Esophageal Siderosis: An Unusual Complication of Oral Iron Therapy

ABSTRACT

Iron is the most common nutritional deficiency encountered in the United States, with over 15% of Americans using some form of daily oral iron supplementation. Although commonly associated with minor gastrointestinal side effects, severe gastrointestinal complications are rare. Direct cytotoxic mucosal damage and subsequent ulcer formation have rarely been reported. Among reported cases, most are found in the stomach with extragastric manifestations of siderosis being less commonly described. We report a rare case of esophageal siderosis related to oral iron supplementation.

INTRODUCTION

Iron is the most common nutritional deficiency encountered in the United States with over 15% of Americans using some form of daily oral iron supplementation. Although commonly associated with minor gastrointestinal side effects, severe gastrointestinal complications are rare. Direct cytotoxic mucosal damage and subsequent ulcer formation have rarely been reported. Extragastric siderosis is uncommonly described.¹ In this case, a patient consuming oral iron supplementation is described developing severe esophageal ulceration and biopsies consistent with esophageal siderosis.

CASE REPORT

A 76-year-old man with a history of iron deficiency anemia and gastroesophageal reflux disease complicated by a history of peptic esophageal strictures necessitating endoscopic dilatation initially presented with severe solid food dysphagia and an approximate 50 lb weight loss. The patient had previously undergone incomplete esophagogastroduodenoscopy secondary to large amounts of distal esophageal food debris. He underwent a follow-up esophagogastroduodenoscopy that demonstrated a 5 cm fungating, ulcerating stricture with numerous whole iron tablets retained in the middle and lower thirds of the esophagus (Figure 1). Complete removal was accomplished with serial Roth Net retrievals (Figure 2). Following retrieval of the iron tablets, a circumferential ulcerated esophageal stenosis 3 cm proximal to the gastroesophageal junction was identified (Figure 3). Endoscopic biopsies were obtained of the ulcer edge and base. Histopathologic assessment demonstrated chronic inflammation with reactive epithelial changes, as well as loose aggregates of tan-brown refractile material compatible with iron in direct association with the epithelium (Figure 4). Interval esophageal mucosa between the ulcerated areas appeared grossly normal. Cross-sectional imaging was obtained postprocedurally and demonstrated no evidence of neoplastic processes. The patient was subsequently instructed to discontinue oral iron supplementation and repeat endoscopy 8 weeks later, which demonstrated healed esophageal ulceration and significant improvement in luminal diameter without evidence of residual siderosis. He was managed chronically with proton-pump inhibitors and serial dilations.

Figure 1.

Retained iron tablets in the lower third of the esophagus.

Figure 2.

Whole iron tablets after retrieval.

Figure 3.

Esophageal ulcers related to the site of iron pill retention.

Figure 4.

(A) 10× Prussian blue stain highlights iron deposition in squamous mucosa. (B) 2× deposition of brown, crystalline material in the esophageal squamous mucosa.

DISCUSSION

This case presents a patient without a known iron overload state presenting with esophageal siderosis and iron pill esophagitis in the setting of esophageal stricture. Mucosal siderosis typically presents with 2 classic patterns. One pattern involves iron deposition in gastric glands and lamina propria. This pattern is associated with iron overload states such as hemochromatosis or serial blood transfusions. The second pattern is characterized by iron deposition more superficially due to oral iron tablets and their local erosive effects on the mucosa. It is likely in this case that the siderosis was due to local stasis of iron tablet in the setting of a known stricture. There are rare case reports of gastric siderosis associated with oral iron supplementation.^2,3 However, there are very few reports of the similar phenomenon of esophageal siderosis.⁴ This patient did not have physiologic risk factors of iron overload but did have a mechanical risk factor of pill retention due to prior peptic stricturing, causing severe stenosis. Risks of iron supplementation have been discussed in patients with gastric motility disorders, as stasis has been known to increase the risk of gastric mucosal siderosis and iron pill gastritis.^5,6 Our case suggests that patients with esophageal motility disorders or obstructive pathology may similarly be at increased risk of mucosal disruption due to iron supplementation.

DISCLOSURES

Author contributions: G. Stoleru: Case report conception, manuscript drafting, manuscript final approval and is the article guarantor. M. Jain: Manuscript drafting. AV Jones: Manuscript drafting. A. Podboy: Case report conception, manuscript drafting, manuscript final approval.

Financial disclosure: None to report.

Informed consent was obtained for this case report.