In this eBook, we rethink the well-known challenges for advancing SLE research by providing innovative solutions to patient reach, recruitment, and biospecimen and data collection. You’ll learn how Sanguine’s patient-powered approach provides the pharmaceutical industry with an enhanced ability to recruit study participants and collect biospecimens and data through a mobile workforce across the United States. Our leading advantage – a mobile direct-to-patient approach – brings research participation into the patient’s home with a primary focus on establishing trusting relationships.
Introduction:
The diversity of genetic factors and variability in symptomatology complicates translational and clinical studies related to systemic lupus erythematosus (SLE, or lupus). As an autoimmune
disease, SLE has been linked to de novo or inherited mutations in various immune-related genes, as well as environmental triggers.3 Moreover, innate and adaptive immune dysfunction cause chronic multisystemic inflammation that progressively worsens over time. The manifestation of symptoms is often unpredictable and increasingly debilitating, with inflammatory flare episodes that have variable recurrence. Although some have chronic disease, most people suffering from SLE experience a recurring and remitting disease phenotype based on flare periods that range in severity and time.
The hallmark of SLE diagnosis is the detection of key autoantibodies, such as anti-nuclear antibodies that bind to DNA and RNA primarily. These autoantibodies, in addition to T cell and B cell
dysregulation, have key roles in cytokine induction and type I interferon stimulation, which drive inflammation.
Impressive scientific advances have extended SLE lifespan from a 4-year survival rate of ~50% in 1950 to a 15-year survival rate of ~85% as of 2013. (4) Even though the disease landscape continues to improve, SLE continues to take lives prematurely as a result of the morbidities that arise through disease progression. To that end, lupus nephritis, which is present in 40% to 70% of SLE patients, represents the most harmful and difficult-to-treat clinical feature that can lead to chronic renal failure.(5)
Although SLE therapeutic development lags when compared with other rheumatic diseases, the elucidation of new molecular pathways and potential therapeutic targets provides great hope to the future of SLE treatment options.