ORIGINAL ARTICLE
Year : 2015  |  Volume : 2  |  Issue : 4  |  Page : 139-145

The Adventitial Angioproliferation in Human Immunodeficiency Virus Associated Large Artery Vasculopathy is Not a Manifestation of Kaposi Sarcoma


1 Department of Vascular/Endovascular Surgery; Nelson R Mandela School of Medicine; University of KwaZulu-Natal, Durban, KwaZulu-Natal, South Africa
2 Department of Anatomical Pathology; School of Laboratory Medicine and Medical Sciences; University of KwaZulu-Natal; National Health Laboratory Service, Durban, KwaZulu-Natal, South Africa
3 Department of Anatomical Pathology , National Health Laboratory Service, Durban, KwaZulu-Natal, South Africa
4 Department of Cardiology; Nelson R Mandela School of Medicine; University of KwaZulu-Natal, Durban, KwaZulu-Natal, South Africa

Correspondence Address:
Balasoobramanien Pillay
Department of Vascular/Endovascular Surgery; Nelson R Mandela School of Medicine; University of KwaZulu-Natal, Durban, KwaZulu-Natal
South Africa
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-0820.180113

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Introduction: Human immunodeficiency virus-associated large artery vasculopathy (HIV-vasculopathy) is characterized by distinctive transmural microanatomical alterations, including adventitial angioproliferation, similar to that described in early cutaneous Kaposi sarcoma (KS). Human herpesvirus-8 (HHV8), the etiological agent of KS, is identifiable in tissue sections. The aim of this study was to investigate, based on HHV8-latent nuclear antigen-1 (HHV8-LNA-1) immunohistochemical and HHV8 polymerase chain reaction (PCR) testing, whether KS is the cause of the angioproliferation. Materials and Methods: Sections from 20 large arteries, ten each with HIV-associated occlusive and aneurysmal vasculopathy and ten biopsies with early cutaneous KS from 30 anti-retroviral therapy naive patients were appraised microscopically and subjected to HHV8-LNA-1 immunostaining. Arterial sections were also subjected to HHV8 PCR investigation with appropriate positive and negative controls. Results: The microscopic large arterial adventitial alterations included a dissecting proliferation of capillary-caliber vasculature, surrounded by mixed inflammation, microhemorrhages, hemosiderin and vasa vasorum intimomedial fibrosis, and hypertrophy. Ten vessels also demonstrated adventitial leukocytoclastic and lymphocytic vasculitis. Immunohistochemical and PCR detection of HHV8 was consistently negative. Skin biopsies of KS shared the vascular adventitial alterations, but vasculitis and thrombosis were absent. Endothelial and dermal spindle cells were immunopositive for HHV8. Conclusion: The adventitial angioproliferation in large arteries with HIV-vasculopathy is not a manifestation of KS. The exact roles of HIV, including interaction with co-infective agents and cellular and subcellular responses in the induction of vasculopathic and vasa vasorum abnormalities, including adventitial angioinflammatory alterations, require accelerated investigation for improved disease understanding and patient management.


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