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Etheresia Pretorius
Stellenbosch University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-9108-2384
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Background Patients infected with the human immunodeficiency virus (HIV) are more prone to systemic inflammation and pathological clotting, and many may develop deep vein thrombosis (DVT) as a result of this dysregulated inflammatory profile. Coagulation tests are not routinely performed unless there is a specific reason. Methods We recruited ten healthy control subjects, 35 HIV negative patients with deep vein thrombosis (HIV negative-DVT), and 13 HIV patients with DVT (HIV positive-DVT) on the primary antiretroviral therapy (ARV) regimen- Emtricitabine, Tenofovir and Efavirenz. Serum inflammatory markers, haematological results, viscoelastic properties (using thromboelastography-TEG) and scanning electron microscopy (SEM) of whole blood (WB) were used to compare the groups. Results DVT patients (HIV positive and HIV negative) have raised inflammatory markers. The HIV positive-DVT group has anaemia in keeping with anaemia of chronic disorders. DVT patients have a hypercoagulable profile on the TEG but no significant difference between HIV negative-DVT and HIV positive-DVT groups. The TEG analysis compared well and supported our ultrastructural results. Scanning electron microscopy of DVT patient’s red blood cells (RBCs) and platelets demonstrates inflammatory changes including abnormal cell shapes, irregular membranes and microparticle formation. All the ultrastructural changes were more prominent in the HIV positive-DVT patients. Conclusions It is well-known that HIV infection is linked to inflammation and inflammation is linked with the presence of a hypercoagulable state. The presence of DVT is also associated with inflammation. Whether HIV is the cause of the DVT is not certain. Although there were trends that HIV infected patients were more hypercoagulable on functional tests (viscoelastic profile) compared to HIV uninfected patients, there were no significant differences between the 2 groups. Morphologically there were inflammatory changes in patients with DVT. These ultrastructural changes, specifically with regard to platelets, appear more pronounced in HIV infected patients which may contribute to increased risk for hypercoagulability and deep vein thrombosis.
Keywords
Hypercoagulability, human immunodeficiency virus (HIV), deep vein thrombosis (DVT), inflammation.
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CURRENT STATUS: Published
View the published article at Retrovirology.
No community comments so far
Editorial decision: Accept
On 14 Jun, 2020
Editor assigned
On 21 Mar, 2020
Submission checks complete
On 20 Mar, 2020
Editor invited
On 20 Mar, 2020
Version 2
Posted 18 Feb, 2020
No comments provided
Editorial decision: Minor revision
On 16 Mar, 2020
Editor assigned
On 18 Feb, 2020
Submission checks complete
On 17 Feb, 2020
Editor invited
On 17 Feb, 2020
No comments provided
Editorial decision: Major revision
On 19 Jan, 2020
Review #2 received
Received 03 Jan, 2020
Review #1 received
Received 29 Dec, 2019
Reviewer #2 agreed
On 20 Dec, 2019
Reviewer #1 agreed
On 18 Dec, 2019
Reviewers invited
Invitations sent on 10 Dec, 2019
First submitted
On 11 Nov, 2019
Editor assigned
On 11 Nov, 2019
Submission checks complete
On 10 Nov, 2019
Editor invited
On 10 Nov, 2019
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PDF Downloads: ...
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Subject Areas
Virology
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A new preprint design is coming!
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See the published version of this preprint at Retrovirology.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Etheresia Pretorius
Stellenbosch University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-9108-2384
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Retrovirology.
No community comments so far
Editorial decision: Accept
On 14 Jun, 2020
Editor assigned
On 21 Mar, 2020
Submission checks complete
On 20 Mar, 2020
Editor invited
On 20 Mar, 2020
Version 2
Posted 18 Feb, 2020
No comments provided
Editorial decision: Minor revision
On 16 Mar, 2020
Editor assigned
On 18 Feb, 2020
Submission checks complete
On 17 Feb, 2020
Editor invited
On 17 Feb, 2020
No comments provided
Editorial decision: Major revision
On 19 Jan, 2020
Review #2 received
Received 03 Jan, 2020
Review #1 received
Received 29 Dec, 2019
Reviewer #2 agreed
On 20 Dec, 2019
Reviewer #1 agreed
On 18 Dec, 2019
Reviewers invited
Invitations sent on 10 Dec, 2019
First submitted
On 11 Nov, 2019
Editor assigned
On 11 Nov, 2019
Submission checks complete
On 10 Nov, 2019
Editor invited
On 10 Nov, 2019
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Virology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Retrovirology.
Background Patients infected with the human immunodeficiency virus (HIV) are more prone to systemic inflammation and pathological clotting, and many may develop deep vein thrombosis (DVT) as a result of this dysregulated inflammatory profile. Coagulation tests are not routinely performed unless there is a specific reason. Methods We recruited ten healthy control subjects, 35 HIV negative patients with deep vein thrombosis (HIV negative-DVT), and 13 HIV patients with DVT (HIV positive-DVT) on the primary antiretroviral therapy (ARV) regimen- Emtricitabine, Tenofovir and Efavirenz. Serum inflammatory markers, haematological results, viscoelastic properties (using thromboelastography-TEG) and scanning electron microscopy (SEM) of whole blood (WB) were used to compare the groups. Results DVT patients (HIV positive and HIV negative) have raised inflammatory markers. The HIV positive-DVT group has anaemia in keeping with anaemia of chronic disorders. DVT patients have a hypercoagulable profile on the TEG but no significant difference between HIV negative-DVT and HIV positive-DVT groups. The TEG analysis compared well and supported our ultrastructural results. Scanning electron microscopy of DVT patient’s red blood cells (RBCs) and platelets demonstrates inflammatory changes including abnormal cell shapes, irregular membranes and microparticle formation. All the ultrastructural changes were more prominent in the HIV positive-DVT patients. Conclusions It is well-known that HIV infection is linked to inflammation and inflammation is linked with the presence of a hypercoagulable state. The presence of DVT is also associated with inflammation. Whether HIV is the cause of the DVT is not certain. Although there were trends that HIV infected patients were more hypercoagulable on functional tests (viscoelastic profile) compared to HIV uninfected patients, there were no significant differences between the 2 groups. Morphologically there were inflammatory changes in patients with DVT. These ultrastructural changes, specifically with regard to platelets, appear more pronounced in HIV infected patients which may contribute to increased risk for hypercoagulability and deep vein thrombosis.
Figure 1
Figure 2
Figure 3
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