Marked Different Responses of rhIGF-1 and Steroid Therapy in Two Patients with Type B Insulin Resistance Complicated by Systemic Lupus Erythematosus

Abstract

Type B insulin resistance syndrome is an autoimmune disease caused by anti-insulin receptor autoantibodies and is frequently accompanied by other autoimmune disorders. The choice of treatment modality may thus be difficult in these patients. We report two patients with type B insulin resistance syndrome associated with systemic lupus erythematosus (SLE), whose responses to therapeutic agents differed markedly. Case 1: A 50-year-old Japanese woman with a SLE activity index (SLEDAI) score of 10 had her hyperglycemia treated successfully with recombinant human IGF-1 (rhIGF-1) (10 mg/day), but not even high dose of insulin were effective. Anti-insulin receptor autoantibodies and SLE activity may be dramatically decreased by SLE therapy with prednisolone (30 mg/day). Case 2: In contrast, a 59 year-old Japanese man with a SLEDAI score of 26 had hyperglycemia resistant to IGF-1 therapy, as were anti-insulin receptor autoantibodies and SLE activities to prednisolone. Only intensive immunosuppressive therapy with cyclophosphamide and cyclosporine A was effective in reducing SLE activity, high plasma glucose, and anti-insulin receptor autoantibody titers. The clinical courses of these two patients are highly indicative of differences considering the choice of therapeutic modalities for type B insulin resistance syndrome associated with other autoimmune diseases.