Circulating Anti-Beta2-glycoprotein Antibodies and Endothelial Dysfunction

Influence of Circulating Anti-beta2-glycoprotein I Antibodies on the Endothelial Function and NO Metabolism in Peripheral Arterial Disease Patients.

Status

Completed

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT01822990

Enrollment

Registered

2013-04-04

Start date

2011-02-28

Completion date

2012-07-31

Last updated

2013-04-04

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Peripheral Arterial Disease

Keywords

Anti-beta2-glycoprotein antibodies, Peripheral arterial disease, Inflammation, Nitric oxide, Endothelial dysfunction

Brief summary

Circulating anti-beta2-glycoprotein antibodies have been associated with coronary artery disease and peripheral arterial disease. This auto-antibodies could activate endothelial cells leading to the expression of leukocyte adhesion molecules and increasing the release of pro-inflammatory cytokines. On the other hand, endothelial dysfunction of atherosclerotic patients acts as a primary pathogenic event, as it occur before structural changes are evident on angiogram or ultrasound scan. Loss of endothelial normal function causes vasoconstriction, local coagulation alterations and an increase arterial wall proliferation. This situation s been attributed to a reduction in nitric oxide bioactivity, and to an increase oxygen-free radical formation in the context of the pro-inflammatory status found in atherosclerosis. Hypothesis: Circulating Anti-beta2-glycoprotein I antibodies could be associated with endothelial dysfunction and nitric oxide metabolism disruption en patients with peripheral arterial disease.

Interventions

None listed

Study design

Observational model

CASE_CONTROL

Time perspective

PROSPECTIVE

Eligibility

Sex/Gender

MALE

Age

18 Years to 90 Years

Healthy volunteers

Yes

Inclusion criteria

* Male gender * Peripheral arterial disease diagnosis * Intermittent claudication. * Hemodynamic confirmation of the disease through non-invasive vascular studies.

Exclusion criteria

* Autoimmune disease * Previous revascularization of the ischemic limb. * Ischemic ulcers * Previous history of organ transplants. * Treatment with immunosuppressors

Design outcomes

Primary

Measure	Time frame	Description
Circulating anti-beta2-glycoprotein I antibodies	12 months	The titer of circulating anti-endothelial cell antibodies directed against beta2-glycoprotein antigens (Circulating ABGPI) could be detected by indirect immunofluorescence using a diagnosis reagent kit and subjects serum.
Flow-mediated arterial dilatation (FMAD)	12 months	FMAD is an ultrasound test based on the ability of endothelial cells to detect changes in shear stress and is one of the most effective and reliable indirect methods for estimating endothelial dysfunction. The ultrasound transducer is applied proximal to the antecubital fossa, and a longitudinal image of the brachial artery is obtained. The basal arterial diameter is determined. A blood pressure cuff is then placed distal to the measurement area and inflated to a pressure of 250 mmHg for five minutes. New measurements of the arterial diameter in the final diastolic phase should be obtained, 60 seconds after the cuff is deflated
Nitrite serum levels	12 months	Nitrite serum levels reflects the nitric oxide metabolism. Serum nitrite concentration could be measured by colorimetric analysis using the Griess reaction. This is a chemical reaction which uses sulphanilamide and naphthylethylenediamine dihydrochloride under acid conditions (phosphoric acid).The system is capable of detecting nitric oxide in a variety of biological and experimental fluids, like human serum samples.
Highly sensitive C-reactive protein.	12 months	Highly sensitive C-reactive protein levels could be measured using a highly sensitive, automated immunoassay with the human serum samples.

Countries

Spain

Outcome results