Cerebral toxoplasmosis is a leading cause of the central nervous system disorders in acquired immune deficiency syndrome. This study aimed to investigate the clinical course of cerebral toxoplasmosis in human immunodeficiency virus (HIV)-infected individuals. The study included 90 HIV-infected patients with cerebral toxoplasmosis, who underwent inpatient treatment. In case of positive enzyme immunoassay, HIV infection was confirmed with the immunoblot test. The HIV-1 ribonucleic acid level was determined using the polymerase chain reaction method. The flow cytometry was used for counting CD4 (cluster of differentiation 4 cells). Pathomorphological examination included the autopsy, gross and microscopic examination of internal organs, histological and other methods. The incidence of cerebral toxoplasmosis significantly increases at the CD4 count below 100 cells/μl, P < 0.001, and at the HIV viral load above 50 copies/ml, P < 0.05. The clinical picture of cerebral toxoplasmosis included focal symptoms, cognitive impairment, toxic syndrome, mild cerebral symptoms and a meningeal symptom. Given the absence of a specific clinical picture and the absence of abnormal laboratory and instrumental findings, the cerebral toxoplasmosis needs to be diagnosed with a number diagnostic methods combined: clinical examination, laboratory testing, immunological examination, molecular genetic testing and neuroradiological imaging.

A feature of the HIV epidemic is currently a large number of comorbid and severe forms of the disease, with frequent involvement in the pathological process of the brain. Methods of in vivo verification of brain damage in clinical practice is sufficient, but in some cases they are limited by financial availability and time factor. Correct and timely deciphering of the nature of brain damage is necessary for the choice of treatment tactics, and as a consequence, reducing mortality. Objective: to study the epidemiology, clinic and pathomorphology of brain damage in HIV infection in conditions of urgent and planned admission of patients to a specialized hospital. Materials and methods. Clinical and pathomorphological studies of HIV-infected patients (n=85) receiving specialized medical care were carried out. The final diagnosis was made taking into account clinical, laboratory and morphological data on the classification of ICD-10 in accordance with the domestic requirements of the formulation of comorbid diagnosis. Conclusion. Brain lesions are clinically and morphologically detected in most HIV-infected patients. Opportunistic and secondary diseases with brain damage have their clinical picture, but it is not specific. From the timely decoding of the nature of brain damage depends on the choice of treatment tactics and, as a consequence, reducing the risk of death. Therefore for verification of the etiological agent, you need to conduct a comprehensive examination: clinical (neurological, psychological distress) and laboratory (cellular composition of CSF protein level and glucose) and bacteriological (seeding of CSF on the flora, on Wednesday Saburo to identify mushrooms on medium Bactec and Lowenstein-Jensen medium for detection of M.tuberculesis); immunological (number of CD4-lymphocytes, at.gondii IgM, at.gondii IgG antibodies), molecular genetic (HIV RNA; DNA HSV1, 2; VZV DNA; DNA EBV; CMV DNA; DNA ВГЧ6; T.gondii DNA; DNA of M.tuberculesis; DNA Cr.neoformans; JC virus DNA) and radiological (MRI brain) research methods. The structure of brain damage in deceased patients was dominated by toxoplasmosis in 28,8% of cases; neuroinfection of unspecified etiology in 28,8% and herpesvirus lesion in 11,9%. Rarely met: tuberculosis 8,47%; candidiasis 8,47%; PML 3,39%; cryptococcosis 3,39%; b-cell lymphoma with brain metastases 3,39%.

A feature of the HIV epidemic is currently a large number of comorbid and severe forms of the disease, with frequent involvement in the pathological process of the brain. Brain lesions can be primary, caused by the human immunodeficiency virus itself and secondary, due to the development of opportunistic and secondary diseases and tumors. Correct and timely deciphering of the nature of brain damage is necessary for the choice of treatment tactics and as a consequence of reducing mortality. Objective. To study the radiological manifestations of brain damage in HIV infection in urgent and planned admission of patients to specialized hospitals. Materials and methods of research. In the work, studies were conducted to study the clinical and radiological manifestations of brain damage in HIV-infected patients admitted to various medical institutions with a diagnosis of HIV infection. Radiation examination of the brain was performed in adult HIV-infected patients (n = 410) using magnetic resonance imaging with intravenous contrast. The final diagnosis was made taking into account clinical, laboratory, radiological studies on the classification of ICD-10 in accordance with the domestic requirements of the formulation of comorbid diagnosis. Conclusion. To correctly decipher the nature of brain damage, it is necessary to use comprehensive studies including clinical, laboratory and radiation examination methods. Magnetic resonance imaging with intravenous contrast is the method of choice in the examination of the brain in HIV-infected patients. The structure of brain damage in HIV-infected patients had a different nature: in 54.4% there were signs of the presence of opportunistic and secondary diseases; in 24.9% signs of HIV encephalopathy; in 13.2% signs of nonspecific changes in small vessels of the brain, indicating premature aging or abnormal development; in 7.56% signs of involvement of the brain in the pathological process were not detected. Structure and opportunistic secondary diseases were presented: toxoplasmosis of the brain 18.3%; herpes lesions 12.2%; chief of 10.24%; neuroinfection unspecified etiology is 12.2%; cryptococcosis 4.39%; TB is 2.44%; lymphoma of the brain is 2.44%; MAC infection is 0.24%. Brain damage in HIV-infected patients is largely characterized by synchronicity (mixed infection in 8.52 %) and multifactorial lesions.

The possibilities to diagnose the non-classical form of 21-hydroxylase deficiency using the low-dose (5 mcg) 1-24 ACTH stimulation test are considered.