[A case report of central pontine and extrapontine myelinolysis in the combination with spinal cord damage in a patient with tuberculosis in the lung]. / Sluchai tsentral'nogo pontinnogo i ekstrapontinnogo mielinoliza v sochetanii s porazheniem spinnogo mozga u bol'nogo tuberkulezom legkikh.

A case report of central pontine and extrapontine myelinolysis in the combination with spinal cord damage is presented. The authors analyze literature data on this problem and discuss the pathogenesis and diagnostic issues of myelinolysis.

[The main principles underlying the pathologo-anatomical diagnostics and coding of the causes of death from tuberculosis].

The objective of the present study was to universalize the approaches to pathologoanatomical diagnostics and coding of the causes of death from tuberculosis and other diseases. We undertook the analysis of 409 medical death certificates of the subjects who died from tuberculosis in Moscow during 2013. It revealed the main errors of pathologoanatomical diagnostics and formulation of the respective medical documentation. The recommendations are proposed for pathologoanatomical diagnostics of tuberculosis, completion of medical death certificates, and formulation of the conclusions of the causes of death. It was shown that tuberculosis should be regarded either as the main independent disease or one of the components of the combined pathology in the structure of pathologoanatomical diagnosis. The diagnosis must reflect the form of the disease, its localization, the extension of the pathological process, phases of the clinical course, and the results of bacteriological studies. Only one form of tuberculosis should be indicated with the emphasis on its chronic or destructive character. The fatal complications of a single form of tuberculosis may differ. The categorization of a "minor" form as the "major" disease is the serious error even if it is confirmed by the results of the bacteriological study. Such nosological forms as acute coronary heart disease, urgent surgical pathology, etc. in the combined "major" disease must be indicated in the first place, even in the presence of progressive tuberculosis. It is concluded that the pathologoanatomical diagnosis structure must include the comparison of the clinical and morphological data, correct assessment of the activity and the extension of the tuberculosis process, its role in tanatogenesis, and the significance of tuberculosis compared with the concomitant diseases.

[Pulmonary histological and ultrastructural changes in HIV infection concurrent with tuberculosis].

OBJECTIVE: To analyze cellular and subcellular disorders in the lung in the presence of HIV-associated tuberculosis. MATERIAL AND METHODS: The investigators made a comprehensive morphological examination of 25 autopsy specimens from patients who had died from HIV-associated tuberculosis. Lung pieces from the foci of caseous necrosis at its boundary and adjacent lung segments and from macroscopically intact perifocal pulmonary segments were microscopically explored. Plain stains and Ziehl-Neelsen histobacterioscopy were used for light microscopy. An immunohistochemical study was conducted using tuberculosis mouse monoclonal antibodies (clone 1.1/3/1, Vector). Seven early autopsy specimens (1-2 hours after statement of biological death) were investigated ultrastructurally. Ultrathin sections were contrasted with Reynolds' lead citrate and looked through a Libra-120 transmission electron microscope (Germany). Semithin sections were stained with toluidine blue. RESULTS: HIV-associated tuberculosis is a disease accompanied by dual aggressive infection. Impaired blood-air barrier integrity gives rise to structural and ultrastructural changes primarily in type I alveolocytes that are responsible for physiological gas exchange and detoxification. Type I alveolocytes have been noted to be in close contact with plasmocytes that are most ultrastructurally preserved and at the same time display the phagocytic and detoxifying functions being redistributed, which is necessary to keep cells viable and which is a characteristic sign of this comorbidity. This redistribution is due to severe damage to macrophages that are unable to ensure complete mycobacterial phagocytosis; thereby the plasma cells partly assume this function, as supported by ultrastructural examination. Severe destruction of granulocyte organelles and partial and complete cell necrosis with its preceding apoptotic changes were established. A study of vessels in the microcirculatory bed has indicated that the ultrastructural changes in the endothelial cells are polymorphic, which is characteristic of an exudative-inflammatory response of lung tissue. CONCLUSION: Cellular and subcellular changes, the pattern of intercellular relationships, and necrotic and apoptotic cell rearrangements, which are in one way or another involved in the pathophysiological processes maintaining definite hemostasis, are an important component in the pathogenesis of HIV-associated tuberculosis.