In addition, differences in GnRH signalling have also been shown to contribute to the onset of SLE. While females are more likely to relapse than males, the intensity of these relapses is the same for both sexes.In addition to hormonal mechanisms, specific genetic influences found on the X chromosome may also contribute to the development of SLE. Studies indicate that the X chromosome can determine the levels of sex hormones. A study has shown an association between Klinefelter syndrome and SLE. XXY males with SLE have an abnormal X–Y translocation resulting in the partial triplication of the PAR1 gene region. Changing rate of disease
The rate of SLE in the United States increased from 1.0 in 1955 to 7.6 in 1974. Whether the increase is due to better diagnosis or an increased frequency of the disease is unknown. History
The history of SLE can be divided into three periods: classical, neoclassical, and modern. In each period, research and documentation advanced the understanding and diagnosis of SLE, leading to its classification as an autoimmune disease in 1851, and to the various diagnostic options and treatments now available to people with SLE. The advances made by medical science in the diagnosis and treatment of SLE have dramatically improved the life expectancy of a person diagnosed with SLE. Etymology
There are several explanations ventured for the term lupus erythematosus. Lupus is Latin for "wolf", and "erythro" is derived from ερυθρός, Greek for "red". All explanations originate with the reddish, butterfly-shaped malar rash that the disease classically exhibits across the nose and cheeks.
Hypocomplementemia is also seen, due to either consumption of C3 and C4 by immune complex-induced inflammation or to congenitally complement deficiency, which may predispose to SLE. Renal disorder: More than 0.5 g per day protein in urine or cellular casts seen in urine under a microscope; sensitivity = 51%; specificity = 94%. Antinuclear antibody test positive; sensitivity = 99%; specificity = 49%. Immunologic disorder: Positive anti-Smith, anti-ds DNA, antiphospholipid antibody, or false positive serological test for syphilis; sensitivity = 85%; specificity = 93%. Presence of anti-ss DNA in 70% of cases (though also positive with rheumatic disease and healthy persons). Neurologic disorder: Seizures or psychosis; sensitivity = 20%; specificity = 98%.Other than the ACR criteria, people with lupus may also have:
Fever (over 100 °F/ 37.7 °C)
Extreme fatigue
Hair loss
Fingers turning white or blue when cold (Raynauds phenomenon)

Criteria for individual diagnosis
Some people, especially those with antiphospholipid syndrome, may have SLE without four of the above criteria, and also SLE may present with features other than those listed in the criteria.Recursive partitioning has been used to identify more parsimonious criteria. This analysis presented two diagnostic classification trees:

Simplest classification tree: SLE is diagnosed if a person has an immunologic disorder (anti-DNA antibody, anti-Smith antibody, false positive syphilis test, or LE cells) or malar rash. It has sensitivity = 92% and specificity = 92%. Full classification tree: Uses 6 criteria. It has sensitivity = 97% and specificity = 95%.Other alternative criteria have been suggested, e.g. the St. Thomas Hospital "alternative" criteria in 1998.