Ingested IFN-alpha preserves residual beta cell function in type 1 diabetes. J Interferon Cytokine Res 2001 Dec;21(12):1021-30
Date
01/19/2002Pubmed ID
11798459DOI
10.1089/107999001317205141Scopus ID
2-s2.0-0035701950 20 CitationsAbstract
Type 1 diabetes mellitus is a chronic disorder that presumably results from an autoimmune destruction of the insulin-producing pancreatic beta cells. The therapeutic potential of interventions aimed at preventing type 1 diabetes can be assessed in newly diagnosed patients. Because there is a historical experience of a low incidence of spontaneous remission in type 1 diabetes mellitus, interventions preserving beta cell function have been used to identify positive therapeutic outcomes. We treated 10 newly diagnosed type 1 diabetes patients with 30,000 IU ingested interferon-alpha (IFN-alpha) within 1 month of diagnosis and examined the difference between baseline and Sustacal-induced (Mead Johnson Nutritionals, Evansville, IN) C-peptide responses, respectively, at 0, 3, 6, 9, and 12 months. Eight of the ten patients showed preserved beta cell function, with at least a 30% increase in stimulated C-peptide levels at 0, 3, 6, 9, and 12 months after initiation of treatment. There was no discernible chemical or clinical toxicity associated with ingested IFN-alpha. Our results support the potential of ingested IFN-alpha to preserve residual beta cell function in recent onset type 1 diabetes mellitus and the testing of IFN-alpha in a placebo-controlled trial.
Author List
Brod SA, Atkinson M, Lavis VR, Brosnan PG, Hardin DS, Orlander PR, Nguyen M, Riley WJAuthor
Staley A. Brod MD Professor in the Neurology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Administration, OralAdolescent
Adult
Autoantibodies
C-Peptide
Cells, Cultured
Child
Cytokines
Diabetes Mellitus, Type 1
Humans
Insulin
Interferon-alpha
Islets of Langerhans
Kinetics
Treatment Outcome
