Yasmina Ferfar1, Léa Savey1, Cloé Comarmond1, Nirvana Sadaghianloo2, Marlène Garrido3, Fanny Domont1, Marc Antoine Valantin4, Valérie Pourcher-Martinez4, Philippe Cluzel5, Pierre Fouret6, Laurent Chiche2, Julien Gaudric2, Fabien Koskas2, Patrice Cacoub1, David Saadoun7. 1. Department of Internal Medicine and Clinical Immunology, Centre de référence des maladies autoimmunes et systémiques rares, Sorbonne University, UPMC Paris VI, AP-HP, Hôpital Pitié-Salpétrière, Paris, France; DHU I2B, Inflammation, Immunopathologie, Biothérapie, Sorbonne University, UPMC Paris VI, AP-HP, Hôpital Pitié-Salpétrière, Paris, France. 2. Department of Vascular Surgery, Sorbonne University, UPMC Paris VI, AP-HP, Hôpital Pitié-Salpétrière, Paris, France. 3. DHU I2B, Inflammation, Immunopathologie, Biothérapie, Sorbonne University, UPMC Paris VI, AP-HP, Hôpital Pitié-Salpétrière, Paris, France. 4. Department of Infectious Diseases, Sorbonne University, UPMC Paris VI, AP-HP, Hôpital Pitié-Salpétrière, Paris, France. 5. Department of Radiology, Sorbonne University, UPMC Paris VI, AP-HP, Hôpital Pitié-Salpétrière, Paris, France. 6. Department of Pathology, Sorbonne University, UPMC Paris VI, AP-HP, Hôpital Pitié-Salpétrière, Paris, France. 7. Department of Internal Medicine and Clinical Immunology, Centre de référence des maladies autoimmunes et systémiques rares, Sorbonne University, UPMC Paris VI, AP-HP, Hôpital Pitié-Salpétrière, Paris, France; DHU I2B, Inflammation, Immunopathologie, Biothérapie, Sorbonne University, UPMC Paris VI, AP-HP, Hôpital Pitié-Salpétrière, Paris, France. Electronic address: david.saadoun@aphp.fr.
Abstract
OBJECTIVE: The objective of this study was to describe large-vessel vasculitis (LVV) in patients with human immunodeficiency virus (HIV) infection. It is a retrospective single-center study conducted between 2000 and 2015 through a university hospital of 11 HIV-infected patients with LVV. METHODS: The characteristics and outcome of 11 HIV-infected patients with LVV (7 patients fulfilled international criteria for Takayasu arteritis, 5 patients had histologic findings of vasculitis, and 5 patients had imaging features of aortitis) were analyzed and compared with those of 82 patients with LVV but without HIV infection. RESULTS: Concerning the HIV-infected patients with LVV (n = 11), the mean age was 40 years (range, 36-56 years), and 55% of patients were female. At diagnosis of LLV, the mean initial CD4 cell count was 455 cells/mm3 (range, 166-837 cells/mm3), and the median HIV viral load was 9241 copies. Vascular lesions were located in the aorta (n = 7), in supra-aortic trunks (n = 7), and in digestive arteries (n = 3). Inflammatory aorta infiltrates showed a strong expression of interferon-γ and interleukin 6. In HIV-negative LVV patients (n = 82), the median age was 42 years, and 88% of the patients were women. Thirty patients had an inflammatory syndrome. Seventy patients had been treated with glucocorticosteroids and 57 with immunosuppressive treatments. Compared with their negative counterparts, HIV-positive patients with LVV were more frequently male (P = .014), had more vascular complications (ie, Ishikawa score; P = .017), and had more frequent revascularization (P = .047). After a mean follow-up of 96 months, four relapses of vasculitis were reported, and one patient died. Regardless of the HIV virologic response, antiretroviral therapy improved LVV in only one case. CONCLUSIONS: LVV in HIV-infected patients is a rare and severe entity.
OBJECTIVE: The objective of this study was to describe large-vessel vasculitis (LVV) in patients with human immunodeficiency virus (HIV) infection. It is a retrospective single-center study conducted between 2000 and 2015 through a university hospital of 11 HIV-infectedpatients with LVV. METHODS: The characteristics and outcome of 11 HIV-infectedpatients with LVV (7 patients fulfilled international criteria for Takayasu arteritis, 5 patients had histologic findings of vasculitis, and 5 patients had imaging features of aortitis) were analyzed and compared with those of 82 patients with LVV but without HIV infection. RESULTS: Concerning the HIV-infectedpatients with LVV (n = 11), the mean age was 40 years (range, 36-56 years), and 55% of patients were female. At diagnosis of LLV, the mean initial CD4 cell count was 455 cells/mm3 (range, 166-837 cells/mm3), and the median HIV viral load was 9241 copies. Vascular lesions were located in the aorta (n = 7), in supra-aortic trunks (n = 7), and in digestive arteries (n = 3). Inflammatory aorta infiltrates showed a strong expression of interferon-γ and interleukin 6. In HIV-negative LVV patients (n = 82), the median age was 42 years, and 88% of the patients were women. Thirty patients had an inflammatory syndrome. Seventy patients had been treated with glucocorticosteroids and 57 with immunosuppressive treatments. Compared with their negative counterparts, HIV-positivepatients with LVV were more frequently male (P = .014), had more vascular complications (ie, Ishikawa score; P = .017), and had more frequent revascularization (P = .047). After a mean follow-up of 96 months, four relapses of vasculitis were reported, and one patient died. Regardless of the HIV virologic response, antiretroviral therapy improved LVV in only one case. CONCLUSIONS: LVV in HIV-infectedpatients is a rare and severe entity.
Authors: Anum S Minhas; Wendy S Post; Bin Liu; Henrique Doria De Vasconcellos; Sabina A Haberlen; Matthew Feinstein; Valentina Stosor; Matthew Budoff; Kara W Chew; Jared W Magnani; Todd Brown; Joao A C Lima; Katherine C Wu Journal: J Am Heart Assoc Date: 2022-03-05 Impact factor: 5.501