RESUMO
Pneumocystis in humans is caused by a unicellular and eukaryotic organism called P. jirovecii. The overall incidence of P. jirovecii pneumonia (PCP) has decreased with the use of highly active antiretroviral therapy and the use of chemoprophylaxis with trimethroprim sulfametoxazole (TMP/SMX) in cases of immunosuppressed patients. However, approximately 85% of patients with advanced HIV infections continue to experience this disease with inadequate management. Pneumocystis infection can present with spontaneous pneumothorax in 2-6% of cases [8] which can be a potentially fatal complication. We report the case of a 32-year-old man presented with P. jirovecii pneumonia who developed cystic lesions and spontaneous bilateral pneumothorax in spite of TMP/SMX treatment. We consider it an interesting clinical case because few simultaneous bilateral pneumothorax cases have been described directly related to the PCP.
RESUMO
The aim of this study was to analyze whether FeNO levels in acute exacerbation of COPD (AECOPD) with hospital admission have better diagnostic value than eosinophilia in blood, and to evaluate its usefulness in predicting a better clinical response. An observational prospective study of patients with AECOPD was carried out. FeNO determinations were made on arrival at the emergency room (ER), at discharge and during stability 3-6 months after discharge. Co-morbidities, bronchodilators, inhaled (IGC) and systemic (SGC) glucocorticoids, eosinophils, systemic inflammation markers (procalcitonin, C-reactive protein), eosinophil cationic protein, and total IgE were collected. Fifty consecutive patients (92% men, mean age 75 ± 6 years) were included in this study. Phenotypes were 26% Asthma-COPD Overlap Syndrome (ACOS), 42% chronic bronchitis (CB) and 32% emphysema. ACOS patients showed significantly higher levels of FeNO (73 ppb) and eosinophils (508 cells/mm3) than the rest (CB: 23 ppb, 184 cells/mm3, emphysema: 27 ppb, 159 cells/mm3; p < 0.05). A significant correlation between FeNO levels measured in ER and eosinophils was observed (r = 0.7; p < 0.001), but not at discharge or in stable phase. No significant association was found with parameters of systemic inflammation and mean stay. In conclusion, the determination of FeNO in AECOPD does not offer advantages over the evaluation of eosinophilia. These parameters rise at arrival in ER, descend at discharge, and remain unchanged in the stable phase. Both present similar diagnostic utility and are able to better identify the ACOS phenotype, which helps select a population that could benefit from a glucocorticoids therapy.
