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Etiology and Risk Factors
In the general population, SLE affect appoximately 1 in 2000 individuals.
Incidence rates have increased over the past 40 years, most likely because of an
increased availability of serologic tests and increased awareness of the diseases.
The disease has a predilection for women in their childbearing years, with young
african-american women the majority group affected. The prevalence of SLE
varies with race, etnicity, and socioeconomic status. The lupus foundation
america (www.lupus.org) estimates that 1.500.000 Americans have either
systemic or limited forms of lupus. The female to male prevalence ratio is 10:1
for women in the childbearing years. However, men and african-american
females have a worse renal outcome than women.
Once considered a fatal disease in young women, SLE now has improved
outcomes. Over 85% of people with the disorder live longer than 15 years after
diagnosis. Increased mortality, however, has been noted in african americans,
asians, puerto ricans, and people of hispanic descent living in the southwest
united states. Poor survival has been associated with high serum creatinine
levels, low hematocrit levels, proteinuria, and the source of medical care funding.
The most common causes of death in SLE are active lupus nephritis, vascular
events, and infections.
An underlying hormonal change may explain why the disease affects so many
more woman. Genetic factors may also be involved. Familial aggregationn occurs
in 10% of people having a first-degree relative with SLE, including its occurance
in identical twins.
The pathologic findings of SLE occur throughtout the body and are manifestased
by inflammation, blood vessel abnormalities that encompass both bland
vasculopathy and vasculitis, and immune complex deposition. SLE results from
an abnormal reaction of the body against its own tissues, cells, and serum
proteins. In the other words, as an autoimune disease, SLE is characterized by a
decreased self tolerance. In the north american caucasian population, there is a
positive association between SLE and two HLA antigens (DR2 dan DR3) that are
coded by the MHC. People with SLE have increased numbers of both self and
non-self antigens, suggesting hyperactivity of the B cells. Interleukin-6 may have
a role in B-cells hyperactivity. Another antibody, anti-DNA of the IgG type, may
be responsible for the development of the engulfed LE bodies in the LE cells. The
relationship between the serum LE factor and the pathologic changes that occur
with SLE is not clear. The absence of the LE factor, however, is a strong
indication that the disease is not (anti-dsDNA) antibodies are associated with
increased disease activity in clients with SLE