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Is lupus hereditary?
It is suspected that people inherit something from their parents that predisposes them to develop lupus. They are not necessarily pre-destined to develop lupus, but they may be more susceptible. Relatives of lupus patients have an approximate 5-12% greater tendency to get the disease if family members have it.
Heredity does seem to play a role. Ten percent of lupus patients have a first-degree relative (sister, daughter, son, mother) or a second-degree relative (aunt, uncle, first cousin) with lupus. Therefore, 90 percent of lupus patients DO NOT have relatives with lupus. Even in identical twins, when one sibling has lupus and the other twin does not, it is believed there are environmental factors that play an important role.
The precise reason for the abnormal autoimmunity that causes lupus is not known. Inherited genes, viruses, ultraviolet light, and drugs may all play some role. Genetic factors increase the tendency of developing autoimmune diseases, and autoimmune diseases such as lupus, rheumatoid arthritis, and immune 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. The 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.