Systemic lupus erythematosus (SLE), commonly known as lupus, can affect nearly any part of the body, including the joints, skin, kidneys, heart, nervous system, and brain. Along with joint pain, muscle pain, unexplained fever, extreme fatigue, and skin rashes, neurologic and psychiatric events often accompany this autoimmune disease. Depending on the study, between 37 and 95 percent of SLE patients experience signs and symptoms of neuropsychiatric (NP) disease. Determining the correct attribution to NP events is a challenge when managing nervous system disease in individual SLE patients, as well as a critical factor in selecting the right treatment and evaluating progress. For guidance in these decisions, doctors need reliable biomarkers -- which, as dedicated researchers know, have proven difficult to find.
Generation of specific autoantibodies is one of the lupus-specific mechanisms underlying NP disease. Attempts to investigate their biomarker potential have been limited by the wide-ranging disease severity and duration of study patients, not to mention lack of standardization in both the classification of NP events and the methodology used for autoantibody detection. With the goal of overcoming these limitations, an international research alliance called the Systemic Lupus International Collaborating Clinics (SLICC) examined the association between a panel of autoantibodies and nervous system events at the time of diagnosis of SLE. Their results, presented in the March 2008 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), indicate two compelling links: one between anti-ribosomal P (anti-P) antibodies and psychosis attributed to SLE and the other between lupus anticoagulant (LAC) and cerebrovascular disease attributed to SLE.
Led by Dr. J.G. Hanly, a Rheumatologist at the Queen Elizabeth II Health Sciences Centre and Professor of
|Contact: Amy Molnar|