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Ingested IFN-alpha preserves residual beta cell function in type 1 diabetes. J Interferon Cytokine Res 2001 Dec;21(12):1021-30

Date

01/19/2002

Pubmed ID

11798459

DOI

10.1089/107999001317205141

Scopus ID

2-s2.0-0035701950   20 Citations

Abstract

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 WJ

Author

Staley A. Brod MD Professor in the Neurology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Administration, Oral
Adolescent
Adult
Autoantibodies
C-Peptide
Cells, Cultured
Child
Cytokines
Diabetes Mellitus, Type 1
Humans
Insulin
Interferon-alpha
Islets of Langerhans
Kinetics
Treatment Outcome