Linagliptin also significantly reduced FPG
levels relative to placebo (table II)'9.iO-53] and was
associated with a significant (p< 0.0001) improvement
in 2-hour PPG in one trial (adjusted
mean change from baseline of -1.9mmol/L
with linagliptin [n = 67 évaluable] vs -1-1.4 mmol/L
with placebo [n = 24]; between-group difference
-3.2 mmol/L; mean baseline values were 14.3 and
13.5 mmol/L)."!
Consistent with the improvements in glycaemic
control seen with linagliptin, the proportion
of patients who required rescue therapy
was up to 2-fold lower with linagliptin than with
placebo (10.2% vs 20.9%, p = 0.0002;"' 11.6% vs
'53!
The beneficial effects of linagliptin monotherapy
on glycaemic control were maintained during longerterm
treatment. In a 34-week extension'*^' of an
18-week trial,'^^' HbAi^ levels remained stable in
patients who continued to receive linagliptin
monotherapy (n= 137) [7.4% at week 52 vs 7.5%
at week 18]. Patients who had received placebo
during the initial 18-week study were switched to
glimepiride 1 mg/day (uptitrated to a maximum
of 4mg/day); HbAj^ levels in these patients (n = 64)
fell from 8.0% at week 18 to 7.2% at week
5.1.2 Versus Voglibose
Monotherapy with linagliptin 5 mg once daily
provided significantly better glycaemic control
than voglibose monotherapy over 26 weeks of
treatment in Japanese patients with type 2 diabetes,
as evaluated by the adjusted mean change
from baseline in HbAi^ (table 11).''°' However,
the two treatments did not significantly differ with
regard to the proportion of patients who achieved
an HbA|c level of