• C Tcherakian, E Rivaud, E Catherinot, D Zucman, A-C Metivier, and L-J Couderc.
• Service de Pneumologie, Hôpital Foch, 40, rue Worth, 92150 Suresnes, France. c.tcherakian@hopital-foch.org
• Rev Pneumol Clin. 2011 Sep 1;67(4):250-7.

AbstractVascular diseases have become the leading cause of mortality in the population treated for HIV infection. Pulmonary arterial hypertension (PAH) related to HIV (PAH-HIV), the fourth cause of PAH in France, has the same histological pattern as other PAH from the group 1 of Dana Point classification. But, conversely to idiopathic PAH in the general population, PAH-HIV is particular by its high frequency in HIV-infected population. This raises the question for the role of inflammation in the PAH-HIV pathophysiology. Its constant occurrence over the decades, despite introduction of combination antiretroviral therapy (CAT), does not preclude the hypothesis of an involvement of inflammation in the genesis of PAH-HIV. Indeed, it is well known that normalization of CD4+ by the CAT does not mean no inflammation. Especially, it persists an increased and continuous production of IL-6, a main cytokine in the genesis of PAH lesions. This inflammation mainly involves the endothelin-1 pathway, which has an action on endothelium and macrophages, leading to high production of IL-6. Moreover, plasmatic level of IL-6 has a prognostic value in PAH-HIV, independently from conventional (functional or hemodynamic) parameters. The use of endothelin receptor antagonist permits major effect on IL-6 production and dramatic effect on PAH in so-called "bosentan responders".2011. Published by Elsevier Masson SAS.

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