (3) leakage of plasma proteins and fibrinogen. Other intestinal and autoimmune disorders, including celiac disease, collagenous enteritis, collagenous colitis, Sjogren syndrome, systemic lupus erythematosus, juvenile arthritis, rheumatoid arthritis, Hashimoto's thyroiditis, Graves' disease, diabetes mellitus type 1, and common variable immune deficiency, have been associated with CG in both the pediatric and adult populations.,,, This suggests that CG may share common autoimmune mechanism in pathogenesis with these diseases. Some of the CG cases have been reported in association with medications such as olmesartan , and antidepressants, for example, venlafaxine., The mechanisms by which these medications predispose to CG are not well understood. Although H. pylori has been associated with cases of lymphocytic gastritis, no prior CG cases have been attributed to H. pylori infection.
The gold standard of diagnosis for CG is endoscopy with biopsy. Endoscopic findings include nodularity, mucosal erythema, hemorrhage, ulceration, and exudates., Characteristic histologic finding includes subepithelial thickening of the collagen band of at least 10 μm in thickness., Three patterns of inflammation have been described, which include lymphocytic gastritis-like pattern,,,, an eosinophil-rich pattern,, and an atrophic pattern., Even though a widely used technique, miss rates of endoscopy are high, reported up to 7% in case of esophageal and gastric cancers. Data on endoscopic miss rates of CG are lacking. EGD findings in CG may be very subtle as in our case. Our patient had a prior EGD and colonoscopy with biopsies, which were deemed completely normal. A repeat EGD with biopsy, however, confirmed the diagnosis at our institute.
Treatment guidelines for CG are not established yet. Various medications have been used in the treatment with variable response. Corticosteroids, H2 receptor blockers, PPI, misoprostol, sucralfate, 5-aminosalicylates, and dietary modification (gluten-free diet) have been used. Long-term disease course and natural history of CG are variable. In most of the cases, CG seems to have a chronic persistent disease pattern but may have complete resolution in occasional cases. It has been suggested that collagen thickness may have a role in the disease course and its severity. There is no definite information on long-term development of dysplasia or malignancy.
In summary, we present another case of CG to add to the limited pool of cases of this rare condition. The symptoms in our patient had been persistent, but the diagnosis was missed in a recent workup. We hope to raise awareness among clinicians to consider CG in the differential diagnosis for a young female presenting with anemia and gastrointestinal symptoms. Our case highlights the need for a more careful examination during endoscopy, and it stresses on the role of an observant pathologist in making this diagnosis.
Informed consent was obtained from the patient.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]