Esophageal tuberculosis during treatment of hepatitis C.

Conflicts of interest The authors disclose no conflicts. © 2013 by the AGA Institute 1542-3565/$36.00 http://dx.doi.org/10.1016/j.cgh.2013.04.018 Apresented with progressively worsening odynophagia and dysphagia for 3 weeks. She had completed 15 weeks of pegylated interferon-alfa-2a and ribavirin during which her course was uncomplicated. She had emigrated from Ethiopia 5 years earlier and was HIV negative. Physical exam and basic laboratory evaluation were unremarkable. Esophagogastroduodenoscopy found a 2.0 1.0 cm ulcer in the proximal esophagus (Figure A). Chest computed tomography scan revealed a right apical cavitating mass (Figure B). Biopsy of the esophageal ulcers showed multiple non-necrotizing granulomas (Figure C). Cultures of biopsy specimens and sputum grew Mycobacterium tuberculosis. Gastrointestinal tuberculosis (TB) is the sixth most frequent site of extrapulmonary TB. Esophageal disease is rarer still, accounting for 0.2%–1.0% of gastrointestinal cases. Site-specific symptoms include retrosternal pain, dysphagia, and odynophagia. Endoscopy typically shows ulcerative lesions in the mid-esophagus. Patients are usually treated with 4-drug antitubercular therapy for 2 months, followed by rifampin and isoniazid to complete 9 months of treatment. The salient question is whether there is a relationship between hepatitis C and TB. Hepatitis C and TB often coexist, especially among patients from regions where TB is endemic. In spite of this association, TB reactivation is not commonly seen in patients being treated for HCV; only 4 cases have been reported in the medical literature thus far. Interferon therapy has been implicated in infectious adverse events. The mechanism of this increased susceptibility to infection has been proposed to be due to either treatmentinduced leukopenia or from direct modulation of the immune system. Although neutropenia occurs in about 20% of patients treated with pegylated interferon, it alone does not seem to be associated with increased risk of infection. In addition to the use of pegylated interferon, other factors found to be associated with increased infectious risk include age and hyperglycemia, both of which have a known association with diminished glycol, the molecule covalently attached to interferon, accumulates in tissue macrophages and also suppresses phagocytic activity. This argues that reducing functional activity, rather than leukocyte quantity, may be more significant in promoting susceptibility to infection. Even more specifically, monocytes and macrophages pretreated with interferon-alfa and then infected with M bovis have demonstrated a striking loss of mycobacteriostatic activity. This patient was treated with rifampin, isoniazid, ethambutol, and pyrazinamide. Her odynophagia and dysphagia resolved after 1 month of treatment. After completing a 9-month course, repeat endoscopy showed healing of the esophageal ulcer. This is, to our knowledge, the first reported case of esophageal TB occurring during treatment of hepatitis C virus. Because of the high rate of coinfection among emigrants from countries where TB is endemic, it seems prudent to implement routine TB screening before initiating treatment of hepatitis C in high-risk patients.