Tuberculous pleurisy

The expansion or new development of tuberculous lesions during ultimately successful therapy has been termed a paradoxical response. It is most often reported in relation to intracranial tuberculomata, but is probably most common in tuberculous lymphadenopathy. It is also described in tuberculous pleurisy and in parenchjmal lung disease. In most cases, the problem eventually settles, but sometimes glucocorticoid therapy is used empirically. 

Dlugovitzky D, Rateni L, Torres-Morales A, Ruiz-SUva J, Pinesky R, Canosa B, Molteni O, Bottasso O. Levels of interleukin-8 in tuberculous pleurisy and the profile of immunocompetent cells in pleural and peripheral compartments. Immunol Lett 1997 55 35-39. 

Mohammed KA, Nasreen N, Ward MJ, Mubarak KK, Rodriguez-Panadero F, Antony VB. Mycobacterium-mediated chemokine expression in pleural mesotheUal cells role of C-C chemokines in tuberculous pleurisy. J Infect Dis 1998 178 1450-1456. 

Nasreen N, Mohammed KA, Ward MJ, Antony VB. Mycobacterium-induced trans-mesothelial migration of monocytes into pleural space role of intercellular adhesion molecule-1 in tuberculous pleurisy. J Infect Dis 1999 180 1616-1623. 

Pokkali, S., Das, S.D., and Selvaraj, A. (2010) Differential upregulation of chemokine receptors on CD56( + ) NK cells and their transmigration to the site of infection in tuberculous pleurisy. FEMS Immunology and Medical Microbiology, in press. 

Indications 1) Suspended rheum and 2) replete water. Tuberculous exudative pleurisy, rheumatic pleurisy, ascites due to cirrhosis, schistosomiasis, nephritis, or uremia from systemic lupus erythematosus. 

The role of chemokines in granulomatous disease of the pleura has been extensively studied in mberculous pleurisy (16,25-28). Tuberculous pleural fluids contain a significant proportion of mononuclear phagocytes and lymphocytes that are responsible for the initiation of the granulomatous inflammatory response and the localization of mycobacteria into granulomas (16,29,30). 

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