Abstract

Herpes simplex esophagitis (HSE) is typically seen in patients with HIV, undergoing chemotherapy, or otherwise immunosuppressed. However, HSV may rarely cause esophagitis in immunocompetent patients, and is likely underdiagnosed as it is typically a self-limited process in this population and resolve spontaneously in one to two weeks. A 68-year-old male with history of peptic ulcer disease due to Helicobacter pylori, gastroesophageal and reflux disease presented to the emergency department after three days of acute onset severe odynophagia. His symptoms had begun suddenly while eating a spicy Cajun gumbo, after which he experienced intense burning pain with all oral intake, accompanied by nausea and vomiting. He denied constitutional symptoms, but recalled a mild sore throat and dry cough two days prior to onset of odynophagia, and two weeks previously had an oral “cold sore” which resolved spontaneously. The patient also endorsed a recent 10-pound weight loss, which he attributed to lifestyle modification. His vital signs, oropharyngeal exam, and abdominal exam were unremarkable, and no laboratory abnormalities were noted. Following initial symptomatic control with gastrointestinal cocktail, he underwent upper endoscopy. Multiple 3-5 mm, shallow, clean-based, irregular ulcerations were found in the distal and mid-esophagus, suggestive of herpes simplex esophagitis, and empiric valacyclovir was started given severity of his presenting symptoms. Biopsy revealed squamous mucosa ulceration with underlying granulation tissue. HSV-1 was subsequently identified in viral culture from esophageal biopsies, with corresponding positive HSV-1 IgG and IgM serology. Further infectious workup was unremarkable. His symptoms resolved entirely with a brief course of oral valacyclovir and he was tolerating a regular diet within a week. HSV is a rare cause of esophagitis in immunocompetent patients, and should prompt consideration of underlying immune deficiency. In this patient with a complex medical history, pill esophagitis, gastroesophageal reflux, or even malignancy would be much more likely causes of his acute odynophagia with alarm symptoms. Data regarding antiviral use in immunocompetent patients is sparse and the decision to treat is based on the severity of symptoms. This case illustrates the importance of keeping HSV in the differential for acute odynophagia regardless of immunologic status.

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