Iron Pill Gastropathy: A Case Report and Review of the Literature

Abstract

Purpose: Despite the widespread use of oral iron supplements, the entity of “iron pill gastritis” has remained largely unrecognized in the Gastreonterology literature. Our patient is an 85 year-old man who presented with a several-month history of melena. Pertinent medications included daily lansoprazole 30 mg and aspirin 81 mg. He had been taking ferrous sulfate 325 mg twice daily for iron deficiency anemia for the prior 8 weeks. History included coronary artery disease, compensated congestive heart failure, and hypertension. The patient had a history of an upper gastrointestinal bleed 2 years prior to this evaluation, secondary to aspirin and celecoxib use. Upper endoscopy revealed a large esophageal ulcer, multiple duodenal ulcers, and no gastric ulcers. Testing for Helicobacter pylori was negative. Physical exam revealed stable vital signs and no orthostasis. Examination was normal except for guaiac-positive stool. Hematocrit was stable at 36%. Subsequent upper endoscopy revealed a normal esophagus and multiple sessile diminutive polyps in the gastric fundus. A non-bleeding 4 × 8 mm gastric ulcer with pigmented material was found in the gastric body. Histopathologic evaluation of gastric biopsies obtained from the ulcer revealed foveolar hyperplasia with abundant granular brown pigment, consistent with iron pill gastropathy. The patient was placed on twice daily oral lansoprazole at a dose of 30 mg, and oral iron was discontinued. A follow-up upper endoscopy performed one month later revealed no evidence of active ulceration. The patient has been maintained on lansoprazole 30 mg twice daily and aspirin 81 mg daily. He has experienced no further gastrointestinal problems. Iron injury is thought to result from a direct corrosive action on the gastrointestinal mucosa. A previous study found gastric ulcers in association with oral iron use. Histology of these biopsies showed heavy iron deposition within ulcer granulation tissue, in connective tissue, and in blood vessels of the lamina propria. Ulceration appeared to have preceded the initiation of iron therapy, suggesting that iron use exacerbated a pre-existing condition. Few clinicians are aware that oral iron has been associated with gastropathy that can lead to the development of peptic ulcer disease. Our case provides an illustration of this rare but important entity and highlights the importance of co-morbidity and concomitant use of low dose aspirin.