Discrepant coagulation profile in HIV infection

Haugaard, Anna Karen; Lund, Thomas Kromann; Birch, Carsten; Rönsholt, Frederikke Falkencrone; Trøseid, Marius; Ullum, Henrik; Gerstoft, Jan; Johansson, Pär I.; Nielsen, Susanne Dam; Ostrowski, Sisse Rye

doi:10.1097/01.aids.0000432462.21723.ed

Cited by 33 publications

(18 citation statements)

References 50 publications

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“…The cohort has previously been described in detail [31]. One individual in the treatment group had detectable viral replication and was excluded from further analyses.…”

Section: Methodsmentioning

confidence: 99%

“…One individual in the treatment group had detectable viral replication and was excluded from further analyses. Clinical characteristics of the study population have previously been described [31]. Briefly, mean age was 40 and 42 years, 90 and 88% were men, 90 and 86% were Caucasian, 42 and 41% were current smokers, and mean current CD4 + T-cell count was 600 and 674 in the HIV-infected untreated and treated individuals, respectively [31].…”

Section: Methodsmentioning

confidence: 99%

“…Briefly, mean age was 40 and 42 years, 90 and 88% were men, 90 and 86% were Caucasian, 42 and 41% were current smokers, and mean current CD4 + T-cell count was 600 and 674 in the HIV-infected untreated and treated individuals, respectively [31]. Baseline characteristics are summarized in Table 1.…”

Section: Methodsmentioning

confidence: 99%

“…Summary of clinical and demographic characteristics of the study population previously published in [31]. from Continuous data are presented as medians and (interquartile ranges) and categorical data as percentages and (total numbers).…”

Section: Methodsmentioning

confidence: 99%

“…Platelet function was determined at inclusion by whole-blood multiple electrode impedance aggregometry, assessing platelet aggregation in a time-dependent manner as area under curve after 6 min after stimulation with adenosine diphosphate (ADP, concentration 6.5 mmol/l, arachidonic acid (ASPI, concentration 0.5 mmol/l), collagen (COL, 3.2 mg/ml), and thrombin receptor agonist peptide (TRAP, concentration 32 mmol/l) on a Multiplate analyzer (Dynabyte GmBH, Munich, Germany), as previously described [31]. …”

Section: Methodsmentioning

confidence: 99%

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Microbiota-dependent metabolite and cardiovascular disease marker trimethylamine-N-oxide (TMAO) is associated with monocyte activation but not platelet function in untreated HIV infection

et al. 2017

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BackgroundHIV infection is associated with increased risk of cardiovascular disease beyond that explained by traditional risk factors. Altered gut microbiota, microbial translocation, and immune activation have been proposed as potential triggers. The microbiota-dependent metabolite trimethylamine-N-oxide (TMAO) predicts myocardial infarction (MI) in the general population and has recently been shown to induce platelet hyperreactivity. In the present study, we investigated if TMAO was associated with platelet function, microbial translocation, and immune activation in both untreated and combination anti-retroviral therapy (cART) HIV infection.MethodsTMAO and the pre-cursors betaine, choline, and carnitine were quantified by mass-spectrometry in plasma samples from a previously established cross-sectional cohort of 50 untreated and 50 cART treated HIV-infected individuals. Whole-blood impedance aggregometry, C-reactive protein, sCD14, and lipopolysaccharide were assessed as measures of platelet function, inflammation, monocyte activation, and microbial translocation, respectively.ResultsTMAO was not associated with platelet aggregation response after stimulation with four different agonists, or with overall hypo- or hyperreactivity in untreated or treated HIV-infected individuals. In contrast, sCD14 a marker of both monocyte activation and microbial translocation was independently associated with TMAO in untreated HIV-infection (R = 0.381, P = 0.008). Lower levels of carnitine [32.2 (28.4–36.8) vs. 38.2 (33.6–42.0), P = 0.001] and betaine [33.1 (27.3–43.4) vs.37.4 (31.5–48.7, P = 0.02], but similar TMAO levels [3.8 (2.3–6.1), vs. 2.9 μM (1.9–4.8) P = 0.15] were found in cART treated compared to untreated HIV-infected individuals, resulting in higher ratios of TMAO/carnitine [0.12 (0.07–0.20) vs. 0.08 (0.05–0.11), P = 0.02] and TMAO/betaine [0.11 (0.07–0.17) vs. 0.08 (0.05–0.13), P 0.02].ConclusionsIn contrast to recent studies in HIV-uninfected populations, the present study found no evidence of TMAO-induced platelet hyperreactivity in HIV infected individuals. Microbial translocation and monocyte activation may affect TMAO levels in untreated individuals. Furthermore, the elevated ratios of TMAO/betaine and TMAO/carnitine in cART-treated individuals could possibly suggest a role of cART in TMAO metabolism.

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“…The cohort has previously been described in detail [31]. One individual in the treatment group had detectable viral replication and was excluded from further analyses.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Microbiota-dependent metabolite and cardiovascular disease marker trimethylamine-N-oxide (TMAO) is associated with monocyte activation but not platelet function in untreated HIV infection

et al. 2017

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Platelet function and microvesicle generation in patients with hemophilia A

Melero-Amor

Romecín

Iyú

et al. 2021

Clinical Case Reports

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Chronic HIV disease and activation of the coagulation system

Baker

2013

Thrombosis Research

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With current effective antiretroviral treatment, the spectrum of morbidity and mortality during chronic HIV disease has shifted away from AIDS defining clinical events. Persistent abnormalities in coagulation appear to contribute to excess risk for a broad spectrum of non-AIDS defining complications, including, but not limited to, venous and arterial thrombotic disease. Mechanisms specific to HIV disease, antiretroviral therapy, and lifestyle or behavioral factors contribute to a pro-coagulant state, in part, through increased tissue factor activity coupled with a paradoxical decline in the anti-coagulant response. Alterations in coagulation biology in the context of HIV disease appear to be largely a consequence of persistent systemic immune activation, micro- and macro-vascular disease, and, potentially, impaired hepatic synthesis of coagulation factors. The clinical consequences of HIV-related changes in coagulation biology, the degree to which they are unique to HIV disease, and whether they can be mitigated through adjunct treatments, remains a focus of current research.

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Discrepant coagulation profile in HIV infection

Cited by 33 publications

References 50 publications

Microbiota-dependent metabolite and cardiovascular disease marker trimethylamine-N-oxide (TMAO) is associated with monocyte activation but not platelet function in untreated HIV infection

Microbiota-dependent metabolite and cardiovascular disease marker trimethylamine-N-oxide (TMAO) is associated with monocyte activation but not platelet function in untreated HIV infection

Platelet function and microvesicle generation in patients with hemophilia A

Chronic HIV disease and activation of the coagulation system

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