Viral load and disease progression as responsible for endothelial activation and/or injury in human immunodeficiency virus-1-infected patients (original) (raw)
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Changes in Endocan Levels and Blood Coagulation in HIV Infection
Biomedical and Pharmacology Journal, 2017
Alteration in endothelial function may precede the development of morphological changes in disorders and may contribute to morbid development and clinical complications. Therefore, this work attempted to evaluate the levels of endocan (endothelial specific molecule-1) and other coagulation parameters and find their prognostic significance with respect to severity of human immuno-deficiency virus (HIV) infection. Sixty HIV infected patients on drugs and antiretroviral (ART) naïve were enrolled in a prospective, cross-sectional study while thirty HIV non reactive, apparently healthy individuals were recruited as control. Endocan was measured using high sensitive Enzyme linked immunosorbent assay. Plasma levels of prothrombin time and activated partial thromboplastin time were determined to check both intrinsic and extrinsic coagulation pathways. CD4+ count and platelet count were also analyzed by standard methods. HIV positive patients who are already on antiretroviral therapy (ART) had significantly increased endocan levels (471.134+92.84 pg/ml) compared to normal control (208.277+106.60 pg/ml) (p<0.05) while patients that are ART naïve had significantly increased endocan levels when compared to those already on drugs (611.60+608.77pg/ml) (p<0.05). HIV-1 infected subjects not on drugs had significantly increased platelet count (145.1+580 cumm) when compared with normal subjects (90.100+40.00 cumm) (P< .0001) however, group on drugs had marginal decrease compared to normal group (85.000+192cumm). Markers of intrinsic and extrinsic coagulation-APTT and PT were significantly elevated in HIV positive patient when compared with apparently healthy controls. This is significantly associated with severity.
Endothelial Function in HIV-Infected Persons
Clinical Infectious Diseases, 2006
Background-Several reports have suggested an increased risk of coronary disease in HIVinfected patients on protease inhibitors (PI). Impaired endothelium-dependent vasodilation is a putative surrogate marker of coronary atherosclerotic disease.
http://bloodjournal.hematologylibrary.org/content/93/12/4232.full.html Updated information and services can be found at: (2497 articles) Hemostasis, Thrombosis, and Vascular Biology Articles on similar topics can be found in the following Blood collections http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#repub\_requests Information about reproducing this article in parts or in its entirety may be found online at: http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#reprints Information about ordering reprints may be found online at: http://bloodjournal.hematologylibrary.org/site/subscriptions/index.xhtml Information about subscriptions and ASH membership may be found online at: Alterations in the vascular system and the onset of angioproliferative lesions such as Kaposi's sarcoma (KS) are common traits of human immunodeficiency virus-1 (HIV-1)-infected patients. To investigate possible factors involved in acquired immunodeficiency syndrome (AIDS)-associated vasculopathy and vascular malfunction, expression of vascular endothelial cell growth factor-A (VEGF-A) was analyzed in HUT 78 T lymphocytes upon infection with HIV-1.
Endothelial markers and HIV infection in the era of highly active antiretroviral treatment
Thrombosis Research, 2003
Many circumstances can induce activation and/or injury of the endothelium that plays a role in the development of vascular complications. Raised plasma levels of endothelial markers such as von Willebrand factor (vWF), soluble thrombomodulin (sTM) and soluble vascular cell adhesion molecule-1 (sVCAM-1) have a prognostic and/or diagnostic value. Human immunodeficiency virus-infected patients (HIV+) have a clustering of conditions that activate or injure the endothelium. Highly active antiretroviral treatment produces adverse effects such as dyslipemia, insulin resistance (IR) and body fat changes (named lipodystrophy syndrome) which may contribute to aggravate their endothelial perturbation.
Effects of HIV Infection on Arterial Endothelial Function
Arteriosclerosis, Thrombosis, and Vascular Biology, 2020
Objective: To determine the effects of HIV serostatus and disease severity on endothelial function in a large pooled cohort study of people living with HIV infection and HIV− controls. Approach and Results: We used participant-level data from 9 studies: 7 included people living with HIV (2 treatment-naïve) and 4 had HIV− controls. Brachial artery flow-mediated dilation (FMD) was measured using a standardized ultrasound imaging protocol with central reading. After data harmonization, multiple linear regression was used to examine the effects of HIV− serostatus, HIV disease severity measures, and cardiovascular disease risk factors on FMD. Of 2533 participants, 986 were people living with HIV (mean 44.4 [SD 11.8] years old) and 1547 were HIV− controls (42.9 [12.2] years old). The strongest and most consistent associates of FMD were brachial artery diameter, age, sex, and body mass index. The effect of HIV+ serostatus on FMD was strongly influenced by kidney function. In the highest te...
Journal of AIDS & clinical research, 2013
The prevalence of cardiovascular disease is increased with human immunodeficiency virus (HIV) infection, but the mechanism is unclear. We hypothesized that HIV increases microvascular reactive oxygen species, thereby impairing endothelial function and enhancing contractility. Subcutaneous microarterioles were isolated from gluteal skin biopsies in premenopausal, African American, HIV positive women receiving effective anti-retroviral therapy, but without cardiovascular risk factors except for increased body mass index (n=10) and healthy matched controls (n=10). The arterioles were mounted on myographs, preconstricted and relaxed with acetylcholine for: endothelium-dependent relaxation, endothelium-dependent relaxation factor (nitric oxide synthase-dependent relaxation), endothelium-dependent hyperpolarizing factor (potassium-channel dependent relaxation) and endothelium-independent relaxation (nitroprusside). Contractions were tested to endothelium-dependent contracting factor (acet...
Journal of the American College of Cardiology, 2008
Objectives-This study evaluated the effects of three class-sparing antiretroviral therapy (ART) regimens on endothelial function in HIV-infected subjects participating in a randomized trial. Background-Endothelial dysfunction has been observed in patients receiving ART for human immunodeficiency virus (HIV) infection. Methods-This was a prospective, multicenter study of treatment-naïve subjects who were randomly assigned to receive a protease inhibitor-sparing regimen of nucleoside reverse transcriptase inhibitors (NRTIs) + efavirenz, a non-nucleoside reverse transcriptase inhibitor-sparing regimen of NRTIs + lopinavir/ritonavir, or a NRTI-sparing regimen of efavirenz + lopinavir/ritonavir. NRTIs were lamivudine + stavudine, zidovudine, or tenofovir. Brachial artery flow-mediated dilation (FMD) was determined by B-mode ultrasound before starting on ART, then after 4 and 24 weeks. Results-There were 82 subjects (median age 35 years, 91% men, 54% white). Baseline CD4 cell counts and plasma HIV RNA values were 245 cells/mm 3 and 4.8 log 10 copies/ml, respectively. At baseline, FMD was 3.68% (interquartile range 1.98-5.51%). After 4 and 24 weeks of ART, plasma HIV RNA decreased by 2.1 and 3.0 log 10 copies/mL, respectively. FMD increased by 0.74% (−0.62-+2.74, p=0.003) and 1.48% (−0.20-+4.30%, p< 0.001), respectively, with similar changes in each arm (p KW >0.600). The decrease in plasma HIV RNA at 24 weeks was associated with greater FMD (r s =− 0.30, p=0.017). Conclusions-Among treatment-naïve individuals with HIV, three different ART regimens rapidly improved endothelial function. Benefits were similar for all ART regimens, appeared quickly, and persisted at 24 weeks.