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The immune system is an important system within the human body that defends against disease and internal malfunction. When there is an invader or a pathogen, the body’s immune system responds accordingly, usually destroying the pathogen before it can infect the body and cause 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 patient no longer identifies foreign versus self correctly. The immune system of a patient with an autoimmune disorder will attack the body’s cells or tissues causing damage or death. (Lettre & Rioux, 2008).
Autoimmune disorders can be genetically predisposed, but just because a patient is predisposed to a particular disorder does not mean they will necessarily experience it. Often times, autoimmune disorders occur through a combination of genetic predispositions and environmental factors. This means a patient may 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 suffer 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 several 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 antibodies 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 body’s 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 pain (arthralgia) and swelling (edema). SLE can also cause fatigue, mouth sores, sensitivity 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 of 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 difficult 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 patient’s immune system to attack the body’s 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 patient’s blood. ANA tests are used when the autoimmune disease may be affecting 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 because they share 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 above: ‘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 treated 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 body’s tissues and cells. HCQ was originally used in the treatment of malaria and is known as a disease-modifying anti-rheumatic drug (DMARD). It is recommended that patients diagnosed with SLE immediately start a HCQ regiment as this drug help prevent further 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 prominent symptom of SLE. Corticosteroids mimic naturally produced strong anti-inflammatory substances within the body. However, treatments come with risk factors. In rare cases, HQC can cause retinopathy; retinopathy is when vision is altered 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 these 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. Research suggests this is due in part to estrogen. 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 primarily 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)
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