LAUSR

We present the case of a boy aged 11 years that sought care for postprandial feeling of fullness and nausea lasting 3 years in the absence of vomiting, heartburn or abdominal pain. The patient had normal bowel movements and development. He reported recurrent orchiepididymitis (with normal biopsy of the testes and epididymis) and a history of juvenile polyps at age 3 years. He had a family history of autoimmune disease (mother: indeterminate inflammatory bowel disease, chronic gastritis and arthritis; father: psoriatic arthritis; maternal side of family: chronic gastritis, pernicious anaemia, Sjögren syndrome and coeliac disease). The results of the diagnostic tests were: haemoglobin, 13.3 g/dL; ferritin 15 g/L; vitamin B12 150 pg/mL. The patient had low levels of pepsinogen I (3.5 ng/mL), pepsinogen II (6.3 ng/mL) and gastrin (19.6 pg/mL). The results of the complete blood count, blood chemistry panel, blood clotting tests, thyroid panel and quantitative immunoglobulin tests were normal. The assays for the detection of ANA, ANCA, ASCA, antitransglutaminase IgA, anti-parietal cell, anti-LKM, anti-smooth muscle, antimitochondrial and anti-intrinsic factor antibodies were negative. The level of faecal calprotectin was normal. The upper GI endoscopy revealed thickening of the folds of the gastric mucosa with a nodular appearance (Fig. 1). Examination of the gastric biopsy revealed inflammatory cell infiltration, a thick sub-epithelial collagen band and marked oxyntic gland atrophy. There was no evidence of Helicobacter pylori infection, gastric metaplasia or epithelial dysplasia (Fig. 2). A colonoscopy ruled out large bowel involvement. The patient was asymptomatic, so he continued treatment with vitamin B12 and iron supplementation. The patient underwent follow-up endoscopic examinations at 6 and 18 months that revealed persistence of collagenous gastritis; he remained asymptomatic. Collagenous gastritis is a rare condition. Approximately 60 cases have been described in the literature. The first case was described in 1989 by Colleti and Trainer in a female patient aged 15 years. At present, its precise aetiology and pathogenesis are not well understood. The deposition of collagen may be due to an abnormal response following exposure to a toxic or infectious agent, with chronic inflammation or increased vascular permeability that would allow extravasation and deposition of plasma proteins and collagen. It usually has onset before adolescence and it is more frequent in the female sex. It is classified into 2