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Published on: October 12, 2017

[Hyperhomocysteine like thrombocytic risk factor in patient with systemic lupus erythematous with antiphospholipid

Laura Onetti1, Susana Villafañe, Emilia Menso

  • 1Servicio de Reumatologia - U.H.M.I 1, Hospital Nacional de Clinicas, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba.

Revista De La Facultad De Ciencias Medicas (Cordoba, Argentina)
|November 12, 2005
PubMed

Insights

Hyperhomocysteinemia (high Hcy) is prevalent in Systemic Lupus Erythematosus (SLE) patients, particularly those with antiphospholipid syndrome. Elevated Hcy levels correlate with antiphospholipid antibodies, suggesting a link to thrombotic events.

Area of Science:

  • Rheumatology
  • Clinical Chemistry
  • Immunology

Context:

  • Systemic Lupus Erythematosus (SLE) is an autoimmune disease with increased thrombotic risk.
  • Antiphospholipid syndrome (APS) is a major contributor to morbidity and mortality in SLE patients.
  • Hyperhomocysteinemia (Hcy > 9) is a potential risk factor for thrombosis.

Purpose:

  • To determine the prevalence of hyperhomocysteinemia in SLE patients with and without antiphospholipid syndrome.
  • To compare Hcy levels between SLE patients and healthy controls.
  • To investigate the correlation between hyperhomocysteinemia and antiphospholipid antibodies in SLE.

Summary:

  • This study included 44 SLE patients (17 with APS, 27 without) and 24 healthy controls.
  • Prevalence of hyperhomocysteinemia was 61.4% in SLE patients.
  • Elevated Hcy levels were significantly higher in SLE patients compared to controls (p=0.002), and in SLE patients with APS (p=0.003) and without APS (p=0.015) versus controls.
  • A significant association was found between hyperhomocysteinemia and anticardiolipin antibodies (aCL(+)) in SLE patients (75% of aCL(+) patients had hyperhomocysteinemia).

Impact:

  • Findings highlight hyperhomocysteinemia as a common metabolic abnormality in SLE.
  • The correlation between Hcy and antiphospholipid antibodies suggests a shared pathway in thrombosis pathogenesis.
  • This research may inform targeted interventions for managing thrombotic risk in SLE patients.
Abstract

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