Management of anticoagulation in patients with human immunodeficiency virus/acquired immunodeficiency virus

Sabourin, Ashley A; Patel, Twisha S; Saad, Samira; Renner, Elizabeth; Mouland, Erin; Adie, Sarah; Ha, Nghi B.

doi:10.1016/j.thromres.2021.01.020

Cited by 6 publications

(2 citation statements)

References 12 publications

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“…Inhibition of CYP 450 enzyme by PIs or pharmacological promoters may lead to an increase in Direct Oral Anticoagulants (DOACs) concentration and potentially increase the risk of bleeding. The induction of CYP450 enzyme by NNRTIs may reduce the concentration of DOACs, resulting in treatment failure [ 129 ]. Management of these interactions should involve careful selection based on patient characteristics; ART and anticoagulants with a low potential for DDI should be chosen.…”

Section: Antithrombotic Agents In Pwhmentioning

confidence: 99%

Elevated Risk of Venous Thromboembolism in People Living with HIV

Zhang

Peng

et al. 2022

Viruses

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Human immunodeficiency virus (HIV) has been generally considered as a highly adaptive and rapidly evolving virus. It still constitutes a major public health problem all over the world despite an effective outcome in the prevention and reversal of the development and prognosis by using antiretroviral therapy. The salient question lies in the more frequent emergence of a series of comorbidities along with the prolongation of the life, which deeply affects the survival in such group. Venous thromboembolism (VTE) has been recognized to be the third most common cardiovascular condition within people living with HIV (PWH). In terms of its mechanism of action, the occurrence of VTE is quite multifactorial and complex in HIV. Prior exploration concerning the etiology of VTE in PWH identifies general, disease-specific, and miscellaneous factors for explaining its occurrence and development. VTE has constituted an important role in PWH and may increase its all-cause mortality. Therefore, it is quite necessary to understand VTE from the following aspects of epidemiology, pathophysiology, molecular mechanisms, and therapeutic interventions so as to balance the risks and benefits of anticoagulation and optimize corresponding treatment.

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Section: Antithrombotic Agents In Pwhmentioning

confidence: 99%

Elevated Risk of Venous Thromboembolism in People Living with HIV

Zhang

Peng

et al. 2022

Viruses

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“…Initial studies on the approval of warfarin and direct oral anticoagulants did not include patients undergoing ART. Sabourin et al (2021) 13 discussed drug-drug interaction based on pharmacokinetics and the effect of medicines on cytochrome P450 and concluded that non-nucleoside reverse transcriptase inhibitors and protease inhibitors may interact with anticoagulant metabolism and that nucleoside reverse transcriptase inhibitors (NRTIs) and integrase strand inhibitors (INSTIs) have no significant interaction (NRTIs and INSTIs were used in the patient discussed in the present case report). In a case study by Liedtke et al (2012), an increased warfarin dose was required to maintain a therapeutic international normalized ratio after the initiation of ritonavir-boosted darunavir, etravirine, and raltegravir therapy for HIV 14 .…”

Section: Discussionmentioning

confidence: 85%

A Case of Deep Venous Thrombosis in an HIV-Infected Patient despite Therapeutic Anticoagulation

Aiman,

Ashar Ali,

Grewal

et al. 2024

IJHOSCR

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Patients with human immunodeficiency virus (HIV) infection have an increased likelihood of venous thromboembolism (VTE) owing to factors such as acquired protein C and S deficiency, antiphospholipid antibody syndrome, and heightened levels of pro-inflammatory cytokines. This case report highlights an exceptionally uncommon occurrence of deep venous thrombosis in an HIV-infected patient receiving a therapeutic dose of enoxaparin. This underscores the need for cautious consideration of the risk of VTE in HIV-infected individuals, even with preventive or therapeutic anticoagulant treatment. Further research is recommended to investigate HIV as a potential risk factor of prophylactic anticoagulation.

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