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Decreasing postprandial C-peptide levels over time are not associated with long-term use of sulphonylurea: an
A Nybäck-Nakell1, J Bergström, U Adamson
1Karolinska Institute, Department of Clinical Sciences, Division of Medicine, Danderyd Hospital, 182 88 Stockholm, Sweden. asa.nyback-nakell@ds.se
Aim:
The present study aimed to describe changes over 10 years in HbA(1c) and beta-cell function, as assessed by postprandial C-peptide (PP-CPT) and C-peptide/glucose (PP-CPT/glucose) ratio, and to investigate whether treatment with sulphonylurea (SU) exerts a deleterious effect on beta-cell function.
Methods:
During 1997-1998, HbA(1c), PP-CPT and PP glucose were measured in 462 patients. Ten years later, 171 of the 341 patients who were still alive were followed-up.
Results:
HbA(1c) decreased from 7.41 to 6.96% (P=0.002) as treatments were intensified. There was a decrease in both PP-CPT (P<0.001) and PP-CPT/glucose ratio (P=0.063). A multivariable-regression model was used to evaluate the effects on beta-cell function changes, using the following variables as effect modifiers: gender; age; BMI; diabetes duration; baseline PP-CPT/glucose ratio; HbA(1c); GAD-antibody class; and SU treatment (continuously, periodically, never). Baseline PP-CPT/glucose ratio was the most important variable (R(2)=45%; P<0.001) for explaining variations in beta-cell function. An increase in HbA(1c) was associated with a decrease in beta-cell function, and beta-cell function remained unchanged if glycaemic control was improved. Long-term treatment with SU had no effect on long-term changes in beta-cell function (R(2)=0.1%; P=0.894).
Conclusion:
Both HbA(1c) and beta-cell function decreased over 10 years with SU treatment, but such treatment was not associated with a pronounced decline in beta-cell function. These results, however, need to be interpreted with caution, as this was an observational study. Nevertheless, the present study findings do not support the notion that SU, as used in clinical practice, is harmful to beta-cell function.
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