ABSTRACT
Os pulmões estão entre os principais sítios acometidos pela paracoccidioidomicose, contudo as alterações nem sempre são fáceis de serem diferenciadas de outros distúrbios respiratórios. O objetivo deste estudo foi verificar a freqüência do comprometimento pulmonar na paracoccidioidomicose e se existe associação clínico-radiológica. Foi realizado um estudo retrospectivo de março de 1996 a novembro de 2006, em pacientes com paracoccidioidomicose no Hospital Universitário Regional de Maringá, PR. No período foram confirmados 45 casos, dos quais 79,5 por cento apresentavam alterações radiológicas em Raios-X de tórax e quatro deles tinham também tuberculose pulmonar. De 40 pacientes com paracoccidioidomicose exclusivamente, 57,5 por cento apresentavam manifestações clínicas respiratórias e 77,5 por cento alterações radiológicas, ficando evidente uma dissociação clínico-radiológica, o tabagismo foi declarado por 80,6 por cento dos pacientes que apresentavam alterações radiológicas. Concluímos que as alterações morfológicas no pulmão, embora freqüentes, nem sempre correspondem a sinais e sintomas respiratórios e são difíceis de serem atribuídas exclusivamente à paracoccidioidomicose.
Lungs are among the main sites affected by paracoccidioidomycosis. However, the alterations are not always easy to differentiate from other respiratory disorders. The objectives of the present study were to investigate the frequency of lung impairment in paracoccidioidomycosis cases and to investigate whether any clinical-radiological association exists. A retrospective study was carried out from March 1996 to November 2006, among patients with paracoccidioidomycosis at the Regional University Hospital of Maringá, Paraná, Brazil. Over this period, 45 cases were confirmed, of which 79.5 percent presented radiological abnormalities on chest X-rays, and four of them also presented pulmonary tuberculosis. Out of the total of 40 patients with paracoccidioidomycosis alone, 57.5 percent presented respiratory clinical manifestations, whereas 77.5 percent presented radiological abnormalities, thus demonstrating clinical-radiological dissociation. On the other hand, 80.6 percent of the patients who presented radiological abnormalities said that they smoked. We concluded that although morphological abnormalities in the lungs are frequent, they do not always correspond to respiratory signs and symptoms and cannot easily be attributed exclusively to paracoccidioidomycosis.
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Lung Diseases, Fungal/diagnosis , Paracoccidioidomycosis/diagnosis , Respiration Disorders/etiology , Acute Disease , Chronic Disease , Lung Diseases, Fungal/complications , Lung Diseases, Fungal , Paracoccidioidomycosis/complications , Paracoccidioidomycosis , Retrospective Studies , Respiration Disorders/diagnosis , Severity of Illness Index , SmokingABSTRACT
To evaluate the role of murine fibrinogen like protein 2 (mfgl2) /fibroleukin in lung impairment in Severe acute respiratory syndrome (SARS), a murine SARS model induced by Murine hepatitis virus strain 3 (MHV-3) through trachea was established. Impressively, all the animals developed interstitial pneumonia with extensive hyaline membranes formation within alveoli, and presence of micro-vascular thrombosis in the pulmonary vessels. MHV-3 nucleocapsid gene transcripts were identified in multiple organs including lungs, spleen etc. As a representative proinflammatory gene, mfgl2 prothrombinase expression was evident in terminal and respiratory bronchioles, alveolar epithelia and infiltrated cells in the lungs associated with fibrin deposition and micro-vascular thrombosis. In summary, the established murine SARS model could mimic the pathologic characteristics of lungs in patients with SARS. Besides the physical damages due to virus replication in organs, the up-regulation of novel gene mfgl2 in lungs may play a vital role in the development of SARS associated lung damage.
ABSTRACT
Objective: To investigate the relationship of murine fibrinogen-like protein 2(mfgl2) / fibroleukin with pulmonary impairment in the murine model of severe acute respiratory syndrome(SARS).Methods: The Balb/cJ mice infected with murine hepatitis virus strain 3(MHV-3) through the trachea were observed for the pathological features and virus distribution in different organs.The expressions of both mfgl2 and fibrino in the lungs were determined by in situ hybridization and immunohistochemistry.Results: The MHV-3 infected mice developed typical interstitial pneumonia with extensive hyaline membrane formation in the alveoli,presented micro-vascular thrombosis in the pulmonary vessels and died within 5 days.MHV-3 virus replication was identified in all the organs observed.The specific expression of mfgl2 prothrombinase was noted in the terminal and respiratory bronchioles,alveolar epithelia and infiltrating cells.Conclusion: The characteristics of the pulmonary impairment of SARS in human can be properly simulated by the MHV-3 induced murine model of SARS.The up-regulation of the specific gene mfgl2 in the lungs involved in fibrino deposition and microvascular thrombosis may be largely responsible for SARS-associated pulmonary damages.