Top 10 HIV Clinical Developments of 2008 - CD8 T cells - The Body
Top 10 HIV Clinical Developments of 2008 - CD8 T cells - The Body
Top 10 HIV Clinical Developments of 2008 - CD8 T cells - The Body
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16 • <strong>HIV</strong> JournalView—<strong>Top</strong> <strong>10</strong> <strong>HIV</strong> <strong>Clinical</strong> <strong>Developments</strong> <strong>of</strong> <strong>2008</strong><br />
Study Snapshot: Inflammatory and Coagulation Biomarkers and Mortality in<br />
INSIGHT SMART Study Groups<br />
Design: A pair <strong>of</strong> investigations were conducted: (1) a nested case-control study <strong>of</strong> <strong>HIV</strong>-infected INSIGHT SMART participants<br />
for studying biomarker associations with mortality, and (2) a study to compare drug conservation versus viral suppression<br />
participants for biomarker changes.<br />
Population: (1) 85 participants who died (55 were in the discontinuation <strong>of</strong> <strong>HIV</strong> therapy arm, the remainder in the continuation<br />
arm) compared to two controls who did not die per each case. (2) About 250 participants without known prior CVD.<br />
Main Results: <strong>The</strong> combined results show that, at baseline, the levels <strong>of</strong> almost all markers were higher in patients who died<br />
(cases) than in the controls. IL-6 and D-dimer stood out as most significantly different between patients who died and those<br />
who did not. Based on models <strong>of</strong> mortality risk generated from the baseline biomarker data, the differences in the change in<br />
levels in the study arms are predicted to lead to a 16% to 24% increased risk <strong>of</strong> death for those stopping antiretroviral therapy.<br />
Significance: Both investigations pin an attractively reasonable causative mechanism to the potentially catastrophic effects <strong>of</strong><br />
treatment cessation. Point to a new way to view the threats to the well-being <strong>of</strong> patients who, despite robust immune function,<br />
have suboptimally controlled <strong>HIV</strong> infection. Irrevocably establish endothelial dysfunction as a dimension <strong>of</strong> the management <strong>of</strong><br />
<strong>HIV</strong> disease.