Global trends, potential mechanisms and early detection of organ damage in SLE

Nat Rev Rheumatol. 2013 May;9(5):301-10. doi: 10.1038/nrrheum.2012.208. Epub 2012 Dec 11.

Abstract

Increased longevity of patients with systemic lupus erythematosus (SLE) leads to chronic organ damage accrual, which reduces the possibility of further survival improvement in patients with the disease. Observations from lupus centres worldwide revealed that the prevalence of damage occurring in the cardiovascular system in patients with SLE has increased over the past four decades. The results of a meta-analysis involving over 70 observational studies demonstrated that lupus-related organ damage involving the neuropsychiatric and renal systems also remains a major factor that limits survival improvement in patients with this disease. While efforts to halt acute lupus-related injury are continuing, through early diagnosis and effective use of immunosuppressive agents, a concomitant strategy to improve survival of patients with SLE would be early detection and timely treatment of lupus-related organ damage with meticulous monitoring. This Review discusses the pattern and trend of organ damage in patients with SLE worldwide, the potential serological and genetic mechanisms of organ damage, and the advances in research on potential tools for early detection of lupus-related organ damage, such as functional brain imaging techniques, measurement of endothelial function, identification of biomarkers from body fluids, and development of risk calculation models.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis / diagnosis
  • Atherosclerosis / etiology*
  • Cognition Disorders / diagnosis
  • Cognition Disorders / etiology*
  • Early Diagnosis
  • Humans
  • Lupus Erythematosus, Systemic / complications*
  • Lupus Erythematosus, Systemic / diagnosis*
  • Lupus Nephritis / complications
  • Osteoporosis / diagnosis
  • Osteoporosis / etiology*
  • Renal Insufficiency, Chronic / diagnosis
  • Renal Insufficiency, Chronic / etiology*