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Impact of short-term antiretroviral therapy (START) on some fibrinolytic markers in HIV-infected Nigerian adults: preliminary findings from the START study

Authors Jeremiah Z, Obazee, Okogun GR, Adias TC, Mgbere, Essien EJ

Received 9 December 2011

Accepted for publication 6 January 2012

Published 10 July 2012 Volume 2012:4 Pages 87—94

DOI https://doi.org/10.2147/HIV.S29027

Review by Single-blind

Peer reviewer comments 2


Zaccheaus A Jeremiah1, Yetunde Obazee2, Godwin R Okogun3, Teddy C Adias4, Osaro Mgbere5,6, Ekere J Essien6

1Hematology and Blood Transfusion Science Unit, Department of Medical Laboratory Sciences, College of Health Sciences, Niger Delta University, Wilberforce Island, Bayelsa State, 2General Hospital, Maitama District, Abuja, Federal Capital Territory, 3Department of Medical Laboratory Science, Ambrose Ali University, Ekpoma, Edo State, Nigeria; 4College of Health Technology, Bayelsa State, Nigeria; 5Houston Department of Health and Human Services, 6Institute of Community Health, University of Houston, Texas Medical Center, Houston, TX, USA

Background: Derangement in fibrinolytic markers can result in thrombosis and cardiovascular problems. Antiretroviral therapy (ART) has been reported to affect the levels of these markers. It is unclear how long a patient can be exposed to ART before the effect of the drugs on the fibrinolytic markers becomes noticeable; this short-term antiretroviral therapy (START) study aimed to answer this question.
Methods: Twenty human immunodeficiency virus (HIV)-positive subjects on ART and 20 controls (non-ART) were progressively monitored for three months. CD4 T-cell count was determined while D-dimer, t-PA, and PAI-1 parameters were determined.
Results: CD4 T-cell count increased from 192 µL/mL at baseline to 323 µL/mL at month 3 among patients on ART. D-dimer concentrations decreased from 301.0 µL/mL at baseline to 172.0 µL/mL at month 2, then increased to 226.0 µL/mL at the end of the third month. The median baseline concentration of PAI-1 at the beginning of therapy was 14.0 µg/mL, which increased progressively to 18.2 µg/mL at the end of the third month. The baseline concentration of t-PA at the beginning of therapy was 5.15 µg/mL. This progressively declined to 1.10 µg/mL at the end of the first month and reached 1.45 µg/mL and 1.5 µg/mL at the end of the second and third months, respectively. D-dimer was positively and significantly correlated with CD4 cell counts in both AIDs-associated retrovirus (ARV) and non-ARV patients (r = –0.304, P < 0.01 vs r = –0.477, P < 0.001). t-PA was negatively correlated with CD4 T-lymphocytes in those undergoing ART (r = –0.294, P < 0.01).
Conclusion: A progressive increase in PAI-1 and steady decline in t-PA concentrations within 3 months of commencement of ART could predispose patients to thrombotic disorders earlier than is expected. Pre-thrombotic assessment during therapy is therefore advocated.

Keywords: fibrinolytic markers, D-dimer, t-PA, PAI-1, START study

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