Lupus erythematosus (LE), an autoimmune disorder that encompasses a broad spectrum of clinical and laboratory manifestations, denies any solitary explanation as to cause and pathogenesis. Search for such ascertainment has spawned a wide range of clinical and laboratory investigations, the most noteworthy of these being the identification of circulating autoantibodies. The development of these antibody-antigen systems is purported to be the consequence of a defective suppressor T-cell regulatory mechanism1-3; whether this represents cause or effect, however, has yet to be clarified.
More important than this consideration, however, has been the application of these serological markers to clinical use. Consequently, the demonstration of antibodies to nuclear and cytoplasmic antigens in a patient's serum samples has been considered to be the sine qua non for diagnosis and classification of systemic LE (SLE). Such developments have been embraced by the physician with much enthusiasm but yet with some consternation. There is concern
Wechsler HL. Lupus ErythematosusA Clinician's Coign of Vantage. Arch Dermatol. 1983;119(11):877-882. doi:10.1001/archderm.1983.01650350005005