A Case of Severe Esophagitis in a Patient with Gout

Abstract

Colchicine is a frequently used medication, most commonly for gout. We present a case of severe esophagitis with histopathologic finds consistent with colchicine toxicity. There are few reported cases of this adverse effect, and histopathology has only recently been documented. We hope to shed light on this significant and potentially under recognized complication of a commonly used medication. A 36-year-old male with alcoholism and gout presented with a week of central chest pain, profound odynophagia, and inability to tolerate solids or liquids. He reported minimal NSAID use. Exam was unremarkable. Elevated creatinine, transaminases and lipase were noted. Esophagogastroduodenoscopy revealed 16cm of LA grade D esophagitis with no bleeding, duodenal bulb erythema and diffuse atrophic mucosa in the second portion of the duodenum. Pathology demonstrated esophageal inflammation extending into the muscular layer with ulcerated mucosa and numerous arrested mitoses consistent with colchicine toxicity. Chronic peptic duodenitis without dysplasia was also noted. Further history revealed patient had been taking very large amounts of colchicine three months prior with doses of more than 20 tablets at a time. Colchicine was discontinued. He was diagnosed with LA grade D esophagitis with evidence of colchicine toxicity, duodenitis, alcoholic hepatitis and pancreatitis, and gout flare. Steroid taper, proton pump inhibitor, sucralfate, and vitamins were prescribed with symptomatic improvement. Alcohol and NSAID cessation were advised. Frequently prescribed for gout and pericarditis, colchicine has a long history of use. Colchicine prohibits polymerization of microtubules which is fundamental to chemotaxis, degranulation, and mitosis. Toxicity, in acute overdose or long-term use, can lead to significant morbidity and mortality such as multi-organ failure and death. Impaired hepatic and renal function decrease clearance of colchicine by ten and three-fold respectively. The most commonly involved areas are those with rapid proliferation, including the duodenum and gastric antrum. Pathologic findings are arrested mitoses, epithelial pseudostratification and loss of polarity. The typical site of gastrointestinal tract injury by colchicine is the small bowel. Our case highlights that there is more widespread involvement of the GI tract in colchicine toxicity than previously reported. Furthermore, colchicine can induce severe esophagitis and significant patient symptomatology.1717_A Figure 1. Esophagogastroduodenoscopy with LA Grade D esophagitis in the middle third of the esophagus.1717_B Figure 2. 400x magnification of H&E stain with arrested mitoses in the esophageal epithelium. Scattered characteristic ring mitoses due to colchicine.1717_C Figure 3. 200x magnification of phosphohistone H3 (PHH3) stain of esophageal epithelium highlighting numerous characteristic ring mitoses (brown) in the setting of colchicine toxicity.