Gastroenterology
Volume 138, Issue 1 , Pages e7-e8, January 2010

The Importance of Unfettered Gastric Motility

  • Ian Wall, DO

      Affiliations

    • Division of Gastroenterology, Department of Internal Medicine, Maimonides Medical Center, Brooklyn, New York
    • ,
  • Nison Badalov, MD

      Affiliations

    • Division of Gastroenterology, Department of Internal Medicine, Maimonides Medical Center, Brooklyn, New York
    • ,
  • Michael Bernstein, MD

      Affiliations

    • Division of Gastroenterology, Department of Internal Medicine, Coney Island Hospital, Brooklyn, New York

published online 23 November 2009.

Article Outline

 

Question: A 46-year-old woman presented with a 3-week history of worsening dyspnea on exertion. Her past medical history was significant for poorly controlled type 2 diabetes with prior treatment for gastroparesis and iron-deficiency anemia. Pertinent medications included metformin, daily aspirin, esomeprazole, and iron supplementation. Physical examination revealed a pale woman in no acute distress. Her abdomen was soft without tenderness to palpation. Rectal examination revealed melena. Laboratory results showed severe anemia with a hemoglobin of 5.3 g/dL and a hematocrit of 18.2%. The iron profile revealed an iron of 46 μg/dL, and transferrin saturation of 11.7%. The patient was stabilized with IV fluid hydration and IV proton pump inhibitor; she was given 2 units of packed red blood cells. An upper endoscopy was performed. An acute gastric ulcer was noted within a dependent portion of the fundus. The ulcer was not actively bleeding and had an abnormal shiny metallic quality, as if it were stained (Figure A). The apparent staining did not wash with repeated flushing. Biopsies were taken from the edge of the ulcer (Figure B, C). What is the etiology of this ulcer? What conditions predispose a patient to this type of ulcer?

See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.

Back to Article Outline

Answer to the Clinical Challenges and Images in GI Question: Image 4: Gastric Siderosis 

The etiology of this patient's acute gastric ulcer with significant hemorrhage was mucosal ulceration owing to gastric siderosis. Biopsies revealed an acute gastric ulcer with superficial mucosal iron deposition in the epithelium and extracellular spaces. This deposition of iron in the gastric mucosa is termed gastric siderosis. Mucosal ulcerations are a potential manifestation of gastric siderosis and are more likely to occur in slowed motility states, like gastroparesis. Interestingly, this lesion was noted in a dependent portion of the patient's gastric fundus where static gastric contents would remain for extended periods of time. Importantly, other common etiologies of peptic ulcer disease were ruled out. Stains for Helicobacter pylori were negative. Second, despite daily aspirin, this patient's concomitant use of double-dose esomeprazole significantly mitigated her risk of nonsteroidal anti-inflammatory drug (NSAID)-related ulceration.

Gastric siderosis occurs in 2 distinct patterns. One form consists mainly of glandular and lamina propria iron deposition in which iron is found microscopically on biopsy without endoscopic findings. This pattern is characteristically found in the clinical setting of systemic iron overload. The second form consists of a more superficial mucosal iron deposition. This form is related to oral iron supplementation and its local corrosive effects. Instead of iron deposition concentrated in the gastric glands, the iron deposits occur in the epithelium, stromal cells, and or extracellularly.1, 2 Frequently there is an associated reactive gastropathy termed iron pill gastritis. At therapeutic doses, the mechanism of cellular injury is not clearly understood. One proposed hypothesis is that pill stasis leads to high local concentrations of iron from an overwhelming mucosal absorption in the area of stasis. Once absorbed, the ferrous and ferric ions catalyze reactive oxygen species and cause localized mucosal injury.3 Stasis is an important component of the corrosive process of iron pill injury.

This case represents the rare instance of a clinically significant gastrointestinal bleed secondary to localized iron injury to the gastric mucosa and highlights the role of stasis in the pathogenesis of Siderosis. Iron-deficient patients can ill afford to suffer additional blood loss from iron-induced mucosal injury. Much like NSAIDS, clinicians should be aware of the potential dangers of iron supplementation, especially in patients with known or suspected gastrointestinal motility disorders.

Back to Article Outline

References 

  1. Haig A, Driman DK. Iron-induced mucosal injury to the upper gastrointestinal tract. Histopathology. 2006;48:808–812
  2. Marginean EC, Bennick M, Cyczk J, et al. Gastric siderosis: patterns and significance. Am J Surg Pathol. 2006;30:514–520
  3. Eckstein RP, Symons P. Iron tablets cause histopathologically distinctive lesions in mucosal biopsies of the stomach and the esophagus. Pathology. 1996;28:142–145

 Conflicts of interest The authors disclose no conflicts.

 For submission instructions, please see the Gastroenterology web site (www.gastrojournal.org).

PII: S0016-5085(09)01133-0

doi:10.1053/j.gastro.2009.05.066

Gastroenterology
Volume 138, Issue 1 , Pages e7-e8, January 2010

Article Tools