Immune reconstitution inflammatory syndrome presenting as chylothorax in a patient with HIV and Mycobacterium tuberculosis coinfection: a case report

A 25-year-old HIV-infected male presented with fever, productive cough, and body weight loss for 2 months. His CD4 cell count was 11 cells/μl and HIV-1 viral load was 315,939 copies/ml. Antituberculosis therapy was initiated after the diagnosis of pulmonary TB. One week after antituberculosis therapy, antiretroviral therapy was started. However, multiple mediastinal lymphadenopathies and chylothorax developed. Adequate drainage of the chylothorax, suspension of antiretroviral therapy, and continued antituberculosis therapy resulted in successful treatment and good outcome.Chylothorax is a rare manifestation of TB-associated IRIS in HIV-infected patients. Careful monitoring for development of IRIS during treatment of HIV-TB coinfection is essential to minimize the associated morbidity and mortality.Patients with human immunodeficiency virus (HIV) infection are at risk for coinfection with Mycobacterium tuberculosis (TB) [1]. Highly active antiretroviral therapy restores the immunity of HIV-infected patients, but immune reconstitution inflammatory syndrome (IRIS) may develop [2,3]. We report a case of HIV and TB coinfection who developed chylothorax as a manifestation of IRIS after the initiation of antituberculosis and antiretroviral therapy within a one-week interval.A 25-year-old HIV-1-infected man presented with fever, productive cough, and body weight loss for 2 months. On admission, physical examination disclosed oral thrush and inspiratory crackles over his lung fields bilaterally. He had a CD4 cell count of 11 cells/μl and an HIV-1 viral load of 315,939 copies/ml. Chest X-ray revealed a consolidation in his right lung and multiple nodular infiltrations in the left lung field (Figure 1A). A sputum smear was positive for acid-fast bacilli and the sputum culture subsequently grew TB. He was treated with rifampin, isoniazid, ethambutol, and pyrazinamide initially, and his fever subsided gradually. Due to a strikingly low CD4 cell count, antiretroviral therapy with