In the United States, systemic lupus erythematosus is reported to be more common in women, particularly black women, than in white men.14,16 One U.S. retrospective study16 of medical records found that the disease is diagnosed 23 times more often in black women than in white men. The prevalence of the disease is also higher in Hispanic and Asian Americans.16 In addition, a familial predisposition to systemic lupus erythematosus has been identified.17-19
Neutrophils, 55% to 70% of all leukocytes, are the most numerous phagocytic cells and are a primary effector cell in inflammation. Eosinophils, 1% to 3% of total leukocytes, destroy parasites and are involved in allergic reactions. Basophils, less than 1% of all leukocytes, contain granules of histamine and heparin and are part of the inflammatory response to injury. Monocytes, 3% to 8% of all leukocytes, become macrophages and phagocytize pathogens and damaged cells, esp. in the tissue fluid. Lymphocytes, 20% to 35% of all leukocytes, have several functions: recognizing foreign antigens, producing antibodies, suppressing the immune response to prevent excess tissue damage, and becoming memory cells.
Systemic lupus erythematosus (SLE) is a complex multisystemic autoimmune disease resulting, oftentimes, in irreversible damage, diminished quality of life and reduced life expectancy.1–3 Genetic and environmental factors play important roles in its pathogenesis.4–8 Disease manifestations and severity vary according to the patients’ racial/ethnic background and socioeconomic status (SES).1 9 10 Data from Grupo Latino Americano de Estudio del Lupus (GLADEL), Lupus in Minorities: Nature vs Nurture (LUMINA) and the Lupus Family Registry and Repository cohorts have demonstrated that Latin American and North American Mestizo patients (mixed Amerindian and European ancestry), African descendants and Native Americans develop lupus earlier11 12 although diagnostic delays may occur.1 They also experience more severe disease, have higher disease activity levels,1 accrue more organ damage2 and have higher mortality rates,1 succumbing mainly to disease activity and/or infections.1 3 13–15
Nonsteroidal anti-inflammatory drugs (NSAIDs) are helpful in reducing inflammation and pain in muscles, joints, and other tissues. Examples of NSAIDs include aspirin, ibuprofen (Motrin), naproxen (Naprosyn), and sulindac (Clinoril). Since the individual response to NSAIDs varies, it is common for a doctor to try different NSAIDs to find the most effective one with the fewest side effects. The most common side effects are stomach upset, abdominal pain, ulcers, and even ulcer bleeding. NSAIDs are usually taken with food to reduce side effects. Sometimes, medications that prevent ulcers while taking NSAIDs, such as misoprostol (Cytotec), are given simultaneously.
Any of a group of glycoproteins with antiviral activity. The antiviral type I interferons (alpha and beta interferons) are produced by leukocytes and fibroblasts in response to invasion by a pathogen, particularly a virus. These interferons enable invaded cells to produce class I major histocompatibility complex surface antigens, increasing their ability to be recognized and killed by T lymphocytes. They also inhibit virus production within infected cells. Type I alpha interferon is used to treat condyloma acuminatum, chronic hepatitis B and C, and Kaposi’s sarcoma. Type I beta interferon is used to treat multiple sclerosis. Type II gamma interferon is distinctly different from and less antiviral than the other interferons. It is a lymphokine, excreted primarily by CD8+ T cells and the helper T subset of CD4+ cells that stimulates several types of antigen-presenting cells, particularly macrophages, to release class II MHC antigens that enhance CD4+ activity. It is used to treat chronic granulomatous disease.
Subacute Cutaneous Lupus can cause skin lesions on any part of the body. These lesions often form red, ring-shaped, scaly patches on the skin. These lesions do not itch and often appear on the chest as well as the upper back and neck; however, they may also be seen on the face and arms. Typically, these lesions occur on areas of the body that are exposed to sunlight or fluorescent lights. Furthermore, it is not uncommon for patients with SCLE to have associated joint disease.
Management of systemic lupus erythematosus (SLE) often depends on disease severity and disease manifestations,  although hydroxychloroquine has a central role for long-term treatment in all SLE patients. The LUMINA (Lupus in Minorities: Nature versus Nurture) study and other trials have offered evidence of a decrease in flares and prolonged life in patients given hydroxychloroquine, making it the cornerstone of SLE management. 
The first mechanism may arise genetically. Research indicates SLE may have a genetic link. SLE does run in families, but no single causal gene has been identified. Instead, multiple genes appear to influence a person's chance of developing lupus when triggered by environmental factors. HLA class I, class II, and class III genes are associated with SLE, but only classes I and II contribute independently to increased risk of SLE. Other genes which contain risk variants for SLE are IRF5, PTPN22, STAT4, CDKN1A, ITGAM, BLK, TNFSF4 and BANK1. Some of the susceptibility genes may be population specific.
Osteoarthritis is the most common form of arthritis, affecting millions of people around the world. Often called wear-and-tear arthritis, osteoarthritis occurs when the protective cartilage on the ends of your bones wears down over time. While osteoarthritis can damage any joint in your body, the disorder most commonly affects joints in your hands, neck, lower back, knees and hips. Osteoarthritis gradually worsens with time, and no cure exists. But osteoarthritis treatments can slow the progression of the disease, relieve pain and improve joint function.
To ensure that the person has lupus and not another autoimmune disease, the American College of Rheumatology (ACR) established a list of clinical and immunologic criteria that, in any combination, point to SLE. The criteria include symptoms that the person can identify (e.g. pain) and things that a physician can detect in a physical examination and through laboratory test results. The list was originally compiled in 1971, initially revised in 1982, and further revised and improved in 2009.
Mortality rates for systemic lupus erythematosus are particularly high in children. In a retrospective study26 of Brazilian children, overall mortality during 16 years of follow-up was 24 percent. Death occurred because of infection (58 percent), central nervous system disease (36 percent), and renal disease (7 percent). When disease onset was before the age of 15 years, renal involvement and hypertension predicted mortality.
While no single test can determine whether a person has lupus, several laboratory tests may help the doctor confirm a diagnosis, or at least rule out other ailments. The most useful tests identify certain autoantibodies that are often present in the blood of lupus patients. A biopsy of the skin or kidneys may also be ordered if those organs are affected. The doctor will look at the entire picture – medical history, symptoms, and test results – to determine if you have lupus. Other laboratory tests are used to monitor the progress of the disease once it has been diagnosed.
Anemia is common in children with SLE and develops in about 50% of cases. Low platelet and white blood cell counts may be due to the disease or a side effect of pharmacological treatment. People with SLE may have an association with antiphospholipid antibody syndrome (a thrombotic disorder), wherein autoantibodies to phospholipids are present in their serum. Abnormalities associated with antiphospholipid antibody syndrome include a paradoxical prolonged partial thromboplastin time (which usually occurs in hemorrhagic disorders) and a positive test for antiphospholipid antibodies; the combination of such findings have earned the term "lupus anticoagulant-positive". Another autoantibody finding in SLE is the anti-cardiolipin antibody, which can cause a false positive test for syphilis.
Since other diseases and conditions appear similar to lupus, adherence to classification can greatly contribute to an accurate diagnosis. However, the absence of four of these criteria does not necessarily exclude the possibility of lupus. When a physician makes the diagnosis of SLE, s/he must exclude the possibility of conditions with comparable symptoms, including rheumatoid arthritis, systemic sclerosis (scleroderma), vasculitis, dermatomyositis and arthritis caused by a drug or virus.
Neonatal lupus erythematosus (NLE) can develop in the babies of mothers with antibodies to SSA/Ro. Neonates with NLE can present with rash around 4-6 weeks of life, elevated liver function test results, thrombocytopenia around 1-2 weeks of life, neutropenia, and hydrocephalus.  NLE can also manifest as a congenital atrioventricular conduction block,  with as many as 1-5% of pregnancies in mothers with anti- SSA/SSB antibodies leading to heart block, rising to a 6-25% risk for subsequent pregnancies after one affected child is born. 
Most patients with systemic lupus erythematosus (unless they’re otherwise advised by their rheumatologist) should be taking an oral antimalarial drug — medications originally used to prevent a malaria infection, but that have been found to help with lupus symptoms, says Dr. Kramer. The antimalarial hydroxychloroquine helps prevent lupus flares, minimizes joint inflammation, and controls fever, fatigue, pleurisy (inflammation of the sac surrounding the lungs), and pericarditis (inflammation of the lining around the heart). The drug is also “the backbone of therapy” for most skin rashes associated with lupus, says Kramer. Mouth sores may also be alleviated with this drug. Chloroquine and quinacrine are other antimalarials drugs used to treat lupus. (3)
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