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Changes in inflammatory/cardiac markers of HIV positive patients

Authors :
Tatiana Montagner Dalcin Bertoldo
Stephen A. Adefegha
João Felipe Peres Rezer
Daniela F. Passos
Renata da Silva Pereira Saccol
Daniela B.R. Leal
Assis Ecker
Source :
Microbial Pathogenesis. 114:264-268
Publication Year :
2018
Publisher :
Elsevier BV, 2018.

Abstract

HIV replication promotes atherogenesis and participates in the immune response to the virus, thereby influencing the inflammatory profile. These changes may, in turn, contribute to the risk of cardiovascular diseases with involvement of platelets. However, adenine nucleotides and nucleosides involved in thromboregulation and modulation of immune response may therefore be affected by these alterations. Objectives This study sought to evaluate the profile of pro and anti-inflammatory cytokines (IL-10, IL-6, IL-17, TNF, IL-4, IL-2 and IFN-gamma), cardiac markers (troponin, CK, CK MB, LDH, CRP) in HIV-positive patients and assess the in vitro effect of antiretroviral therapy on the activities of ectonucleotidases (E-NTPDase and E-5′-nucleotidase) in human platelets. Design and Methods Blood samples were obtained from ten HIV positive patients at the Infectious Disease Clinic of the University Hospital of Santa Maria, Brazil and ten HIV negative individuals (control group) for this study. Results The results revealed that there were significant (P 0.05) changes in the serum levels of the cardiac markers investigated (CK, CK-MB, troponin, LDH and CRP). In addition, the ectonucleotidases (E-NTPDase and E-5′-nucleotidase) activities were not altered (P > 0.05) in human platelets when incubated with different antiretroviral drugs in vitro. Conclusions The results of this study suggest that, despite successful treatment, a proinflammatory state is not altered in HIV patients, and that antiretroviral therapy per se does not change the purinergic profile.

Details

ISSN :
08824010
Volume :
114
Database :
OpenAIRE
Journal :
Microbial Pathogenesis
Accession number :
edsair.doi.dedup.....4ffdf6da140e170463606796e6c492c3
Full Text :
https://doi.org/10.1016/j.micpath.2017.11.045