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Inturlekin L33 in Ankylosing Spondylities Patients and Its Relation to Subclinical Atherosclerosis

Inturlekin 33 in Ankylosing Spondylitis Patients and Its Relationship to Subclinical Atherosclerosis

Status
Not yet recruiting
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT06564155
Enrollment
45
Registered
2024-08-21
Start date
2024-09-30
Completion date
2026-12-31
Last updated
2024-08-22

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

Conditions

Ankylosing Spondylitis

Brief summary

detect level of Inturlekin 33 in ankylosing spondyilits patient measure CIMT (carotid intima media thickness ) by carotid duplex to detect subclinical atherosclerosis in ankylosing spondyitis patients detect the relation between IL33 and subclinical atherosclerosis in Ankylosinig Spondylitis patients

Detailed description

Ankylosing spondylitis (AS), a type of SpA, is an autoimmune disease that mainly involves, sacroiliac joints (SIJs) and their adjacent soft tissues, such as tendons and ligaments. The main clinical manifestations include back pain and progressive spinal rigidity as well as inflammation of the hips, shoulders, peripheral joints and fingers/toes. In addition, there are extra-articular manifestations. Cardiovascular disease has become the first cause of death for patients with ankylosing spondylitis (AS). Patients with ankylosing spondylitis (AS) have an increased cardiovascular morbidity and mortality . Accelerated atherosclerosis caused by a systemic inflammatory response has been reported to be an important risk factor for increased cardiovascular risk for autoimmune diseases. Interleukin (IL)-33 is a cytokine belonging to the IL-1 family and was recently identified as a ligand for ST2, .the serum levels of IL-33/sST2 were remarkably higher in the patients with AS than the healthy groups . Pervious studies confirm the importance of IL-33/ST2 axis in the process of atherosclerosis, and indicate its ambiguous function in immune response, whether as proinflammatory cytokine in advanced atherosclerotic lesions, or as profibrotic, in early lesions. Previous study shows increased CIMT in AS patients without traditional cardiovascular risk factors compared to healthy controls.

Interventions

measure Carotid intima media thickness

Sponsors

Assiut University
Lead SponsorOTHER

Study design

Observational model
CASE_CONTROL
Time perspective
CROSS_SECTIONAL

Eligibility

Sex/Gender
ALL
Age
20 Years to 40 Years
Healthy volunteers
Yes

Inclusion criteria

* patient diagnosed as Ankylosing Spondylitis * Age (20-40)

Exclusion criteria

* Patients with other rheumatic diseases/other SPA types * Participants with history of CVD event in past or present * Patient experiencing cardiovascular revascularization surgery or cerebrovascular disorder within past 6 months. * Patient with other risk factor for atherosclerosis.

Design outcomes

Primary

MeasureTime frameDescription
detect level of IL33 in AS patients3 yearsmeasure level of IL33 in the serum of AS patients measure caroid intima media thickness CIMT in AS patients

Secondary

MeasureTime frameDescription
detect the reation between IL33 and subclinical atherosclerosis in AS patients3 yearsmeasure caroid intima media thickness CIMT in AS patients

Contacts

Primary ContactAya AbuAli, master
ayaa.m.abuali471@gmail.com01097833248
Backup ContactShimaa Mahmoud, Dr
Shaimaasalah@aun.edu.eg01062084082

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026