title: The reduction of serum B-lymphocyte activating factor levels following quinacrine add-on therapy in systemic lupus erythematosus.
abstract: B-Lymphocyte-activating factor (BAFF/BLyS) is a survival factor for B cells, belonging to the tumor necrosis ligand super family. Serum BAFF levels have been found to be elevated in patients with systemic lupus erythematosus (SLE). Neutralization of BAFF activity was suggested as an additional therapeutic approach in SLE. To determine the effect of add-on Quinacrine (Qn) treatment on serum BAFF levels and the effect of this treatment on SLE disease activity index (SLEDAI), antidsDNA and anticardiolipin (aCL) antibody levels, we treated 29 stable SLE patients, who were maintained on prednisolone and hydroxychloroquine and in some on azathioprine (AZT), with additional Qn (100 mg/d) with an aim to further reduce disease activity. SLEDAI, antidsDNA, aCL antibodies and serum BAFF levels were assessed before and 3 months after the addition of Qn. Three months following Qn initiation, a reduction in SLEDAI was noticed in 19/29 patients (mean 8.8 +/- 2.3 to 3.3 +/- 1.5, P = 0.009), followed by reduction or discontinuation of prednisolone in all patients and the discontinuation of AZT in five patients. Serum BAFF levels were significantly reduced in 8/12 patients (mean 6.3 +/- 0.5 to 3.0 +/- 0.56 ng/ml P = 0.0001). This reduction was found in correlation with a decrease in aCL titres. However, the decrease in SLEDAI scores and antidsDNA antibody titres was unrelated to the decrease in serum BAFF or aCL levels. We conclude that the addition of Qn to previous therapeutic regimens in active SLE is beneficial and seems to reduce SLEDAI scores, serum BAFF and aCL levels and therefore should be considered in many of our SLE patients before aggressive treatments are given.
authors.affiliation: Division of Clinical Immunology and Allergy, Bnai-Zion Medical Center, Haifa, Israel. elias.toubi@b-zion.org.il
authors.forename: E
authors.initials: E
authors.lastname: Toubi
authors.forename: A
authors.initials: A
authors.lastname: Kessel
authors.forename: I
authors.initials: I
authors.lastname: Rosner
authors.forename: M
authors.initials: M
authors.lastname: Rozenbaum
authors.forename: D
authors.initials: D
authors.lastname: Paran
authors.forename: Y
authors.initials: Y
authors.lastname: Shoenfeld
mesh_terms: D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000032:analysis*; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001379:Azathioprine / Q000627:therapeutic use; D053264:B-Cell Activating Factor; D016022:Case-Control Studies; D004359:Drug Therapy, Combination; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D006886:Hydroxychloroquine / Q000627:therapeutic use; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D008297:Male; D008565:Membrane Proteins / Q000097:blood*; D008875:Middle Aged; D011239:Prednisolone / Q000627:therapeutic use; D011796:Quinacrine / Q000008:administration & dosage / Q000627:therapeutic use*; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha
chemical_list: D017153:Antibodies, Anticardiolipin; D018501:Antirheumatic Agents; D053264:B-Cell Activating Factor; D008565:Membrane Proteins; C505719:TNFSF13B protein, human; D014409:Tumor Necrosis Factor-alpha; D006886:Hydroxychloroquine; D011239:Prednisolone; D011796:Quinacrine; D001379:Azathioprine