É possível diferenciar derrames pleurais linfocíticos secundários a tuberculose ou linfoma através de variáveis clínicas e laboratoriais? / Differentiating between tuberculosis-related and lymphoma-related lymphocytic pleural effusions by measuring clinical and laboratory variables: Is it possible?

OBJETIVO: Descrever características clínicas e laboratoriais em pacientes com derrames pleurais linfocíticos secundários a tuberculose ou linfoma, a fim de identificar as variáveis que possam contribuir no diagnóstico diferencial dessas doenças. MÉTODOS: Estudo retrospectivo com 159 pacientes adultos HIV negativos com derrame pleural linfocítico secundário a tuberculose ou linfoma (130 e 29 pacientes, respectivamente) tratados no Ambulatório da Pleura, Instituto do Coração, Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo (SP), entre outubro de 2008 e março de 2010. RESULTADOS: A média de idade e de duração dos sintomas foi menor no grupo tuberculose que no grupo linfoma. Os níveis pleurais de proteínas, albumina, colesterol, amilase e adenosina desaminase (ADA), assim como os níveis séricos de proteínas, albumina e amilase, foram maiores no grupo tuberculose, enquanto os níveis séricos de colesterol e triglicérides foram maiores no grupo linfoma. As contagens de leucócitos e linfócitos no líquido pleural foram maiores no grupo tuberculose. Células malignas estavam ausentes no grupo tuberculose, entretanto, linfócitos atípicos foram observados em 4 desses pacientes. No grupo linfoma, a citologia para células neoplásicas foi positiva, suspeita e negativa em 51,8%, 24,1% e 24,1% dos pacientes, respectivamente. A imunofenotipagem do líquido pleural foi conclusiva na maioria dos pacientes com linfoma. CONCLUSÕES: Nossos resultados demonstram semelhanças clínicas e laboratoriais entre os pacientes com tuberculose ou linfoma. Embora os níveis de proteínas e ADA no líquido pleural tendam a ser mais elevados no grupo tuberculose que no grupo linfoma, mesmo essas variáveis mostraram uma sobreposição. Entretanto, nenhum paciente com tuberculose apresentou níveis de ADA no líquido pleural inferiores ao ponto de corte (40 U/L).

OBJECTIVE: To describe clinical and laboratory characteristics in patients with tuberculosis-related or lymphoma-related lymphocytic pleural effusions, in order to identify the variables that might contribute to differentiating between these diseases. METHODS: This was a retrospective study involving 159 adult HIV-negative patients with tuberculosis-related or lymphoma-related lymphocytic effusions (130 and 29 patients, respectively), treated between October of 2008 and March of 2010 at the Pleural Diseases Outpatient Clinic of the University of São Paulo School of Medicine Hospital das Clínicas Heart Institute, in the city of São Paulo, Brazil. RESULTS: Mean age and the mean duration of symptoms were lower in the tuberculosis group than in the lymphoma group. The levels of proteins, albumin, cholesterol, amylase, and adenosine deaminase (ADA) in pleural fluid, as well as the serum levels of proteins, albumin, and amylase, were higher in the tuberculosis group, whereas serum cholesterol and triglycerides were higher in the lymphoma group. Pleural fluid leukocyte and lymphocyte counts were higher in the tuberculosis group. Of the tuberculosis group patients, none showed malignant cells; however, 4 showed atypical lymphocytes. Among the lymphoma group patients, cytology for neoplastic cells was positive, suspicious, and negative in 51.8%, 24.1%, and 24.1%, respectively. Immunophenotyping of pleural fluid was conclusive in most of the lymphoma patients. CONCLUSIONS: Our results demonstrate clinical and laboratory similarities among the patients with tuberculosis or lymphoma. Although protein and ADA levels in pleural fluid tended to be higher in the tuberculosis group than in the lymphoma group, even these variables showed an overlap. However, none of the tuberculosis group patients had pleural fluid ADA levels below the 40-U/L cut-off point.

Inflammation and clinical repercussions of pleurodesis induced by intrapleural talc administration

Although reports on pleurodesis date back to the beginning of the 20th century, the search for the ideal sclerosing agent is ongoing. Several agents have been studied and used, but talc continues to be the most popular. However, potentially harmful systemic side effects have been associated with talc pleurodesis. In this article we discuss the likely mechanisms of pleural inflammation and pleurodesis with emphasis on the systemic response due to the instillation of talc into the pleural space.

Apesar dos relatos sobre pleurodese remontarem ao início do século XX, ainda hoje se busca o agente esclerosante ideal. Diversos agentes foram estudados e utilizados, mas o talco é considerado o mais popular. No entanto, efeitos sistêmicos potencialmente tóxicos tem sido associados à pleurodese pelo talco. Neste artigo discutimos os prováveis mecanismos de inflamação pleural e pleurodese, com ênfase na resposta sistêmica produzida pela instilação intrapleural de talco.

Avaliação dos efeitos do talco de diferentes tamanhos de partículas na pleurodese experimental / Systemic and pleural effects of talc with different size particles in experimental pleurodesis

Introdução: diversos efeitos colaterais sistêmicos têm sido associados à pleurodese induzida pelo talco. No entanto, o mecanismo pelos quais o talco produz efeitos sistêmicos é pouco conhecido. Especulamos que as pequenas partículas de talco instiladas na cavidade pleural podem migrar para a circulacao sanguínea com mais facilidade e causar uma resposta / Study objectives: talc-induced pleurodesis has been associated with several systemic effects. However, the mechanisms by which talc pleurodesis produce a systemic inflammatory response are poorly understood...

Reexpansion pulmonary edema

Reexpansion pulmonary edema (RPE) is a rare, but frequently lethal, clinical condition. The precise pathophysiologic abnormalities associated with this disorder are still unknown, though decreased pulmonary surfactant levels and a pro-inflammatory status are putative mechanisms. Early diagnosis is crucial, since prognosis depends on early recognition and prompt treatment. Considering the high mortality rates related to RPE, preventive measures are still the best available strategy for patient handling. This review provides a brief overview of the pathophysiology, diagnosis, treatment, and prevention of RPE, with practical recommendations for adequate intervention.