Problemy tuberkuleza
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Problemy tuberkuleza · Jan 1997
Review[Intravascular activation of hemostatic system and DIC syndrome in pulmonary tuberculosis].
The paper summarizes his own findings and literature data on the status of the hemostatic system in patients with pulmonary tuberculosis. It discusses various terms used to designate intravascular coagulation and variants of this process in patients with tuberculosis.
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Problemy tuberkuleza · Jan 1997
[Changes and patterns of drug resistance of mycobacterium tuberculosis in patients with pulmonary tuberculosis (by data of the microbiological laboratory of research production association "Phthysiology")].
Changes in and patterns of drug resistance of Mycobacterium tuberculosis were analyzed in Yakutia. It was shown that in the past 5 years, there had been no rise in the total resistance; however, its patterns changed: a proportion of polyresistant strains had increased with decreases in monoresistant strains. The rate of Mycobacterium tuberculosis resistance to most antituberculous drugs was found to be growing. The pattern of resistance is varying in different areas of Yakutia.
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Open parietal pleural biopsy was made in 223 patients with pleurisy. The biopsy specimens were histologically and microbiologically studied (Mycobacterium tuberculosis (MT) being found). The etiology of pleurisy was established to be tuberculous in 118 patients, nonspecific in 96, cancerous in 9. The detection rate of MT in the biopsy specimens with histological evidence for tuberculosis was no more than 53.8%.
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Problemy tuberkuleza · Jan 1997
[Intravascular coagulation as a typical concomitant of acute pulmonary tuberculosis].
Hemostasis and fibrinolysis, markers of intravascular coagulation (IC), hemorrhagic parameters, and platelet aggregatory properties were studied in 119 patients with various types of pulmonary tuberculosis. In patients with active pulmonary tuberculosis, IC was found to be a persistent and important component of a pathological process which both plasma factors and circulating cells were involved in. In most critical patients, the degree and rate of spontaneous and stimulated platelet aggregation were decreased, when stimulated, the rate of increases in the mean volume of aggregates was yet higher in these patients than in the controls. The latter created an additional prerequisite for progression of microthrombogenesis.