[Post-infectious clinical-immunological syndrome and its place in clinical practice].

The progression of chronic-relapsing infectious disease (CRID) depends on a combination of cumulative immune-mediated responses of the human body, which, in turn, are united by a number of the common mechanisms. The mechanisms are called as the post-infectious clinical-immunological syndrome (PICIS) to demonstrate the features and scale of imbalances of immune homeostasis. PICIS usually accompanies most of the known CRID to define the type of the disease, to predict the progression of and risks for the complications to be risen as well. PIFIS is generally provoked by either infectious pathogens of various nature or by the atypical immune responses from the infected patient, or by the onset of the disease itself, or by the inadequate antimicrobial therapy. Three forms of PICIS which depend on two key factors have been described. These included: (i) the spectrum of a microbial colonization landscape; (ii) the antimicrobial immunity itself to generate, for instance, either of three alternative PICIS, namely, (1) postinfectious secondary immunodeficiency syndrome (PISIS); (2) postinfectious autoimmune syndrome (PIAIS), and (3) PISIS combined with PIAIS, i.e. PISIDAS. The dominant monosyndrome-like form of associated immune imbalances in CRID patients is PISIS. PISIS occurs in more than a third of the clinical cases to stress the autoaggression (PIFAS), or combininative form of the immune-mediated imbalances, i.e. PISIDAS. In the process of the development of CRID, PISIS can give a way to either PIAIS or PISIDAS. Besides the immune-mediated imbalances, an essential role in the pathogenesis of CRID and PICIS is also attributed to the infectious factors capable of forming microbial associates in the pathogenesis of PICIS. Therefore, treatment of such patients should be directed not only at the elimination of the infectious pathogen(s), but also at the restoration of the physiological level of the immune homeostasis impaired by PICIS.

[Architectonics of cell subpopulations of peripheral blood in patients with autoimmune myocarditis: clinical and pathogenetic aspects].

AIM: To compare the most significant architectonic parameters of peripheral blood cell subpopulations in patients with different variants of an autoimmune myocarditis (AIM) course and their clinical value in therapeutic practice. MATERIAL AND METHODS: Blood cell subpopulations were studied with flow cytometry in 99 blood samples from patients having different AIM variants and myocardiosclerosis as well as in 40 healthy donors. RESULTS: Severe (malignant) AIM was characterized by growing indices of T-/B lymphocyte activation, expression of activation markers on the cells of both differentiation lines, disproportions in composition of subpopulations of the immunoregulatory cells, parallel rise in specific weight of dendritic cells, reduced intensity of apoptosis of autoreactive T-lymphocytes. In benign AIM marked immunopathology was not found. This group can be considered as a separate variant of AIM course necessitating an individual approach to planning pathogenetically sound therapeutic and rehabilitation measures. CONCLUSION: The study of activation markers expression on peripheral blood cells is superior to the study of endomyocardial biopsies providing a non-invasive method of immunodiagnosis.