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Atherosclerosis and antiphospholipid syndrome.
Luis J Jara1, Gabriela Medina, Olga Vera-Lastra
1Clinical Research Unit and Rheumatology Department, Hospital de Especialidades Centro Medico La Raza, Mexico City, México.
Clinical Reviews in Allergy & Immunology
|June 10, 2003
Summary
Atherosclerosis, an autoimmune disease, involves immune responses to factors like oxidized LDL. In systemic lupus erythematosus and antiphospholipid syndrome, specific autoantibodies and reduced PON1 activity contribute to accelerated atherosclerosis.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Autoimmune Diseases
Background:
- Atherosclerosis is an inflammatory disease influenced by infectious, inflammatory, and autoimmune factors.
- Humoral and cellular immune mechanisms are implicated in atheromatous lesion development.
- Autoantigens like heat-shock protein (hsp), oxidized low-density lipoprotein (LDL), and beta2-GPI trigger immune responses within lesions.
Purpose of the Study:
- To explore the role of immunological alterations in accelerated atherosclerosis in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS).
- To investigate the relationship between paraoxonase (PON1) activity and antiphospholipid antibodies (aPL) in SLE and APS patients.
- To identify methods for early atherosclerosis detection in SLE and APS.
Main Methods:
- Analysis of humoral and cellular immune responses to autoantigens (hsp, oxidized LDL, beta2-GPI).
- Assessment of autoantibody titers (anti-oxidized LDL, aPL, anti-beta2-GPL, anti-prothrombin) in SLE and APS patients.
- Measurement of paraoxonase (PON1) activity and its association with IgG anti-HDL and IgG anti-beta2-GPI antibodies.
- Utilizing Doppler carotid ultrasound for early atherosclerosis detection.
Main Results:
- Autoantigens expressed in atherosclerotic lesions elicit immune responses influencing lesion progression.
- Patients with SLE and APS exhibit accelerated atherosclerosis, not fully explained by traditional risk factors.
- Immunological alterations, including specific autoantibodies, are linked to premature atherosclerosis in SLE and APS.
- Reduced PON1 activity was associated with IgG anti-HDL and IgG anti-beta2-GPI antibodies in SLE and primary APS patients.
Conclusions:
- Specific autoantibodies and reduced PON1 activity are key factors in accelerated atherosclerosis in SLE and APS.
- Early detection using autoantibody titers and Doppler carotid ultrasound is crucial for managing atherosclerosis in these patients.
- Integrated therapeutic strategies, including early disease control and risk factor management, are essential to reduce morbidity and mortality.