[Day tuberculous exudative pleurisy: morphological and morphometric aspects].

Visceral pleural pathomorpholodical changes were studied in 50 patients. Group 1 included 25 patients with isolated tuberculous pleurisy; Group 2 consisted of 7 patients with tuberculous exudative pleurisy in the presence of a specific process in the lung; a comparison group comprised 18 who had not died from diseases of the lung and pleura. The exudative productive type of specific pleural inflammation was prevalent in 15 (60%) and 4 (57.1%) patients, respectively. In Group 1, the pleural thickness was 144.0 +/- 3.3 microm, which was 8.3 times greater (p < 0.01) than that in the comparison group (17.35 +/- 4.78 microm). In Group 2, the visceral pleural thickness was 151.1 +/- 3.4 microm, which was 8.7 times greater (p < 0.01) than that in the comparison group and 1.05 times greater than that in Group 1. The study has established that in both Group 1 and Group 2, exudative pleurisy is accompanied by early visceral pleural fibrosing with a tendency to be more pronounced in Group 2 patients, which raises the question as to whether it is necessary to use resolution therapy at the early stages of treatment, to inject isoniazid lymphotropically, and to apply physical methods to prevent pleural cavity obliteration.

[The diagnostic value of adenosine deaminase coefficient in patients with tuberculous exudative pleurisy].

The authors examined 51 patients aged 37.74 +/- 2.17 years who had tuberculous pleurisy and aged 49.8 +/- 4.6 years who had nonspecific pleurisy. Group 1 comprised 18 patients with isolated tuberculous exudative pleurisy. Group 2 included 13 patients with tuberculosis complicated by tuberculous pleurisy. Group 3 consisted of 10 patients with nonspecific exudative pleurisy. Catarrhal endobronchitis was the leading form of tracheo-broncheal tree lesion among patients with tuberculous exudative pleurisy (n = 20 (64.5%)). The activity of adenosine deaminase (ADA) was 2.18 +/- 0.73, 2.41 +/- 0.80, and 2.47 +/- 1.52 U/l in Groups 1, 2, and 3, respectively. Thus, the measurement of bronchoalveolar fluid ADA separately from other parameters is of no informative value in the differential diagnosis of the etiology of pleurisy. While analyzing the parameters, the authors introduced the coefficient of ADA (CADA) that was calculated using the formula: K(ADA) = ADA/cytosis. In patients with tuberculous pleurisy, K(ADA) was 0.65 +/- 0.17 (this was 0.52 +/-0.13 in isolated tuberculous exudative pleurisy and 0.84 +/- 0.36 in tuberculous exudative pleurisy complicated by pulmonary tuberculosis (p < 0.05), and 0.20 +/- 0.06 in nonspecific pleurisy (p < 0.05). The ADA coefficient of 0.52 or more confirms the tuberculous etiology in isolated pleurisies and permits a differential diagnosis to be made between specific and nonspecific pleurisy with and without lung changes.