Systemic Lupus Erythematosus (SLE) is a chronic, potentially fatal autoimmune disease characterized by exacerbations and remissions with many clinical manifestations, and may mimic infectious mononucleosis, lymphoma or other systemic disease. SLE is a complex disorder resulting from the production of antibodies that attack the DNA and proteins within healthy cells and the generation of circulating immune complexes. The complications from this involve multiple organs and are potentially life-threatening. The hallmark of the disease is recurrent, widespread, and diverse vascular lesions. The idea that lupus is generally a fatal disease is one of the gravest misconceptions about this illness. In fact, the prognosis of lupus is much better today than ever before. It is true that medical science has not yet developed a method for curing lupus and some people do die from the disease. However, with current methods of therapy, deaths from lupus are uncommon, and 80-90% of people with lupus live more than 10 years after diagnosis.

There is clinical involvement of the joints, skin, kidney, brain, and membranes of the lung, heart and gastrointestinal tract. The symptoms are often vague, can be mild or severe and are often unrelated to lab tests. A patient can have many lupus symptoms in a lifetime. Women and non-Caucasians are disproportionately affected and SLE is most common in women of child-bearing age although it has been reported in all ages. The incidence is about 1 in 200 people in America.

Among children, SLE occurs three times more commonly in females than in males. In the 60% of SLE patients who experience onset between puberty and the fourth decade of life, the female to male ratio is 9:1. The disorder is three times more common in African American blacks than American Caucasians. SLE is also more common in Asians.

The cause of SLE remains unknown. A genetic predisposition, sex hormones, and environmental trigger(s) are strongly implicated in this disordered immune response. One of many suspected factors is a genetic mutation that disrupts the body's waste disposal mechanism in cells. The health status of a patient with SLE is related not only to disease activity, but also to the damage that results from recurrent episodes of disease flareups.

A tentative diagnosis can be made through examining a patient's medical history and performing a physical exam and screening tests (positive ANA). Once SLE is suspected, additional tests are valuable to confirm or rule it out. These include anti-double stranded DNA, anti-RNP, anti-Sm, anti-Ro, anti-La, C3, and C4. 30-70% of patients with SLE will be anti-DNA positive. 30% of patients with SLE will be anti-Sm positive. The presence of anti-double stranded DNA antibodies and low complement levels strongly suggests the diagnosis of lupus and identifies the patient at increase risk of kidney damage.

Treatment
The majority of lupus symptoms are due to inflammation and so the treatment is aimed at reducing that inflammation. There are four families of medications used in the treatment of lupus - Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, antimalarials, and cytotoxic drugs.

The treatment of infections in lupus patients is basically the same as for other patients. To prevent possible infections, patients at high risk of infection often benefit from taking antibiotics before dental treatment or surgical procedures. In general, individuals with lupus should avoid exposure to people with colds or other infections.