Systemic Lupus
Erythematosus
(SLE or Lupus)
Medical Author: William C. Shiel Jr., MD, FACP, FACR
Medical Editor: Melissa Conrad Stöppler, MD
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A Lupus Widower Laments to Friends
 By Mr. D.R.
Medical Editor: William C. Shiel Jr., MD, FACP, FACR
So many people have had comments like, "I had no idea Susan was so sick."
That was because Susan did not want anybody to know.
Because lupus is such a crafty disease and flies under the general public's
radar, this is a good opportunity to clear things up.
Lupus is an autoimmune disease, not an infectious disease like HIV. People
with lupus have an overactive immune system. The body's defenses actually attack
healthy tissue. This has been happening to Susan for 30 years or more.
She was diagnosed around 1990, but she had symptoms way before then.
Originally, the disease would manifest itself as flu-like symptoms for about
three weeks out of every three months, with fatigue extending a month after
every flare-up.
In 2000, lupus attacked her central nervous system and involved her brain.
The original result of this new development was pain. From late in January 2000
until the day before she died, she was in pain. On the scale of 1 to 10, there
was no day that she didn't feel pain on an 8 to 10 level. (With 10 being
all-encompassing.)
Lupus attacked her lungs, causing shortness of breath, sleeping problems, and
more pain in the form of pleurisy. In addition to Hashimoto's thyroiditis
(causing cold extremities) and Sjogren's syndrome (extremely dry eyes) and a few
more isms that I have forgotten, life was getting difficult.
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What is lupus? 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. Patients with lupus produce abnormal antibodies in their blood
that target tissues within their own body rather than foreign infectious agents.
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 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 to 45 years of age. Statistics
demonstrate that lupus is somewhat more frequent in African Americans and people
of Chinese and Japanese descent.
What causes lupus? Is it 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 patients 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, suggest that female
hormones play an important role in the expression of SLE. This hormonal
relationship is an active area of ongoing study by scientists.
More recently, 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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