Liver pathologies and infection with Toxoplasma gondii (Nicolle et Manceaux, 1908) are widespread among HIV-infected patients. However, a possible contribution of toxoplasmosis to the development of various forms of liver diseases in HIV-infected individuals has not yet been determined. This research is a retrospective cohort study. Medical cards of 907 HIV-positive patients, including 119 individuals who died, were studied. The patients were divided into two groups: 531 patients were seropositive to T. gondii and 376 seronegative. General liver pathology was more widespread among patients seropositive to T. gondii than in seronegative patients (63.1 ± 2.1% and 51.9 ± 2.6%, respectively, p < 0.001). The association of seropositive to T. gondii with general liver pathology is weak both in the whole cohort (Pearson's contingency coefficient C = 0.112), and among the deceased patients (C = 0.228). Chronic HBV-HCV coinfection was more common in the seropositive than in seronegative individuals as it was found both in entire cohorts (26.0 ± 1.9% and 18.6 ± 2.0%, respectively, p = 0.010) and in died patients (31.0 ± 5.5% and 14.6 ± 5.1%, respectively, p = 0.041). Toxoplasma gondii had a weak role in distributing of HBV-HCV coinfection between cohorts (C = 0.187). In both cohorts in patients with chronic hepatitis, regardless of its etiology, there was no significant difference in alanine transaminase activity (ALT). Cirrhosis of the liver occurred 4.5 times more often in deceased seropositive patients than in the entire seropositive cohort (23.9 ± 5.1 and 5.3 ± 2.0, respectively, p = 0.0006) whereas it no significantly increased in seronegative cohort (10.4 ± 4.4 against 4.8 ± 1.1, p > 0.05). In them T. gondii is weakly involved in cirrhosis formation (C = 0.168). Thus, in HIV-infected patients, T. gondii is a weak nonspecific adjunct that supports chronic liver inflammation and progression of cirrhosis, regardless of etiology, but does not influence the degree of hepatitis activity. The increased prevalence of HBV-HCV coinfection in patients seropositive for T. gondii may be related to their risk factor behaviour associated with uncontrolled blood contacts.

Pulmonary pathology is common in HIV-infected individuals, but the possible role of the parasitic protist Toxoplasma gondii (Nicolle et Manceaux, 1908) is not completely known. The present account reports result of a retrospective cohort study. Medical cards of 907 HIV-positive people, which included 120 deceased patients, were analysed. During a three-year follow-up, the pulmonary pathology was diagnosed in 306 patients (33.7 ± 1.6%): pneumocystis pneumonia in 124 (13.7 ± 1.1%), primary pulmonary tuberculosis in 113 (12.5 ± 1.1%), bacterial pneumonia in 58 (6.4 ± 0.8%) toxoplasmosis pneumonia in two (0.2 ± 0.2%), and others. All patients were divided into two cohorts: 531 individuals seropositive for T. gondii and 376 seronegative ones. It has been found out that general lung pathology is more common in patients with seropositivity to T. gondii than in seronegative ones (43.3 ± 2.2% vs. 20.1 ± 2.0%, p < 0.001). The diagnosis of pneumocystis pneumonia was made ten times more often in the cohort of seropositive patients than in the cohort of seronegative ones (21.9 ± 1.8% vs. 2.1 ± 0.7%, respectively, p < 0.001) and in deceased patients of these cohorts it was 5.5 times more (45.1 ± 5.9% vs. 8.2 ± 3.9, respectively, p < 0.001). In patients with fatal outcome and seropositivity to T. gondii, the incidences of pneumocystis pneumonia increased by 23.2% (p < 0.001) and bacterial pneumonia by 12.4% (p < 0.05), whereas in seronegative individuals only pulmonary tuberculosis increased by 13.1% (p < 0.05) сompared with corresponding whole cohorts. Pearson's contingency coefficient showed the mean strength association between infection with T. gondii and incidence of pneumocystis pneumonia both in whole cohort (C = 0.272) and in patients with fatal outcomes (C = 0.368). In сonclusion, significantly increasing rate of pneumocystis pneumonia in patients with HIV/AIDS and T. gondii infection can be caused by certain synergism between T. gondii and Pneumocystis jirovecii and in some cases overdiagnosis pneumocystis pneumonia due to undiagnosed toxoplasmosis pneumonia.

The aim: To determine changes of FSG of neutrophilic granulocytes of peripheral blood (NGPB) of patients with CHC with concomitant DM-2. Materials and methods: We’ve examined 180 patients with CHC: 160 with concomitant diabetes mellitus and 20 ones without it. The NGPB genome was studied using cytogenetic method. There were analyzed 100 interphase NGPB nuclei in the preparation, structural characteristics were evaluated according to indices: chromatization (IC), nucleolar (IN), pathologically altered nuclei (PAN), micronuclei (MNI). Results: Violations of FSG OF NGPBwere found according to all indices in patients with CHC, they were more pronounced in patients with concomitant DM-2. Conclusions: FSG NGPB is more disordered in CHC with concomitant DM-2. The reduction of IC in CHC with concomitant DM-2 is more pronounced in men. Reduction of IN in patients with CHC with and without DM-2 is a marker of violations of the second stage of realization of hereditary information. The tendency to change the components of the cytogenetic status of all examined patients due to the frequency of MNI was determined.

No abstract

Встановлено, що у ВІЛ-інфікованих осіб із токсоплазмовою інвазією були підвищеними рівні цитокінів: TNF-α, . Після застосування препарату рибонуклеїнової кислоти впродовж 1 місяця спостерігалося зростання рівнів ІЛ-2 та INF-γ, натомість, знижувався TNF-α. Після 3-го місяця лікування знизилися рівні ІЛ-10 та TNF-α, зросла кількість CD4+Т-лімфоцитів та усувався ризик токсоплазмозного енцефаліту Ключові слова: ВІЛ-інфекція, токсоплазмозна інвазія, токсоплазмоз мозку, імунореабілітація, антиретровірусна терапія, препарат рибонуклеїнової кислоти Дикий Богдан Миколайович, доктор медичних наук, професор, кафедра інфекційних хвороб та епідеміології, ДВНЗ «Івано-Франківський національний медичний університет», вул. Галицька,