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Tuberculous pleural effusions in HIV-negative patients

INTRODUCTION

Tuberculous pleural effusion accounts for approximately 5 percent of disease due to Mycobacterium tuberculosis and is the second most common form of extrapulmonary tuberculosis (TB) after lymphatic involvement [1,2].

Issues related to the diagnosis and treatment of tuberculous pleural effusions in HIV-negative patients will be reviewed here. Issues related to tuberculous pleural effusions in HIV-infected patients are discussed separately. (See "Tuberculous pleural effusions in HIV-infected patients".)

PATHOGENESIS

Tuberculous pleural effusions are thought to result from a delayed hypersensitivity reaction to mycobacteria and mycobacterial antigens in the pleural space [3]. These organisms and/or their antigens probably enter the pleural space due to leakage or rupture of a subpleural focus of disease. In one study of 24 patients with tuberculous pleural effusions who underwent thoracotomy, for example, a caseous focus in the lung contiguous with the diseased pleura was found in half of cases [4]. Development of pleural effusion occurs largely as a result of hypersensitivity reaction, but tuberculous pleurisy must be considered to be due to infection since culture of the fluid grows mycobacteria in some cases and culture of the pleural tissue usually grows mycobacteria. Tuberculous pleural effusions are usually self-limited and resolve spontaneously with or without treatment in most cases. However, the condition can potentially progress and worsen and become a tuberculous empyema.

A tuberculous empyema represents chronic active infection of the pleural space and can occur in the setting of a large pleural effusion that progresses, usually leading to an unexpandable lung [5]. Simple tuberculous pleural effusion and tuberculous empyema can be considered a continuum of the same process. Tuberculous empyema can also develop via extension of infection from thoracic lymph nodes or subdiaphragmatic focus, via hematogenous spread, or in the setting of therapeutic pneumothorax therapy leading to an unexpandable lung.

In an experimental model of tuberculous effusion in which Bacille Calmette-Guérin (BCG) was injected into the pleural space of rabbits that had been previously sensitized with intradermal BCG, a sequential influx of cells into the pleural space was observed [6]. An initial neutrophilic response is necessary for the subsequent mononuclear influx [7]. Macrophages are the predominant mononuclear cells until day four, with lymphocytes predominating thereafter [6]. The local release of cytokines probably induces the sequential expression of specific cell adhesion molecules in vascular endothelium that direct the influx of the different inflammatory cells.

           

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Literature review current through: Sep 2014. | This topic last updated: Aug 26, 2014.
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