Systemic Lupus Erythematosus Autoimmune Disorder

Systemic Lupus Erythematosus autoimmune DisorderAUTOIMMUNE DISORDERSThe immune governing body is an important system inwardly the human consistency that defends against indisposition and internal malfunction. When there is an invader or a pathogen, the bodys immune system responds accordingly, usually destroying the pathogen before it can infect the body and ca work illness. The immune system also helps identify malfunctioning cells and eliminates them before faulty DNA is replicated. Autoimmune disorders occur when the immune system of a persevering no longer identifies foreign versus self correctly. The immune system of a patient with an autoimmune disorder will attack the bodys cells or tissues causing wrongfulness or death. (Lettre Rioux, 2008).Autoimmune disorders can be genetically predisposed, but just because a patient is predisposed to a particular disorder does not taut they will necessarily experience it. Often times, autoimmune disorders occur through a combinatio n of genetic predispositions and environmental factors. This means a patient whitethorn have a genetic predisposition for systemic lupus erythematosus but the disorder is triggered by an invading virus the patient encounters and only thereafter do they digest from the symptoms of SLE. There are now 68 genetic precursors that are linked to the development of autoimmune disorders, while in the past only about 15 had been identified. Symptoms of autoimmune diseases vary depending on what part of the body the immune system is attacking (Understanding Autoimmune Diseases, 2016) (Lettre Rioux, 2008).Within the immune system there are some(prenominal) types of cells. B-cells and T-cells play key roles within the immune system and in autoimmune diseases. There are two types of T-cells, CD4 T-helper cells that identify an invader and make the antibody creating B-cells aware and CD8 cytotoxic T-cells which will destroy a previously encountered threat without stimulating the creation of ant ibodies by B-cells. CD4 T-cells are also known as regulatory T-cells (Treg cells). These Tregs play a role in preventing autoimmunity by maintaining the ability to identify self. When these cells no longer identify self properly or at all, an autoimmune disease occurs. When T-helper cells do not identify self-versus-foreign properly they stimulate B-cells to create antibodies to destroy the bodys tissues or cells, called autoantibodies, or the cytotoxic T-cells will destroy the tissue or cells of oneself. (Venes et al., 2005, pp. 132, 135, 203, 204) (Corthay, 2009) (Hampe, 2012).SLE or Systemic Lupus Erythematosus is an autoimmune disease most commonly characterized by joint inconvenience oneself (arthralgia) and swelling (edema). SLE can also cause fatigue, mouth sores, aesthesia to sunlight, and butterfly rash across the cheeks and nose of the face, and hair loss. Other symptoms depend on where the body is being attacked by the immune system. For instance, if the immune system o f a patient with SLE is attacking the heart of the patient an additional symptom of arrhythmia may be experienced. (Systemic Lupus Erythematosus, 2016).Diagnosis of SLE can be operose as it can be associated with varying symptoms. A test known as antinuclear antibody test (ANA) is used to help diagnose SLE. An antinuclear antibody is an antibody created by the patients immune system to attack the bodys tissues and cells. Some ANA tests are enzyme-linked immunosorbent assay (ELISA) and indirect florescent antibody (IFA). These tests examine how many antinuclear antibodies are present in a patients blood. ANA tests are used when the autoimmune disease may be call foring more than one area of the body this is called a systemic autoimmune disease. Because SLE is systemic, an ANA test helps confirm that SLE is the diagnosis as opposed to rheumatoid arthritis. However, having a positive ANA test does not mean that a patient has SLE. SLE is often misdiagnosed as rheumatoid arthritis bec ause they distribute common symptoms such as edema and arthralgia this is why doctors often use an assortment of other tests to diagnose SLE, along with a physical exam as four of the eleven common symptoms of SLE must be present before a patient can be diagnosed. Some of those common symptoms were listed to a higher place butterfly rash across the face, joint pain, sensitivity to sunlight, hair loss, fatigue, and edema. (Antinuclear Antibody, 2017)(Starkebaum, 2016)(Bocco, 2017).Systemic Lupus Erythematosus can be case-hardened but not cured. Because it is an autoimmune disease, SLE is treated with immunosuppressants. Hydroxychloroquine (HCQ) is an immunosuppressant that slows down the immune system and its attack on the bodys tissues and cells. HCQ was originally used in the treatment of malaria and is known as a disease-modifying anti-rheumatic medicate (DMARD). It is recommended that patients diagnosed with SLE immediately start a HCQ regiment as this drug help prevent shap e up damage from the disease process. HCQ is usually used in chorus with other pain relief drugs because HCQ itself does not provide immediate pain relief. NSAIDS (nonsteroidal anti-inflammatory drugs) are often used in joint pain management for patients with SLE. Over time, HCQ will help relieve joint pain in SLE sufferers as well as help stop further damage to any other affected organs and joints. Corticosteroids are often also prescribed to those with SLE as joint pain is a fully grown symptom of SLE. Corticosteroids mimic naturally produced strong anti-inflammatory substances within the body. However, treatments come with jeopardize factors. In rare cases, HQC can cause retinopathy retinopathy is when vision is transfigureed or complete blindness occurs. Likewise, long term use of corticosteroids has adverse effects including osteoporosis, hyperglycemia (high blood sugar), and cataracts. Dosage of corticosteroids are adjusted for long term use in patients with SLE to avoid th ese side effects and routine eye exams are done on those using HCQ to prevent retinopathy. (Plaquenil (hydroxychloroquine), 2014) (Bartels, 2016) (Mayo Clinic Staff, 2015).Systemic Lupus Erythematosus predominantly affects women. search suggests this is due in part to oestrogen. For every one man diagnosed with SLE, there are nine to twenty women diagnosed. Within the population of women who are at risk for SLE, women who are not white are at a higher risk for SLE as well as women under the age of 15 and over the age of 45. The discrepancy in race may have to do with the fact that colored females have higher recorded levels of estrogen than do white females. Estrogen is thought to make women more susceptible to an autoimmune disease such as SLE because of its intracellular transcription ability to alter DNA. The effects of estrogen have also been studied holistically in association with the disease. Estrogen may encourage systemic inflammation in SLE and affect the severity of the disease and acute instances of it. Although estrogen has been identified as causing inflammation it has also been identified as prohibiting inflammation thus meaning estrogen can act oppositely as it does in SLE in terms of another autoimmune disease. The discrepancy between the genders cannot completely be accounted for mainly with estrogen levels, however. Sex hormones are not the only determining factor for autoimmune diseases, others include epigenetics, infections, genetics, and external environment. (Pierdominici Ortona, 2013, pp. 25-27) (Khan Ahmed, 2015) (Isherwood Witter, 2012)ReferencesAntinuclear Antibody (ANA). (2017, troop 22). Retrieved March 23, 2017, from Lab Tests Online website https//labtestsonline.org/understanding/analytes/ana/ contraceptive pill/test/Bartels, C. M. (2016, September 19). Systemic Lupus Erythematosus (SLE) Treatment and Management (H. S. Diamond, Ed.). Retrieved March 23, 2017, from Medscape website http//emedicine.medscape.com/article/33224 4-treatmentBocco, D. (2017, January 3). The Difference Between Lupus and RA (N. Carteron, Ed.). Retrieved March 23, 2017, from Healthline website http//www.healthline.com/health/lupus-and-raOverview1Corthay, A. (2009, June 27). How do Regulatory T Cells Work? Retrieved March 22, 2017, from NCBI website https//www.ncbi.nlm.nih.gov/pmc/articles/PMC2784904/Hampe, C. S. (2012, September 23). B Cells in Autoimmune Diseases. Retrieved March 22, 2017, from Hindawi website https//www.hindawi.com/journals/scientifica/2012/215308/Hansen, M. S., Schuman, S. G. (2011, June). Hydroxychloroquine-Induced Retinal Toxicity. Retrieved March 23, 2017, from American Academy of Ophthamology website https//www.aao.org/eyenet/article/hydroxychloroquine-induced-retinal-toxicityIsherwood, D., Witter, J. (2012, July 16). Lupus fact sheet (B. Diamond, Ed.). Retrieved March 24, 2017, from Womenshealth.gov website https//www.womenshealth.gov/publications/our-publications/fact-sheet/lupus.htmlKhan, D., Ahmed, S. A. (2015, December 3). The Immune System Is a Natural Target for Estrogen Action Opposing Effects of Estrogen in Two Prototypical Autoimmune Diseases. Retrieved March 24, 2017, from NCBI website https//www.ncbi.nlm.nih.gov/pmc/articles/PMC4701921/Mayo Clinic Staff. (2015, November 26). Prednisone and other corticosteroids. Retrieved March 23, 2017, from Mayo Clinic website http//www.mayoclinic.org/steroids/art-20045692?pg=2Pierdominici, M., Ortona, E. (2013). Estrogen Impact on Autoimmunity Onset and Progression the Paradigm of Systemic Lupus Erythematosus. global Trends in Immunity, 1(2), 24-34. Retrieved from http//researchpub.org/journal/iti/number/vol1-no2/vol1-no2-3.pdfPlaquenil (hydroxychloroquine). (2014, February 10). Retrieved March 23, 2017, from Netdoctor website http//www.netdoctor.co.uk/medicines/aches-and-pains/a7356/plaquenil-hydroxychloroquine/Starkebaum, G. A. (2016, January 16). Systemic lupus erythematosus. Retrieved March 23, 2017, from MedlinePlus website https//medlineplus.gov/ency/article/000435.htmUnderstanding Autoimmune Diseases. (2016, March). Retrieved March 22, 2017, from National Institute of Arthritis and Musculoskeletal and cutis Diseases website https//www.niams.nih.gov/%5C/Health_Info/Autoimmune/default.aspVenes, D., Biderman, A., Adler, E., Fenton, B. G., Enright, A. 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