Faculty Collaboration Database

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 (requires institutional sign-in at Scopus site)   21 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

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