David J Bromberg1, Jeffrey A Gill2. 1. Department of Internal Medicine, University of South Florida Morsani College of Medicine, Tampa, FL. 2. Department of Gastroenterology, Division of Digestive Diseases and Nutrition, James A. Haley Veterans Affairs Hospital, University of South Florida, Tampa, FL.
A 51-year-old white man presented to the emergency department with a 3-month history of atypical chest pain, odynophagia to solids and liquids, and a 18-kg weight loss. He was febrile to 39ºC and tachycardic. Physical exam was remarkable for bilateral submandibular lymphadenopathy and thrush in the posterior oropharynx. He was diagnosed with AIDS with CD4 count 146 cells/mm and viral load 423,000 copies/mL. Esophagogastroduodenoscopy (EGD) showed a large, deep, irregular esophageal ulcer (Figure 1). Biopsies of the ulcer margins and bases were negative for malignancy or infection. He was diagnosed with an idiopathic esophageal ulcer (IEU) secondary to AIDS. He was started on a proton pump inhibitor and highly active anti-retroviral therapy (HAART). Three weeks later, repeat EGD revealed complete resolution of the esophageal ulcer (Figure 2). More than 1 year after diagnosis, he continued to do well with a viral load of 53, CD4 count of 708, and without any recurrence of odynophagia.
Figure 1
An idiopathic esophageal ulcer of the distal esophagus prior to initiation of HAART.
Figure 2
The resolved esophageal ulcer after less than 3 weeks of HAART.
An idiopathic esophageal ulcer of the distal esophagus prior to initiation of HAART.The resolved esophageal ulcer after less than 3 weeks of HAART.The gastrointestinal tract—particularly the esophagus—can have disease involvement in up to 40% of AIDSpatients not on HAART. Herpes simplex virus typically causes shallow ulcers, whereas cytomegalovirus (CMV) often affects the distal esophagus with very large and deep ulcers. CMV ulcers and IEUs often have a similar appearance endoscopically, and require multiple biopsies to differentiate. Kaposi sarcoma is the most common esophageal neoplasm with typical-appearing bulky purple-tinged mucosa with submucosal nodular lesions. The diagnosis of IEU is one of exclusion after endoscopy with multiple biopsies. The pathogenesis of IEU formation is hypothesized to be from T-cell activation and subsequent apoptosis of the esophageal mucosa. Numerous possible inducers of apoptosis have been identified, including cytokines from HIV, tumor necrosis factor-α, and bacterial toxins. Treatment of IEUs should target the underlying AIDS virus with HAART. This case demonstrates that even the largest IEUs can be healed by immune reconstitution with HAART and acid suppression.
Disclosures
Author contributions:Author contributions: DJ Bromberg wrote the manuscript and is the article guarantor. JA Gill conceptualized, edited, and approved the manuscript.Financial disclosure: None to report.Informed consent was obtained for this case report.
Figure 1
Figure 2