Eighty-one patients with acutely progressive pulmonary tuberculosis (APPT) (a study group) and 63 patients with involutive pulmonary tuberculosis (a control group) were examined. The magnitude of a systemic inflammatory response was estimated by the values of acute phase reagents (APR) and the blood protein spectrum; the body's iron provision, the state of the hemostatic and fibrinolytic systems, the functional status of mononuclear leukocytes and neutrophils were determined by the basal level of oxygen-dependent and nitrite oxide metabolism and by the capacity of these systems to respond to specific stimulation. In APPT, along with increased APR levels reflecting the mobilization of various components of endogenous defense, the serum (plasma) was found to show the signs of metabolic decompensation as increased catabolic processes and hepatic protein-synthesizing dysfunction in the presence of intravascular inactivation of functionally significant proteins. Noteworthy is hypochromic anemia caused by the body's redistribution of iron (in the absence of its genuine deficiency) and by the reduced plasma concentration of transferring. The patients with APPT had a significant hypercoagulation syndrome with the signs of latent intravascular blood coagulation. Antimicrobial defensive processes involved mononuclear leukocytes and neutrophils wherein free radical oxidation and nitric oxide generation became intensive. In APPT, the permanent reirritation of these systems led to the exhaustion of functional reserves of cells and their response to specific stimulation diminished. In the neutrophils, rearrangement of their metabolism correlated with other manifestations of a systemic inflammatory response and in the mononuclear leukocytes, this correlated with the size of a bacterial population and with the presence of drug sensitivity/resistance of the causative agent.