Risk Factors and Causes for Systemic Lupus Erythematosus (SLE)
Lupus results from an abnormal immune system response, the exact cause of which is unknown. The condition appears to result from the interaction of genetic (inherited), hormonal, and environmental factors.
A number of genes related to SLE have been identified. Fortunately, most people who inherit these genes do not develop SLE. In people who have these genes, other environmental or hormonal factors are necessary to trigger the condition. SLE may develop when the immune system mistakes normal cells in the body for foreign cells, possibly following an environmental trigger, such as an infection with an invading organism (e.g., virus) that is similar to normal proteins in the body. Other environmental triggers include exposure to the sun and certain medications.
Studies have shown that women are more likely to experience autoimmune disorders, such as SLE than men, which may help to explain the higher prevalence of lupus in women. The prevalence of lupus in women of childbearing age (i.e., after puberty and before menopause) may indicate that hormone production or the metabolism (physical and chemical processes) of hormones can also contribute to the condition. In addition, lupus symptoms can worsen during periods of female hormone changes (e.g., pregnancy and during the menstrual cycle).
In rare cases, medications (e.g., procainamide [Pronestyl®], hydralazine [Apresoline®]) can cause a syndrome that is similar to SLE (called drug-induced lupus). This condition, which has a genetic risk factor, causes general symptoms (e.g., fever, malaise), joint pain (arthralgia) and inflammation (polyarthritis), and inflammation of the membranes surrounding the lungs (pleurisy) and heart (pericarditis).
Patients who experience drug-induced lupus are withdrawn from the medication and symptoms usually improve within a few weeks. In severe cases, corticosteroids are administered for 2 to 10 weeks.