Assessment of immune response during chrysotherapy. Comparison of gold sodium thiomalate vs. auranofin

• Published in: Scandinavian journal of rheumatology Vol. 10; no. 2; p. 129
• Main Authors: Lorber, A, Jackson, W H, Simon, T M
• Format: Journal Article
• Language: English
• Published: England 1981
• Subjects: Arthritis, Rheumatoid - drug therapy; Arthritis, Rheumatoid - immunology; Auranofin; Aurothioglucose - analogs & derivatives; Aurothioglucose - blood; Aurothioglucose - therapeutic use; Female; Gold - analogs & derivatives; Gold Sodium Thiomalate - blood; Gold Sodium Thiomalate - therapeutic use; Humans; Immunoglobulins - analysis; Lymphocyte Activation; Lymphocytes - immunology; Lymphocytes - ultrastructure; Male; Microscopy, Electron, Scanning; Phosphines - blood; Phosphines - therapeutic use; Rheumatoid Factor - analysis; Skin Tests
• ISSN: 0300-9742
• DOI: 10.3109/03009748109095285

Auranofin (AF) differs significantly from gold sodium thiomalate (GST) in formulation, i.e., aurous gold is stabilized by dual sulfur and phosphorus ligands, has hydrophobic rather than hydrophilic characteristics, and lacks ionic charge. These attributes facilitate: oral absorption of AF, plasma membrane penetration, increase in intracellular lymphocyte gold concentration and perhaps thereby influence lymphocyte function. AF therapy was observed to affect primarily T rather than B lymphocyte function in 16 RA subjects receiving 6 mg of AF per day for an average of 45 weeks (range 20-74 weeks) compared with GST-treated RA subjects. Lymphocytes from AF-treated subjects manifested prompt and sharp declines in mitogen-induced lymphoproliferative response (LPR); suppressed response to skin testing with dinitrochlorobenzene (DNCB); and blebbing of lymphocyte membranes as shown by scanning electron microscopy. Suppression of LPR with AF was approximately 60% after the first week and 80% after 20 weeks of therapy, contrasting with 0% and 30% for the respective intervals in GST-treated subjects. DNCB skin testing of AF patients, indicated 11 of 14, failed to respond, whereas all GST patients responded. Local or systemic fungal, bacterial and/or opportunistic infections were not encountered. The effect of AF on B cell effector function, e.g., suppression of immunoglobulins and rheumatoid factor titer, was less marked when contrasted with GST therapy in RA subjects, as previously reported.