Response to apheresis: problems of assessment in immune disease.
Systemic lupus erythematosus (SLE) was one of the first diseases to be treated by plasmapheresis, because of the abundance of serological disturbances, and the strong evidence that tissue damage is related to the deposition of immune complexes. Early results in small, uncontrolled studies were promising, but no large-scale controlled trials have yet been reported. The conditions for which well-controlled trials are now available are either diseases affecting a single organ-system, in which clinical abnormalities are readily measurable, such as Guillain-Barre syndrome, or conditions in which serological abnormalities correlate closely with clinical disturbances, such as myasthenia gravis. Definitive answers are also available in rheumatoid arthritis, where many years of clinical experience have led to the development of well-validated indices of clinical activity. Many studies of SLE suggest that serological abnormalities, though important, are often not quantitatively linked to the clinical manifestations of the disease. Attempts to develop indices of clinical activity for SLE are handicapped by the range of different organ systems which may be involved. Progress in the development of clinical trials of plasmapheresis in SLE is most likely to result from multicenter cooperative groups, which will have the capacity to study large enough numbers of patients for adequate stratification, and from the development and validation of indices of clinical activity, which will make possible the quantitation of clinical response, and the measurement of the rate of accumulation of permanent organ damage.
D001172:Arthritis, Rheumatoid / Q000628:therapy; D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000628:therapy*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000628:therapy; D009157:Myasthenia Gravis / Q000628:therapy; D010391:Pemphigoid, Bullous / Q000628:therapy; D010392:Pemphigus / Q000628:therapy; D010956:Plasmapheresis; D011129:Polyradiculoneuropathy / Q000628:therapy
D001323:Autoantibodies