Endoscopy 2008; 40: E157-E158
DOI: 10.1055/s-2007-995380
Unusual cases and technical notes

© Georg Thieme Verlag KG Stuttgart · New York

Herpes simplex virus esophagitis in an immunodeficient patient with non-small-cell lung cancer following a disseminated herpes zoster infection

F.  Gundling1 , H.  Rohrbach2 , A.  Nerlich2 , W.  Schepp1
  • 1Second Department of Medicine, Bogenhausen Academic Teaching Hospital, Technical University of Munich, Munich, Germany
  • 2Department of Pathology, Bogenhausen Academic Teaching Hospital, Technical University of Munich, Munich, Germany
Further Information

Publication History

Publication Date:
30 July 2008 (online)

Preview

Herpes simplex virus (HSV) esophagitis is rare. It usually occurs in the setting of immunodeficiency, for example in patients with malignancy [1], patients on immunosuppressive therapy [2], or patients with AIDS [3].

A 62-year-old patient with non-small-cell lung cancer (T3N2M1) presented with a 1-month history of persistent dysphagia and odynophagia. Eight weeks before, he had undergone whole-brain radiation therapy for multiple cerebral metastases. A few days later, the patient developed disseminated herpes zoster, secondary to the immunosuppression caused by the radiation. He received systemic therapy with intravenous aciclovir (10 mg/kg per day) for 14 days, resulting in complete recovery of the skin lesions.

Upper gastrointestinal endoscopy revealed numerous, coin-shaped, white pseudomembranous lesions, 1 – 2 cm in diameter, with a discrete central ulcer in the proximal portion of the esophagus which bled readily ([Fig. 1]). The stomach and duodenum were normal. Herpes virus infection was not suspected as the cause of the esophagitis at endoscopy. However, biopsy specimens showed typical herpetic histological changes, including a ground-glass appearance of the nuclear chromatin, nuclear inclusions, and multinucleation ([Fig. 2]), and positive immunostaining with specific anti-HSV type 1 antibodies ([Fig. 3]), appearances supporting the diagnosis of herpetic esophagitis.

Fig. 1 Upper gastrointestinal endoscopy revealed coin-shaped, white pseudomembranous lesions, 1–2 cm in diameter, with a discrete central ulcer in the proximal portion of the esophagus (arrows).

Fig. 2 A histological view showing typical histological changes associated with herpetic lesions, including a ground-glass appearance of the nuclear chromatin, nuclear inclusions, and multinucleation (periodic acid–Schiff reaction, original magnification × 100).

Fig. 3 Positive immunohistochemical staining with monoclonal antibody (red color) to herpes simplex virus types 1 and 2 (original magnification × 100).

Because inflammatory parameters were not significantly elevated and because the patient showed no signs of systemic herpes virus infection or relapse of herpes zoster, he was not given antiviral chemotherapy. A repeat endoscopy 2 weeks later showed a marked spontaneous improvement and the patient’s initial symptoms had resolved. To date, the HSV esophagitis has not relapsed (after 3 months).

Proper endoscopic interpretation is a prerequisite for the recognition of herpes esophagitis because biopsy and culture results can be negative in the early stages of this condition [4]. However, failure to diagnose HSV esophagitis can result in gastrointestinal bleeding caused by herpetic esophageal ulcers [5]. We conclude that physicians who are treating patients with malignancies should be aware of the potential of patients to develop HSV esophagitis, especially as effective antiviral agents are now available.

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References

F. Gundling, MD 

Department of Gastroenterology, Hepatology and Gastrointestinal Oncology

Bogenhausen Academic Teaching Hospital

Technical University of Munich

Englschalkinger Straße 77

81925 Munich

Germany

Fax: +49-89-92702486

Email: Gastroenterologie@kh-bogenhausen.de