HIV Infection Clinical Trial
Official title:
Auto-immunity and Prognosis of Pulmonary Arterial Hypertension
The investigators have recently evidenced the presence of antibodies to endothelial cells and
fibroblasts in patients with idiopathic or SSc-associated PAH. The investigators also have
identified several target antigens of anti-fibroblasts antibodies.
The objective of this study is to further investigate for the presence of antibodies to
endothelial cells and fibroblasts in patients and characterize the antigen specificity of
autoantibodies in patients with different types of non idiopathic and non SSc-associated PAH,
such as PAH associated with HIV infection, porto-pulmonary hypertension, congenital heart
diseases, systemic lupus erythematosus, mixed connective tissue disease and Sjögren's
syndrome
Two hundred and fifty patients with PAH will be included: 65 patients with idiopathic PAH
(iPAH), 20 with PAH associated with HIV infection, 20 with porto-pulmonary hypertension, 20
with PAH secondary to congenital heart disorders, 40 with SSc, 20 with SLE, 20 with MCTD and
10 with a PAH associated with a Sjögren's syndrome.
Two hundred patients without PAH will also be included: 80 patients with SSc and 20 in each
of the following groups: HIV infection, porto-pulmonary hypertension, SLE, congenital heart
disorders, MCTD and with Sjögren's syndrome.
Twenty patients with proximal chronic thromboembolic pulmonary hypertension (CTPH) will also
be included in a control arm of the study.
Two hundred and fifty healthy blood donors age and sex-matched with patients with PAH, will
be included as controls.
By using 2D-immunoblotting techniques, we will evidence IgG antibodies to fibroblasts, EC,
vascular smooth muscle cells (SMC) in multiple groups of patients and we will characterize
target antigens of these autoantibodies. We will also assess the production of ROS: nitric
oxide (NO), hydrogen peroxide (H2O2) and the effect of the whole serum (and the IgG
particularly) on in VITRO proliferation of EC, fibroblasts and vascular SMC. For sera that
will induce the production of ROS, we will study the effect of different vasodilatator
(prostacycline, endothelin receptor antagonist, type 5 phosphodiesterase inhibitors) and
anti-oxidant therapies.
Expected results We will characterize target antigens of autoantibodies of patients with
non-idiopathic and non SSc-associated PAH. We will compare these target to those previously
identified in idiopathic or SSc-associated PAH. We will then, distinguish subpopulations of
PAH patients whose serum or purified IgG (possibly specific for a given antigen) are able to
induce ROS production or cell proliferation. For the population of ROS-producer patients, we
will correlate the clinical response to vasodilatator therapy to results of in VITRO
inhibition experiments with vasodilatators and anti-oxidant molecules.
Perspectives The characterization of target antigens of EC, fibroblasts and vascular SMC
specifically
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