1 / 10

Systemic lupus erythematosus (SLE)

Systemic lupus erythematosus (SLE). Presented by Rachael Haun & Avery Medina. Image From http://www.medicinenet.com/image-collection/systemic_lupus_erythematosus_1_picture/picture.htm. Introduction. “Prototype” autoimmune disease Typically seen in women of childbearing age (Mock, 2011)

nuncio
Télécharger la présentation

Systemic lupus erythematosus (SLE)

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Systemic lupus erythematosus (SLE) Presented by Rachael Haun & Avery Medina Image From http://www.medicinenet.com/image-collection/systemic_lupus_erythematosus_1_picture/picture.htm

  2. Introduction • “Prototype” autoimmune disease • Typically seen in women of childbearing age (Mock, 2011) • Cause officially unknown • Genetic predisposition coupled with environmental trigger? • More common in African American, Hispanic, Asian & Native American populations (National Institute of Arthritis, Musculoskeletal and Skin Diseases, 2009)

  3. Introduction • Defect: Mechanisms of lupus still poorly understood • Body loses “self-tolerance” • Abnormal DNA methylation leads to over-expression of genes resulting in autoimmunity • The body forms its own antibodies to nuclear components (antigens) • Abnormal T cells • activate B cells, create autoantibodies • Exacerbate autoimmune response and autoantibody formation (Gorelik & Richardson, 2010)

  4. Introduction • Autoantibodies Image from: http://www.nature.com/nri/journal/v4/n10/fig_tab/nri1456_F1.html

  5. Brief History and Diagnostics • Characteristic “butterfly rash” first described by physician Rogerius in 13th century  • Kaposi (1872) described other systemic features: arthritis & psychosis • Current estimated incidence in US: 40-50 per 100,000 cases • Life expectancy: 5 years of diagnosis (10%) • Many deaths result from long term treatment & immunosuppression • Current diagnostic tests: American College of Rheumatology criteria (4 of 11) • Antinuclear antibody (ANA), malar rash, discoid rash on cheeks, photosensitivity (sunlight), painless mucocutaneous ulcers, nonerosive arthritis (2+ joints), renal dysfunction (proteinuria/cellular casts), neurologic disorder (seizure/psychosis), serositis (pleuritis/pericarditis), hematologic disorders (anemia, thrombocytopenia, leukopenia), immunologic dysfunction • Other tests • complete blood count; urinalysis; serum creatinine level; antiphospholipid antibodies

  6. Clinical Consequences of Untreated Disease • Can affect any bodily tissue • Can damage joints, heart, lungs, kidneys, blood vessels, skin and brain • Symptoms are unpredictable and vary • Pain, swelling, fatigue, anemia, rashes/photosensitivity, ulcers and more… (UMMC, 2011) Image from: http://www.medicinenet.com/lupus_pictures_slideshow/article.htm

  7. Clinical Consequences of Untreated Disease • 90% of those with SLE have a 10 year survival rate, 63-75% have a 20 year survival rate (UMMC, 2011) • Kept unchecked, SLE can be fatal • Why? • The body is attacking itself! Widespread damage, often to major organs Image from: http://kronstantinople.blogspot.com/2011/07/lupus-rash-quest-for-truth.html

  8. Recent Research: RAGE polymorphisms • Study conducted in 2012 at University Medical Center Groningen, Netherlands • Compared patients suffering from SLE and lupus nephritis to healthy controls • Found that RAGE polymorphisms associated with pro-inflammatory response had significant involvement with susceptibility to SLE, severity of LN symptoms

  9. References • Gorelik, G., & Richardson, B. (2010). Key role of erk pathway signaling in lupus. Autoimmunity, 43(1), 17-22. doi: 10.3109/08916930903374832 • Martens, HA, Nienhuis, HLA, Gross, S, der Steege, G van, Brouwer, E, Berden, JHM, Sévaux, RGL de, Derksen, RHWM, Voskuyl, AE, Berger, SP, Navis, GJ, Nolte, IM, Kallenberg, CGM, Bijl, M (2012). Receptor for advanced glycation end products (RAGE) polymorphisms are associated with systemic lupus erythematosus and disease severity in lupus nephritis. Lupus, 21(9). pg 959-968. • Mok, C. C. (2011). Epidemiology and survival of systemic lupus erythematosus in Hong Kong Chinese. Lupus, 20(7), 767-771. doi:10.1177/0961203310388447

  10. References • National Institute of Arthritis, Musculoskeletal and Skin Diseases. (2009, Oct.). What is lupus?. Retrieved from http://www.niams.nih.gov/Health_Info/Lupus/lupus_ff.a sp • Robinson, M, Sheets Cook, S, and Currie, LM (2011). Systemic lupus erythematosus: A genetic review for advanced practice nurses. Journal of the American Academy of Nurse Practitioners, 23(12). pg 629-637. • UMMC. (2011). Systemic lupus erythematosus. Retrieved from http://www.umm.edu/altmed/articles/systemic-lupus- 000161.htm

More Related