Abstract
Esophageal ulcer is a common complication in acquired immune deficiency syndrome patients, especially in the final stages and in patients who develop an acute retroviral syndrome. Although, it can be caused by various infectious agents, such as candida, Cytomegalovirus (CMV) and herpes simplex virus 1 (HSV-1), no etiological agent is successfully identified in a proportion of patients. A 38-year-old male presented to our hospital with a two-month history of progressive dysphagia, odynophagia to solids and liquids, and atypical chest pain. He was previously diagnosed with AIDS with a viral load of 130904 copies/ml and CD4 count of 1 cell/ml, who was not on anti-retroviral therapy. Esophagogastroduodenoscopy (EGD) revealed many large, circumferential, very deep esophageal ulcers without bleeding, 22 to 35 cm from incisors. Biopsies showed ulcerated mucosa with fibrinopurulent exudate, with acute and chronic inflammation, and Immunohistochemical stains were negative for fungal, CMV, HSV-1, and human herpesvirus 8 (HHV-8) viral inclusions. A diagnosis of AIDS-related Idiopathic Esophageal Ulcers (IEU) was made and the patient was started on highly active anti-retroviral therapy (HAART) and oral prednisone 40 mg daily. Follow up visits showed complete clinical improvement after two weeks of treatment with corticosteroid. The postulated pathogenesis of IEU is mainly based on T-cell activation and subsequent apoptosis of the esophageal mucosa. It is usually diagnosed in patients with CD4 cell counts less than 100/μL. Esophageal ulcer in HIV-positive patient includes a vast differential diagnosis, and IEU can only be diagnosed after ruling out microbial pathogens and other possible causes. IEUs are considered to be associated with HIV infection, therefore differentiation between infectious and noninfectious causes is essential as viral or fungal ulcers are usually treated with potentially toxic antimicrobial drugs and idiopathic ulcers are treated with steroids. Both systemic and intralesional steroids, are reported to be effective in the treatment of idiopathic esophageal ulcers. In our case clinical improvement was noted after the initiation of HAART treatment and a short course of systemic steroids. EGD was not repeated due to complete resolution of symptoms.1835_A Figure 1. Large, very deep esophageal ulcer1835_B Figure 2. Circumferential esophageal ulcer1835_C Figure 3. Fibrinopurulent exudate and inflamed granulation tissue
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