Flow Mediated Dilation in Association With Hyperuricemia

A

Assiut University

Status

Enrolling

Conditions

SLE
Cardiovascular Diseases
Atherosclerosis

Treatments

Diagnostic Test: Flow mediated dilation

Study type

Observational

Funder types

Other

Identifiers

NCT05342285
FMD

Details and patient eligibility

About

Assess cardiovascular affection and subclinical atherosclerosis in patients with systemic lupus using the non invasive flow mediated dilation. evaluate the role of uric acid as independent marker of cardiovascular risk in systemic lupus patient

Full description

Systemic lupus erythematosus (SLE) is a complex autoimmune disease that is characterized by multiple end-organ damage and predominantly affects premenopausal women. Cardiovascular disease is a major cause of morbidity and mortality in systemic lupus erythematosus (SLE) patients. These patients have a higher incidence and an earlier age of onset of ischemic heart disease, carotid atherosclerosis, cerebrovascular stroke, and peripheral vascular Disease. Traditional cardiovascular risk factors, including hypertension, diabetes mellitus, dyslipidemia, and physical inactivity, only account partially for the elevated vascular risk in SLE patients . Vascular stiffness proven to have better predictive value for fatal and non-fatal cardiovascular events than traditional risk factors in hypertensives and patients with end-stage renal disease or coronary artery disease . Endothelial dysfunction represents the initial step of atherosclerosis and correlates with arterial stiffness which is associated with incident cardiovascular events. Brachial artery reactivity testing (BART) is used to noninvasively assess responsiveness to reactive hyperemia (flow-mediated dilation [FMD]) and evaluate nitric oxide [NO]-dependent large vessel endothelial function. Reduced FMD reflects impaired endothelial-dependent vasodilation indicative of vascular dysfunction. Uric acid (UA), the final product of purine degradation, is formed in the liver from precursor proteins and is excreted by the kidneys and intestines. At physiologic concentrations, UA exhibits excellent antioxidant activity; however, when UA exceeds its physiologic levels, it can propagate oxidative damage. Furthermore, chronic elevation of UA constitutes a risk factor for many diseases, as it can promote inflammation and endothelial dysfunction . Higher prevalence of hyperuricemia in patients with SLE might be owing to several endogenous and exogenous mechanisms such as inflammation, hypertension, and renal involvement, which are prevalent in patients with SLE and have been identified as provoking hyperuricemia through different mechanisms. On the contrary, increased levels of UA can aggravate inflammation, hypertension, and renal disease, thus creating a vicious cycle. Hyperactivity of the xanthine oxidase enzyme in patients with SLE and some of the drugs used in the treatment of SLE are among the other possible reasons for the higher prevalence of hyperuricemia in patients with SLE. Studies have shown that increases in serum uric acid levels may be tied to an increased risk of cardiovascular disease and mortality. In addition, hyperuricemia has been shown to be associated with endothelial dysfunction as well as the oxidation of lipoproteins within atherosclerotic plaques (contributors to cardiovascular disease risk). Several studies have highlighted the role of uric acid as an independent biomarker of cardiovascular disease risk. . The link between hyperuricemia and the risk of atherosclerotic cardiovascular and cerebrovascular disease has been well-established. . In an observational cohort study testing the association between hyperuricemia and coronary artery calcification, the results showed that hyperuricemia is an independent risk factor for sub-clinical atherosclerosis in young adults . Depending on the microenvironment, uric acid may act as an antioxidant or an oxidant. Under ischemic conditions, xanthine oxidase uses oxygen as an electron acceptor instead of nicotinamide adenine dinucleotide (NAD+) resulting in the formation of superoxide anion and hydrogen peroxide. Oxidants cause endothelial dysfunction by reacting with and removing nitric oxide (NO), which prevents vasodilation of the endothelium. This promotes a pro-inflammatory state that causes endothelial dysfunction and contributes to atherosclerosis and cardiovascular disease .Uric acid can also induce vascular smooth muscle cell proliferation in vitro by producing pro-inflammatory, pro-oxidative, and vasoconstrictive substances. Uric acid stimulates the production of monocyte chemoattractant protein-1 (MCP-1), a chemokine involved in atherosclerosis. Increased production of MCP-1 increases cell proliferation and production of pro-inflammatory mediators. Uric acid stimulates monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2 . This study aims to emphasize the role of flow mediated dilation in the detection of endothelial dysfunction in SLE patients and linking it to hyperuricemia as a predictor and contributor of cardiovascular affection which can be useful to guide therapeutic decisions in these patients in the future.

Enrollment

60 estimated patients

Sex

Female

Ages

18 to 45 years old

Volunteers

Accepts Healthy Volunteers

Inclusion criteria

  • female patient with SLE aged more than 18

Exclusion criteria

  • male patients
  • patient with established cardiovascular disease, patients with end stage renal disease

Trial design

60 participants in 3 patient groups

normal FMD
Description:
SLE femals patientd with normal flow mediated whose ages from 18 to 45yrs
Treatment:
Diagnostic Test: Flow mediated dilation
abnormal FMD
Description:
SLE femals with abnormal flow mediated dikation ages between 18 to 45yrs old
Treatment:
Diagnostic Test: Flow mediated dilation
Normal female
Description:
normal femals whise ages from 18 to 45yrs old
Treatment:
Diagnostic Test: Flow mediated dilation

Trial contacts and locations

1

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Central trial contact

lobna ahmed hassan mohamed, resident doctor; Eman mohamed, doctor

Data sourced from clinicaltrials.gov

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