Abstract
Chronic pulmonary aspergillosis (CPA) is a severe fungal infection usually seen in immunocompetent patients with underlying respiratory disorders [1]. Estimates suggest that ∼3 million people suffer from CPA globally [2]. The precise prevalence is unknown. Pulmonary tuberculosis (TB) seems to be the most relevant driver for the global burden of CPA with estimates suggesting about 1.2 million patients with CPA as a sequel to TB [3]. Given that there were 10.4 million new TB cases in 2015, CPA represents a serious sequela to pulmonary TB [4]. However, any search for CPA in the Global Tuberculosis Report of the World Health Organization (WHO) is still in vain [4]. The relative frequency of CPA after standard antituberculous treatment is estimated to be 17% after 12 months and increases to 22% after 48 months. This data, however, is based on two historic UK studies from 1968 and 1970 in which fungal evidence was confirmed by Aspergillus precipitins (59% sensitivity, 100% specificity) and radiological features considered only aspergilloma [3, 5, 6]. Thus, the frequency of CPA might even be higher, when using Aspergillus -specific IgG antibody assays, which are superior to Aspergillus precipitins with a sensitivity of up to 96% and a specificity of 98%, and when radiological criteria consider all CPA entities, especially chronic cavitary pulmonary aspergillosis (CCPA) [7]. Follow-up visits of TB patients, especially those with cavitary TB, should always include a diagnostic work-up for CPA. Whether CPA plays even a larger role in multidrug-resistant (MDR) and extensively drug-resistant (XDR)-TB patients is entirely unknown. MDR/XDR-TB patients experience a more progressive destruction of the lung and global rates of MDR/XDR-TB are increasing considerably [4, 8]. Predictors of mortality in chronic pulmonary aspergillosis
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