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Introduction
Lupus is a chronic autoimmune that can impact any part of the body resulting in a range of clinical symptoms. The affected part by Lupus may include brain, lungs, kidneys, skin, joints, blood vessels and other internal organs (Pisetsky, Gilkeson & St Clair, 1997). Lupus impacts the immune system by interfering with its capability of differentiating between antigens and normal healthy tissues. This incidence results in the misinterpretation by the immune system, and it directs the antibodies against the healthy tissues causing pain, tissue damage, and swelling. It is also known as systemic lupus erythematosus (SLE). In simple language, SLE makes the body allergic to itself. This situation is just reverse of cancer (Wallace, 2008). In SLE, the body’s immune system becomes over expressive and shows hyperactivity against the unknown stimulus, which stimulates the overproduction of antibodies (Wallace, 2008).
Types
There are several kinds of Lupus that are Systemic Lupus Erythematosus (SLE), cutaneous, and drug-induced. When autoimmune reactions are restricted to skin, then this stage is called cutaneous or discoid lupus erythematosus (DLE). SLE patients with the symptoms of fatigue, pain, and swollen glands but no internal organs associated symptoms are further categorized into the non-organ threatening disease. SLE, which involves the heart, kidneys, liver, lungs or severe blood abnormalities, is categorized as an organ-threatening disease. Lupus also develops as a response to any prescription drug, which is called drug-induced Lupus erythematosus, this is a less severe form (Wallace, 2008).
Epidemiology and incidence
The incidence of SLE is manifested under a criterion that includes three types namely skin, systemic and laboratory criteria. Skin criteria include butterfly rash, discoid rash, sun sensitivity and oral ulcerations. Systemic criteria include arthritis, serositis, kidney and neurologic disorders. Laboratory criteria include blood abnormalities, immunologic disorders, and positive ANA (Anti-Nuclear Antibody) blood tests (Tan et al., 1982). Lupus has impacted 1.5 million Americans and 90% impacted individuals are women, mostly between the ages of 15-44. The colored women are 2-3 times more prone to Lupus than Caucasians (Lupus Fact Sheet/Lupus Research Institute, 2016). DLE contributes to 10% of Lupus cases while SLE contributes to 70%. Non-organ and organ threatening disease are equally responsible for SLE (35%) while drug-induced lupus is attributed to 10% cases (Wallace, 2008).
History of Lupus
The earlier cases of Lupus were published in the 1800s, which were associated with skin deep internal organs. In the 1890s, the first writing on SLE was published by Sir William Osler that demonstrated the involvement of CNS, pulmonary and cardiac system to this disease. Between the 1920s and 1930s in the era of pathology, its pathologic descriptions were revealed. The next breakthrough was 1941 when it was assumed as collagen disease, but this approach led to the current classification of Lupus as an auto-immune disease. In 1948, Mayo Clinic pathologists described the LE cell that represented the systemic inflammatory process which was followed by the discovery of cortisone hormone in 1949 that showed the lifesaving impact on SLE patients. Finally, in 1950 SLE was confirmed to be a part of anti-nuclear antibody or ANA reaction (Wallace, 2008).
Etiology and pathophysiology
SLE is a multisystem inflammatory autoimmune condition which is manifested by uncontrolled hyper-reactivity of B and T lymphocytes that leads to the overproduction of autoantibodies. The main characteristic of the disease is the collapse of tolerance capabilities. There are multiple intrinsic and extrinsic mechanisms that include genetics, deficiency of regulatory T and B cells as well environmental and hormonal factors. It also shows familiar links as a sibling of SLE patient is twenty times more susceptible to develop the disease. In more than 90% cases, the genetic causes have been dominant that are associated with deficiencies in C1q, C2, C4 and CR1 receptor, mannose-binding lectin gene (MBL2) (Genetics of Systemic, 2016). Certain leukocyte antigens (Class-II) and tumour necrosis factor (TNF) gene variants are also associated with Lupus etiology. Environmental factors such as infections are another significant cause of mortality and morbidity in SLE patients (Cuchacovich & Gedalia, 2009).
Involved Microorganisms
Approximately 80% of SLE infections are triggered by bacteria that directly infect the respiratory tract, skin, and urinary tract. The disturbed IL12 release by polymorph nuclear cells among SLE patients is considered significant in acute infections such as bacterial pneumonia and urinary tract infection. Anti-granulocyte antibodies can develop into neutropenia due to cytotoxicity. The most frequent microorganisms observed in SLE patients are Staphylococcus aureus (Lupus Risk Linked to Staph Bacteria: Study, 2016), E. coli, Nontyphoidal Salmonella, Streptococcus pneumonia, Klebsiella spp Acinetobacter spp. and Haemophilus influenza. Other causative agents include Viruses that are Cytomegalovirus, Parvovirus B19, Herpes simplex/varicella zoster, Epstein-Barr virus and Human papillomavirus. It is also caused by certain fungi that include Candida spp, Cryptococcus neoformans, Aspergillus spp, Mycobacterium, Nocardia spp., Nontuberculous mycobacterium and Mycobacterium chelonae (Wallace, 2008). A recent study discovered that Staphylococcus aureus colonizing the nasal and skin tissues releases superantigen (SAg). The long term exposure to a small extent of this SAg is found associated with developing the SLE and may play a role in its etiology (Chowdhary et al., 2012).
Diagnosis and Treatment
Lupus is a very complex disease, difficult to diagnose. Its symptoms are very similar to other diseases and can change frequently. Thus, to diagnose the Lupus the doctors analyze a range of multiple tests along with medical history and physical exam, the tests includes ANA panel covering antiphospholipid, anti-Ro/SSA and anti-La/SSB. Other diagnostic laboratory tests include complete blood count, blood chemistries, Urine tests and complement levels.
Lupus is a very complex disease with a range of hundreds of symptoms. Thus the accurate cure and treatment are still under research. For mild cases, over the counter (OTC) pain relievers and anti-inflammatory therapeutic agents can be used. For advance stage of Lupus where internal organs are affected, various stronger agents are prescribed. Non-steroidal anti-inflammatory agents and cyclooxygenase inhibitors are used for their anti-inflammatory actions. For treating the DLE associated symptoms, anti-malarial drugs are used. Several other agents include corticosteroids and immune-suppressants. The interventions designed for Lupus focuses on certain lifestyle changes that can reduce the chances of symptoms exacerbations. Adopting a healthy lifestyle is the foremost recommendation for SLE patients. Avoiding sun exposure, proper rest, regular exercise, consuming a balanced diet with sufficient fruits and vegetables are recommended as a positive approach to fight the Lupus. The patient should be encouraged to be hygienically clean, use warm water and mild shampoos. The use of prophylactic pressure relieving devices is recommended to prevent skin breakdown (Gulanick Myers, 2013).
Various clinical studies have proposed novel therapies to avoid SLE. Lu et al. (2009), presented a seven-year analysis of using B cell depletion therapy for SLE patients. Using this immune-suppressive approach, the researchers have claimed positive effects of this therapy for SLE patients. Moreover, Burt et al. (2006), proposed a concept of using hematopoietic stem cells for severe and treatment-resistant SLE patients which have shown a potential for future SLE treatment options (Burt et al., 2006).
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