Study of the Efficiency of Hydroxychloroquine on the Endothelial Dysfunction and Its Vascular Consequences During the Antiphospholipid Syndrome

NCT ID: NCT02595346

Last Updated: 2016-12-07

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Clinical Phase

PHASE2

Total Enrollment

30 participants

Study Classification

INTERVENTIONAL

Study Start Date

2016-06-30

Study Completion Date

2018-12-31

Brief Summary

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This study evaluates the benefits of hydroxychloroquine on arterial function in antiphospholipid syndrome.

Briefly, the patients will be randomized in two groups, one will receive hydroxychloroquine and standard treatment, the other will receive placebo in addition of standard treatment.

Detailed Description

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Antiphospholipid syndrome (APS) is an autoimmune disease characterized by recurrent thrombotic events and miscarriages, with persistently positive antiphospholipid antibodies (aPL). APS may be isolated (primary APS) or associated to a connective tissue disease, most often systemic lupus erythematous (SLE).

Pathogenic effects of aPL were first described by the demonstration that in vitro incubation of endothelial cells or monocytes with aPL induce an endothelial dysfunction characterized by pro-coagulant (overexpression of tissue factor and modulation of protein C and S), pro-inflammatory (increased level of IL-6(interleukin 6) , IL-1β and TNFα) and pro-adhesive (increased levels of ICAM-1(intercellular adhesion molecule ), VCAM-1 (vascular endothelial cell adhesion molecule) and E-selectin) phenotypes. In parallel the investigators and others reported that endothelial function, assessed by flow mediated dilatation, is altered in patients with primary and secondary forms of APS. Although a role for TLR (toll-like receptor )-mediated NFkB translocation has been advanced, the pathogenic mechanisms that lead to in vivo endothelial injury in APS are incompletely understood.

In an experimental model, the investigators demonstrated that passive transfer of human aPL to mice induced a marked endothelial dysfunction assessed ex vivo in small resistance arteries, and an increase in TNFα levels. Moreover, the investigators group have demonstrated that patients with primary arterial APS display endothelial dysfunction and structural arterial changes, associated with a pro-oxidative and pro-coagulant state and with activation of the TLR2 and TLR4 signalling pathways.

Recently, in a preliminary study the investigators have found that endothelial glycocalyx which is an important part of the vascular barrier and which is intimately linked to the homeostatic functions of the endothelium was altered in APL patients.

Hydroxychloroquine (HCQ) is an antimalarial drug, also used to treat rheumatic diseases such as SLE. There is experimental evidence to suggest a direct role of hydroxychloroquine on the pathophysiology of APS: it directly reduces the binding of antibodies on the phospholipid bilayers, protects the annexin A5 anticoagulant shield and it reverses platelet adhesion induced by aPL.

Furthermore it is known to decrease the expression of lysosomal TLRs, but also extra lysosomal TLR2 and TLR4.

The aim of this study is to investigate whether treatment with hydroxychloroquine modulates vascular endothelial function in patients.

Conditions

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Antiphospholipid Syndrome (APS)

Study Design

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Allocation Method

RANDOMIZED

Intervention Model

PARALLEL

Primary Study Purpose

TREATMENT

Blinding Strategy

SINGLE

Outcome Assessors

Study Groups

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hydroxychlorquine

hydroxychloroquine 200 mg twice a day for 6 months

Group Type EXPERIMENTAL

Hydroxychloroquine

Intervention Type DRUG

endothelial function is assessed by measuring the flow mediated dilatation of humeral artery in response to ischemia. the dilatation is evaluated by echotracking.

glycocalyx thickness is measured by the study of sublingual microcirculation with SDF imaging.

oxydative, inflammatory and coagulation parameters is assessed on plasma samples.

control

placebo 2 pills a day for 6 months

Group Type PLACEBO_COMPARATOR

placebo

Intervention Type DRUG

endothelial function is assessed by measuring the flow mediated dilatation of humeral artery in response to ischemia. the dilatation is evaluated by echotracking.

glycocalyx thickness is measured by the study of sublingual microcirculation with SDF imaging.

oxydative, inflammatory and coagulation parameters is assessed on plasma samples.

Interventions

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Hydroxychloroquine

endothelial function is assessed by measuring the flow mediated dilatation of humeral artery in response to ischemia. the dilatation is evaluated by echotracking.

glycocalyx thickness is measured by the study of sublingual microcirculation with SDF imaging.

oxydative, inflammatory and coagulation parameters is assessed on plasma samples.

Intervention Type DRUG

placebo

endothelial function is assessed by measuring the flow mediated dilatation of humeral artery in response to ischemia. the dilatation is evaluated by echotracking.

glycocalyx thickness is measured by the study of sublingual microcirculation with SDF imaging.

oxydative, inflammatory and coagulation parameters is assessed on plasma samples.

Intervention Type DRUG

Other Intervention Names

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plaquenil

Eligibility Criteria

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Inclusion Criteria

* Patients who fulfilled Sidney criteria for APS (antiphospholipid Syndrome
* Women of childbearing potential must have a contraceptive method
* Written informed consent
* no severe, progressive, or uncontrolled kidney, liver, blood, stomach, lung, heart, or brain disease.

Exclusion Criteria

* secondary antiphospholipid syndrome
* Pregnancy and breastfeeding
* Patients with a history of severe depression, psychosis, or suicidal ideation
* story of intolerance or contra-indication to hydroxychloroquine, lactose, trinitrin
* Prior use of hydroxychloroquine in the last 6 months
* Chronic heart failure
* atrial fibrillation
* severe pulmonary hypertension
* severe kidney failure clearance \< 30ml/mn
* uncontrolled arterial hypertension
* secondary arterial hypertension
* diabetes mellitus diagnosed in the last 3 months
* body mass index \> 35
* Patient has been committed to an institution by legal or regulatory order
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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University Hospital, Rouen

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Sébastien MIRANDA, MD

Role: PRINCIPAL_INVESTIGATOR

University Hospital, Rouen

Locations

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Rouen University Hospital

Rouen, , France

Site Status RECRUITING

Countries

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France

Central Contacts

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Sébastien MIRANDA, MD

Role: CONTACT

Email: [email protected]

Julien BLOT

Role: CONTACT

Phone: +3323288

Email: [email protected]

Other Identifiers

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2015/074/HP

Identifier Type: -

Identifier Source: org_study_id