A 32-year-old man presents to the clinic because of a frequent “upset stomach” with indigestion and epigastric discomfort for the past 6 months. His symptoms often worsen after meals, and he has had significant fatigue for the past month. He has not had weight loss, blood in the stool, or melena. He does not smoke or drink alcohol. His family history is not significant for any GI conditions, but his brother has type 1 diabetes mellitus. His blood pressure is 134/80 mm Hg, his pulse is 90/min, and his respiratory rate is 14/min. On physical examination, the patient looks pale. Laboratory findings are significant for a hemoglobin of 10.0 g/dL, leukocyte count of 7,000/mm3, an MCV of 110 fL/cell, and an elevated serum gastrin level. A urease breath test is negative. An upper GI endoscopy shows erythema in the body and fundus of the stomach and hypertrophy of the gastric antrum but no bleeding or lines of demarcation. Histology shows parietal cell destruction. What is the most likely cause of this patient’s condition?
Correct answer: Autoimmune metaplastic atrophic gastritis
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This patient has autoimmune metaplastic atrophic gastritis (AMAG). There are 2 types of metaplastic (chronic) atrophic gastritis, autoimmune and environmental. (see Option D). AMAG shares some clinical features with chronic H. pylori gastritis (environmental metaplastic atrophic gastritis or EMAG), but this patient had a negative urease breath test. AMAG may be asymptomatic (and present after pernicious anemia develops), or patients may have dyspepsia with postprandial indigestion.
The pathogenesis of AMAG is the autoimmune destruction of gastric parietal cells, which are principally found in the gastric body and fundus of the stomach. Reduced acid production and loss of intrinsic factor may lead to vitamin B12 deficiency and macrocytic anemia, accounting for this patient’s fatigue. There is an increased incidence of AMAG in patients with autoimmune thyroid disease and type 1 diabetes mellitus. Low gastric acid levels lead to antral G-cell hyperplasia and elevated serum gastrin levels. Patients with AMAG have an increased risk for gastric adenocarcinoma (Option A) and carcinoid tumors