Search

The Lupus Foundation of America (LFA) convened an international working group to obtain a consensus definition of disease flare in lupus. With help from the Paediatric Rheumatology International Trials Organization (PRINTO), two web-based Delphi surveys of physicians were conducted. Subsequently, the LFA held a second consensus conference followed by a third Delphi survey to reach a community-wide agreement for flare definition. Sixty-nine of the 120 (57.5%) polled physicians responded to the first survey. Fifty-nine of the responses were available to draft 12 preliminary statements, which were circulated in the second survey. Eighty-seven of 118 (74%) physicians completed the second survey, with an agreement of 70% for 9/12 (75%) statements. During the second conference, three alternative flare definitions were consolidated and sent back to the international community. One hundred and sixteen of 146 (79.5%) responded, with agreement by 71/116 (61%) for the following definition: “A flare is a measurable increase in disease activity in one or more organ systems involving new or worse clinical signs and symptoms and/or laboratory measurements. It must be considered clinically significant by the assessor and usually there would be at least consideration of a change or an increase in treatment.” The LFA proposes this definition for lupus flare on the basis of its high face validity.

Sex hormone binding globulin (SHBG) is a transport protein in human plasma which regulates the bioavailability of sex hormones, mediates membrane receptor signaling and may affect inflammatory processes, suggesting a regulatory role for this protein in the prevention of atherosclerosis. The current report summarizes literature implicating several members of the SHBG family in the regulation of hormonal and inflammatory processes which may be pertinent to the accelerated atherosclerosis seen in systemic lupus.

The heterogenous immunoglobulins known as antiphospholipid antibodies (APLA) or . lupus 'anticoagulants' (LA) are prevalent in lupus patients and have been implicated in life-threatening thromboembolic events1-3. Unfortunately, observing the presence of these antibodies in an individual does not predict the likelihood of an event nor does it predict when it may occur4-6. A pathogenic role for these antibodies is supported by the observ ation that high titers and IgG isotype confer an increased risk of thromboembolism7. Addi tionally, numerous reports indicate that isolated patient antibodies interfere with various elements of the coagulation cascade8-15. Nevertheless, attempts to correlate specific anti body characteristics with the future likelihood of a hypercoagulable event in an individual patient16have been unsuccessful to date. Given such uncertainty combined with the poten tial complications of anticoagulant medications, patients are generally not treated until sig nificant morbidity has occurred. Finally, because of the apparent high rate of reoccurrence17most patients must remain on anticoagulant therapy indefinitely, regardless of need.