[Post-infection clinico-immunologic syndrome: fundamentals of etiopathogenesis and immunogenodiagnostic strategy].

Professor Yu.M. Lopukhin, an ardent advocate of translation of scientific achievements into clinical medicine, is a founder of new scientific disciplines including clinical immunology that evolved from the fusion of new knowledge, original clinical thought, high-tech diagnostic and therapeutic modalities. Highly promising investigations into molecular pathogenetic mechanisms of various diseases, their diagnosis, and prevention make up a most important aspect of his scientific work. The progress of chronic recurring infectious diseases (CRID) is closely related to the associated immune disorders, e.g. post-infection clinico-immunologic syndrome (PIKIS) that reflects the character and severity of disturbances of immune homeostasis. This syndrome associated with CRID is as a rule provoked by infectious agents of different nature, immunopathologic processes inherent in individual patients, specific clinical course ofCRID or inadequate application of antimicrobial medicines. Three forms of PIKIS are described in this paper: (1) post-infection secondary immunodeficiency syndrome:, (2) post-infection autoimmune syndrome, (3) combination of the two.

[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.