Type 1 diabetes patients did not benefit from isoform of glutamic acid decarboxylase

Ludvigsson J. N Engl J Med. 2012;366:433-442.

Issue: March 2012

Stimulated C-peptide levels demonstrated similar declines in patients with type 1 diabetes who were treated with alum-formulated 65-kD isoform of glutamic acid decarboxylase and patients treated with placebo, according to recent findings.

The study was conducted based on the hypothesis that alum-formulated 65-kD isoform of glutamic acid decarboxylase can preserve beta-cell function in those with recent-onset type 1 diabetes.

There were 334 participants aged 10 to 20 years evaluated in the study. Eligibility criteria included type 1 diabetes, fasting C-peptide levels of more than 0.3 ng/mL (0.1 nmol/L) and detectable serum 65-kD isoform of glutamic acid decarboxylase autoantibodies.

One of three treatment regimens was assigned randomly to study participants within 3 months of diagnosis. Those regimens included four doses of alum-formulated 65-kD isoform of glutamic acid decarboxylase, two doses of the alum formulation followed by two doses of placebo, or four doses of placebo.

The primary outcome measure was the change in the stimulated serum C-peptide level (after a mixed-meal tolerance test) from baseline to 15-month evaluation. Glycated hemoglobin level, mean daily insulin dose, rate of hypoglycemia, and fasting and maximum stimulated C-peptide levels constituted the secondary outcome measures.

Results indicated that all study groups experienced a similar decline in stimulated C-peptide levels. Fifteen-month results indicated no significant differences between study drug groups and the placebo group with regard to the primary outcome measure (P=.10). Insulin dose, glycated hemoglobin level and hypoglycemia rate also were not affected by the use of the study drug.

There were also no significant differences in the adverse event profiles, with infrequent and mild events reported in all three groups.

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