Sunday, June 10, 2012

Lupus erythematosus



Systemic lupus erythematosus (SLE) rash on the skin of the face in a male patient, an autoimmune disease where the immune system attacks the body's connective tissue, mainly in the skin, joints and kidneys.

Systemic lupus erythematosus facts

Systemic lupus erythematosus (SLE) is an autoimmune disease.
SLE is characterized by the production of unusual antibodies in the blood.
SLE is eight times more common in women than men.
The cause(s) of SLE is (are) unknown, however, heredity, viruses, ultraviolet light, and drugs all may play some role.
Up to 10% of people with lupus isolated to the skin will develop the systemic form of lupus (SLE).
Eleven criteria help doctors to diagnose SLE.
Treatment of SLE is directed toward decreasing inflammation and/or the level of autoimmune activity.
People with SLE can prevent "flares" of disease by avoiding sun exposure and not abruptly discontinuing medications and monitoring their condition with their doctor.

What is systemic lupus erythematosus? What are the types of lupus?

Lupus is an autoimmune disease characterized by acute and chronic inflammation of various tissues of the body. Autoimmune diseases are illnesses that occur when the body's tissues are attacked by its own immune system. The immune system is a complex system within the body that is designed to fight infectious agents, such as bacteria and other foreign microbes. One of the ways that the immune system fights infections is by producing antibodies that bind to the microbes. People with lupus produce abnormal antibodies in their blood that target tissues within their own body rather than foreign infectious agents. These antibodies are referred to as autoantibodies.

Because the antibodies and accompanying cells of inflammation can affect tissues anywhere in the body, lupus has the potential to affect a variety of areas. Sometimes lupus can cause disease of the skin, heart, lungs, kidneys, joints, and/or nervous system. When only the skin is involved, the condition is called lupus dermatitis or cutaneous lupus erythematosus. A form of lupus dermatitis that can be isolated to the skin, without internal disease, is called discoid lupus. When internal organs are involved, the condition is referred to as systemic lupus erythematosus (SLE).

Both discoid lupus and systemic lupus are more common in women than men (about eight times more common). The disease can affect all ages but most commonly begins from 20-45 years of age. Statistics demonstrate that lupus is somewhat more frequent in African Americans and people of Chinese and Japanese descent.


What causes systemic lupus erythematosus? Is lupus hereditary?

The precise reason for the abnormal autoimmunity that causes lupus is not known. Inherited genes, viruses, ultraviolet light, and certain medications may all play some role.

Genetic factors increase the tendency of developing autoimmune diseases, and autoimmune diseases such as lupus, rheumatoid arthritis, and autoimmune thyroid disorders are more common among relatives of people with lupus than the general population. Some scientists believe that the immune system in lupus is more easily stimulated by external factors like viruses or ultraviolet light. Sometimes, symptoms of lupus can be precipitated or aggravated by only a brief period of sun exposure.

It also is known that some women with SLE can experience worsening of their symptoms prior to their menstrual periods. This phenomenon, together with the female predominance of SLE, suggests that female hormones play an important role in the expression of SLE. This hormonal relationship is an active area of ongoing study by scientists.

Research has demonstrated evidence that a key enzyme's failure to dispose of dying cells may contribute the development of SLE. The enzyme, DNase1, normally eliminates what is called "garbage DNA" and other cellular debris by chopping them into tiny fragments for easier disposal. Researchers turned off the DNase1 gene in mice. The mice appeared healthy at birth, but after six to eight months, the majority of mice without DNase1 showed signs of SLE. Thus, a genetic mutation in a gene that could disrupt the body's cellular waste disposal may be involved in the initiation of SLE.

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