Pleuro-Pulmonary Nocardiosis as Opportunistic Infection in a Patient with Chronic Hepatitis C under Combination Treatment with Pegylated Interferon, Ribavirin, and Boceprevir

Nocardiosis is an infrequent but serious pulmonary infection caused by Gram-positive aerobic actinomycetes. In this paper, we report on a 48-year-old patient with pleuropulmonary nocardiosis and cirrhosis due to chronic hepatitis C virus infection treated with triple antiviral treatment complicated by prolonged neutropenia. 1. Introduction Pleuropulmonary nocardiosis is an uncommon infection and may cause radiologic findings that vary from vague pulmonary infiltrates to cavitary lesions. It is found more commonly in patients with underlying lung disease and in immunocompromised patients. We describe the first case of this atypical bacterial infection in a patient with hepatitis C virus related liver cirrhosis undergoing antiviral therapy with pegylated interferon alpha, ribavirin, and boceprevir (Merck Sharp & Dome Ltd, Hertforshire, United Kingdom) complicated by prolonged neutropenia. 2. Case Report A 48-year-old Caucasian male was admitted to our inpatient liver clinic in October 2012. He was in poor general condition with ascites, fever (39.4°C), and a dry cough. In 1997, the patient had been diagnosed with chronic hepatitis C (CHC) subtype 1b which was unresponsive to a 3-month course of interferon (IFN)-alpha monotherapy. In June 2007, he had been admitted to the internal medicine department because of portal decompensation following a period of higher alcohol consumption. CT scan at that time revealed, besides signs of cirrhosis, a right-sided nodular pulmonary lesion measuring ？cm, which was interpreted as posttuberculosis infiltration without structural changes of the bronchial architecture. Following abstinence from alcohol, liver function had stabilized from August 2008 onwards. Antiviral combination treatment with pegylated interferon (pegIFN) alpha-2a 180？μg given weekly and ribavirin (RBV) (600？mg/12？h) had been started in September 2009. Due to the rapid virological response with no detectable hepatitis C virus (HCV) RNA determined with the COBAS AmpliPrep/COBAS TaqMan HCV Test (lower limit of detection 15？IU/mL) at week 4 of treatment, the antiviral therapy had been shortened to 24 weeks. Three months after the end of treatment, the patient developed a virological relapse. In May 2012, the patient had been evaluated for triple antiviral combination treated with the protease inhibitor boceprevir. In June 2012, a 4-week lead-in phase with pegIFN alpha-2a 180？μg given weekly and ribavirin (600？mg/12？h) was started. At week 4, the pegIFN dosage was reduced to 135？μg weekly due to neutropenia and boceprevir (800？mg/8？h) being added. The