Factor VIII concentration is greater in female than male patients with HIV infection

Abdollahi, Alireza; Morteza, Afsaneh; Khalilzadeh, Omid; Ahmadzadeh, Ahmad

doi:10.1007/s12185-010-0736-0

Cited by 4 publications

(4 citation statements)

References 35 publications

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“…Our results were similar to another analysis from the WIHS study which showed decreases in Protein S and increases in factor VIII among women with advancing HIV disease compared to controls 22 , and a study by Abdollahi et al showing greater Factor VIII and decreased Protein S in HIV-infected patients compared to controls in Tehran, Iran 97 . Trotti et al showed significantly higher levels of PAI-1 in a small number of HIV infected patients compared to healthy controls 17 .…”

Section: Discussionsupporting

confidence: 91%

“…HIV has known associations with the markers of hemostasis measured here 17–19,21,23,97,98 . Our results were similar to another analysis from the WIHS study which showed decreases in Protein S and increases in factor VIII among women with advancing HIV disease compared to controls 22 , and a study by Abdollahi et al showing greater Factor VIII and decreased Protein S in HIV-infected patients compared to controls in Tehran, Iran 97 .…”

Section: Discussionmentioning

confidence: 88%

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Association of Hepatitis C With Markers of Hemostasis In HIV-Infected and Uninfected Women in the Women's Interagency HIV Study (WIHS)

Kiefer¹,

Shi²,

Hoover³

et al. 2013

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Coinfection with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) is common. HIV infection and treatment are associated with hypercoaguability; thrombosis in HCV is under-investigated. Proposed markers of hemostasis in HIV include higher D-dimer, Factor VIII% and Plasminogen Activator Inhibitor-1 (PAI-1Ag), and lower total Protein S% (TPS), but have not been examined in HCV. We assessed the independent association of HCV with these four measures of hemostasis in a multicenter, prospective study of HIV: the Women’s Interagency HIV Study (WIHS). We randomly selected 450 HCV-infected (anti-HCV+ with detectable plasma HCV RNA) and 450 HCV-uninfected (anti-HCV−) women. HCV was the main exposure of interest in regression models. 443 HCV+ and 425 HCV− women were included. HCV+ women had higher Factor VIII% (124.4% ±3.9 vs. 101.8% ±3.7, p <0.001) and lower TPS (75.7% ±1.1 vs. 84.3% ±1.1, <0.001) than HCV−, independent of HIV infection and viral load; there was little difference in PAI-1Ag or log10 D-dimer. After adjustment for confounders, these inferences remained. HIV infection was independently associated with higher Factor VIII% and log10 D-dimer, and lower TPS. HCV was independently associated with higher Factor VIII% and lower TPS consistent with hypercoaguability. Higher Factor VIII % and D-dimer and lower total Protein S % were also strongly associated with HIV infection and levels of HIV viremia, independent of HCV infection. Further investigation is needed to determine if there is increased thrombotic risk from HCV. Studies examining hemostasis markers in HIV infection must also assess the contribution of HCV infection.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 88%

Association of Hepatitis C With Markers of Hemostasis In HIV-Infected and Uninfected Women in the Women's Interagency HIV Study (WIHS)

Kiefer¹,

Shi²,

Hoover³

et al. 2013

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…PKA does not appear to inhibit NF-κB-driven transcription by disrupting IkBα degradation or NF-κB DNA binding activity ( Takahashi et al, 2002 ). Rather, NF-κB transcriptional activity may be inhibited either directly, through phosphorylation of the NF-κB subunit, p65, on serine 536 of the C-terminal transactivation domain (p-p65) ( Takahashi et al, 2002 ) and blocking p65 nuclear translocation ( Abdollahi et al, 2011 ), or indirectly, through phosphorylation and competition for the transcriptional coactivator CREB binding protein (CBP), or its homologue, p300 ( Parry and Mackman, 1997 ).…”

Section: Introductionmentioning

confidence: 99%

East Indian Sandalwood Oil Is a Phosphodiesterase Inhibitor: A New Therapeutic Option in the Treatment of Inflammatory Skin Disease

Sharma

Levenson²,

Browning

et al. 2018

Front. Pharmacol.

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Cyclic adenosine monophosphate phosphodiesterases (PDEs) regulate pro-inflammatory cytokine production. One isoform, PDE4, is overactive in chronic relapsing inflammatory skin diseases: psoriasis and eczema/atopic dermatitis, and in several cancers. East Indian sandalwood oil (EISO) has significant anti-inflammatory properties. Here, we report that 75% of pediatric eczema/atopic dermatitis patients treated with topical EISO formulations achieved a >50% reduction in their Eczema Area and Severity Index score. EISO treatment of a psoriasis model reduced PDE4 expression and reversed histopathology. EISO directly inhibited PDE enzymatic activity in vitro . In lipopolysaccharide-stimulated human dermal fibroblast, BEAS-2B, A549, and THP-1 cells, EISO suppressed total cellular PDE activity, PDE4, and 7 transcript levels, nuclear factor kappa B (NF-κB) activation, and pro-inflammatory cytokines/chemokine production. These results suggest that EISO anti-inflammatory activity is mediated through suppressing PDE activity, thus facilitating cAMP-regulated inhibition of NF-κB and indicate EISO as an attractive natural therapeutic for chronic and acute inflammatory disorders.

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“…Fibrinogen levels have been shown to be similar between treated and untreated HIV infected persons and controls [ 13 – 15 ]. Regarding anticoagulant factors, treated and untreated HIV infected persons have been shown to have lower levels of protein S and protein C than uninfected controls [ 10 , 16 ] and untreated HIV infected persons have lower levels than treated [ 17 ]. Further, untreated HIV infected persons show signs of increased fibrinolysis with increased d-dimer [ 15 ] and some studies find persistently elevated levels after cART [ 18 ] whereas others find normalization of D-dimer with cART [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Thromboelastography on plasma reveals delayed clot formation and accelerated clot lyses in HIV-1 infected persons compared with healthy controls

et al. 2015

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BackgroundThromboembolic events among HIV infected persons are a recognized clinical problem but the underlying mechanisms are poorly understood. To assess whether coagulation and fibrinolysis differ between long-term treated HIV infected individuals (HIV+) and healthy controls (CON), we investigated functional plasma coagulation by thrombelastography (TEG) and plasma markers of endothelial and platelet activation.MethodsIn 67 successfully long-term treated HIV+ and 15 CON we analyzed stored plasma samples by TEG, with or without addition of tissue-type plasminogen activator (tPA), and measured levels of C-reactive protein, thrombomodulin, syndecan-1, sVE-cadherin, soluble CD40 ligand (sCD40L), adrenaline and noradrenaline.ResultsCompared to CON, HIV+ had delayed clot formation (reaction (R)-time 14.2 min. vs. 11.2 min., p = 0.0004) and reduced clot formation rapidity (angle 22.6° vs. 48.6 °, p = <0.0001). Clot lyses induced by tPA was accelerated in HIV+ displaying enhanced clot degradation after 30 and 60 min (53.9 % vs. 24.2 %, p < 0.0001 and 77.4 % vs. 59.9 %, p < 0.0001, respectively). sCD40L and TEG R-time correlated negatively in both HIV+ and CON (Rho =−0.502, p < 0.001 and rho =−0.651, p = 0.012).DiscussionNo previous studies have examined plasma coagulation by TEG in HIV, however, we have previously demonstrated that HIV+ display hypocoagulability in whole blood by TEG in accordance with the results of this study. Others have reported of HIV associated changes in the hemostatic system in a pro-coagulant direction based on measurements of isolated components of the coagulation pahways. In disease conditions, the flowing blood may change from “normal” to hyper- or hypocoagulant or to hyper- or hypofibrinolytic. A balance may exist in the flowing blood, i.e. between blood cells and the plasma phase, so that pro-coagulant blood cells are balanced by a hypocoagulable plasma phase; thus alterations that may promote thromboembolic events in the patient may at the same time appear as a hypocoagulable profile when evaluated in vitro.ConclusionPlasma from long-term treated HIV infected persons displays a hypocoagulable profile with reduced fibrinolytic resistance as compared to healthy controls.

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Factor VIII concentration is greater in female than male patients with HIV infection

Cited by 4 publications

References 35 publications

Association of Hepatitis C With Markers of Hemostasis In HIV-Infected and Uninfected Women in the Women's Interagency HIV Study (WIHS)

Association of Hepatitis C With Markers of Hemostasis In HIV-Infected and Uninfected Women in the Women's Interagency HIV Study (WIHS)

East Indian Sandalwood Oil Is a Phosphodiesterase Inhibitor: A New Therapeutic Option in the Treatment of Inflammatory Skin Disease

Thromboelastography on plasma reveals delayed clot formation and accelerated clot lyses in HIV-1 infected persons compared with healthy controls

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