PURPOSE: To observe the effects of systemic glucocorticoids on tuberculous pleural effusions.
METHODS: Ninety Wistar rats were intrapleurally injected with standard human mycobacterium tuberculous bacilli H37Rv each to develop an experimental tuberculous pleurisy. Then the rats were divided into two groups, one group were injected with 0.03mg of injection of triamcinolone acetonide (SG) and another group as control were received 1 ml of saline (CG) in their right thighs at 24 hours after they intrapleurally received tuberculous bacilli. Five rats were killed in groups in 8h, 24h, 32h, 48h, 3d, 5d, 7d, 10d, 15d respectively after the day of intrapleural injection. Then the pathology of the pleura and lung tissues and biochemical indices of the pleural effusion were observed and analyzed.
RESULTS: The amount of pleural effusions (PE) in SG significantly decreased from 8h to 48h after intrapleural injection when compared with CG and completely disappeared on day 3, while the PE were persistently present to day 15 and reached great amount on day 5 in CG. The LDH in early stage were greatly decreased in SG than in CG, while LDH was elevated over time and reached its peak on day 15 in CG. The concentrations of sICAM-1and TGF-β1 in effusions were significantly increased at 8h and then decreased at 48h in SG than in CG. The levels of IFN-γ; in effusions were persistently increased in SG than CG. The thickness of pleura in SG was greatly thinner than that in CG no matter in early or late stages. Pulmonary interstitial and pleura showed decreased congestion and edema in SG when compared with that of CG.
CONCLUSION: The use of systemic glucocorsteroids in experimental tuberculous pleurisy leads to a significantly decrease in the inflammatory response of pleural cavity to tuberculous bacilli, resulting in smaller amount of pleural effusions and shortening the duration of pleural effusions. Moreover, glucocorsteroids lessen the degree of adhesions and thickness of pleura.
CLINICAL IMPLICATIONS: Gucocorsteroids is effective in relieving pleural inflammatory reaction to tuberculous bacilli.
DISCLOSURE: Xie Can-mao, None.