Introduction
Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune rheumatic disease characterized by autoantibody production towards nuclear antigen.1 Almost all patients with SLE have antinuclear antibodies (98%), and some also have autoantibodies against double-stranded DNA (dsDNA) (76%), hypocomplementemia (71%), and antibodies to Ro (SSA) (35%). SLE has a wide range of clinical symptoms and the potential to affect nearly all organs and tissues.2
In the 1970s, a pulse dose of 500-1000 mg/day for 1 to 3 days of MEP was established to treat life-threatening complications associated with SLE.3 Pulse-dose MEP is the fastest immunosuppression therapy for life- or organ-threatening SLE.3 It is effective for renal involvement and other severe symptoms such as pulmonary hemorrhage and neuropsychiatry.3 Conventional treatment with intravenous MEP can reduce activity and complement activation in lupus nephritis.3 However, some patients continue to develop increasing renal impairment, and even those with favorable responses are at risk for relapse. Currently, objective measures to estimate the rate of response to pulse-dose MEP are unavailable, and the safety profile for the increased risk of infection is high.
Sixty to seventy percent of SLE patients have elevated blood BAFF levels, which positively correlate with SLEDAI 2k and anti-dsDNA levels.4 In addition, the BLISS-52 clinical trial demonstrated that belimumab, an inhibitor of BAFF, can reduce serology activity, prevent flares, and reduce corticosteroid use.5 A study by Milz et al. showed that blood BAFF levels were elevated compared to healthy controls in different autoimmune diseases, such as Idiopathic Thrombocytopenic Purpura (ITP), and that Glucocorticoid (GC) therapy dramatically reduces serum BAFF levels.6 This may be related to GC receptor binding in the promoter region.6
Interferon-gamma-induced protein 10 is a member of T-helper 1 lymphocyte chemokines produced and released in response to stimulation by infiltrating monocytes, macrophages, and endothelial cells.7 These cells subsequently bind to the T-lymphocyte-expressed CXCR3 receptor, essential for T-lymphocyte trafficking into SLE patients’ afflicted organs.8 IP-10 levels are significantly higher in the acute phase of SLE.9 Additionally, SLE treatment modalities such as prednisolone, mycophenolate, and hydroxychloroquine significantly lower serum IP-10 levels.10
The goal of this study is to use clinical manifestations, routine laboratory examinations, and more specific protein examinations such as sBAFF, BAFF-R, and IP-10 to predict SLEDAI 2k score following pulse-dose MEP, given that the spectrum of clinical manifestations and response to treatment varies from patient to patient.
